Cattle - Diseases & Conditions
This presents some information about the more important diseases affecting cattle in the U.K.. It is not comprehensive and always seek veterinary advice about any disease affecting your stock.
LEFT-SIDED DISPLACEMENT OF THE ABOMASUM
A disease which occurs mainly, although not exclusively, in high producing dairy cows during the first 6 weeks of lactation.
AETIOLOGY
Abomasal( 4th stomach) motility is known to be reduced when cattle are fed a diet with a high fat and/or high protein content and once the abomasum becomes hypotonic it will become distended with food material and gas. It has been suggested that the abomasum moves forward and to the left under the rumen during late pregnancy when the gravid uterus causes the rumen to lift slightly from the abdominal floor, and then becomes trapped when the rumen re-expands after calving. A secondary acetonaemia usually develops.
Concentrate feeding and lack of exercise are also important factors in the aetiology.
CLINICAL FINDINGS
In the period following calving (may vary from a few days to weeks) there will be a selective anorexia (roughage eaten, concentrates refused), accompanied by a marked drop in milk yield and a ketotic smell from the breath, milk and urine
Rectal temperature, cardiovascular and respiratory findings are all within the normal range. Quite often a concurrent septic focus may be detected e.g. mastitis/metritis/lameness etc.
Rumenal movements are reduced in frequency and strength and faecal output is reduced and slightly soft, but in some cases intermittent profuse diarrhoea may occur
The displaced abomasum can be heard on the left flank, usually between the ninth and twelfth ribs over the upper two thirds of the abdominal wall. Abomasal sounds are typically high pitched with tinkling and splashing sounds which are often peristaltic; these sounds may be heard spontaneously or after gently ballotting the lower part of the abdomen in that area.
These sounds often disappear if an animal is moved and great care must be taken to conduct a thorough examination before a diagnosis of left sided displacement of the abomasum is ruled out, in some cases it may be necessary to re-examine the cow the next day.
TREATMENT
On diagnosis of a left abomasal displacement in a dairy cow three options are open to the veterinary surgeon:
- Conservative treatment e.g. rolling
- Surgical correction
- Cull.
Conservative treatment is often employed as an initial treatment and if this fails then surgery is performed. The technique of rolling is used often but the majority of cases recur. The cow is cast on her right side and rolled on to her back. At this stage the abomasum normally tends to move towards its correct position, and can be ballotted over midline. The cow is then rolled on to her left side and the abomasum can be percussed over the right flank. She should remain in left lateral recumbency for several minutes. After rolling, the animal should be encouraged to eat as much roughage as possible.
Culling should be considered if the cow had been marked for cull in the near future for some other reason eg. mastitis; old age; poor feet. Also if the animal has had a reduced milk yield for a long period prior to examination then even if surgery is performed she will be unlikely to perform well in that lactation.
However in almost all cases surgical correction should be the first option if economically viable. Many cows which have been successfully treated conservatively have a recurrence of the condition in the subsequent lactation and surgery should be considered. The earlier after diagnosis that surgery is performed the better the likelihood that the cow will perform to her potential in that lactation.
RIGHT-SIDED DILATATIONS and TORSION OF ABOMASUM
Cases of right-sided dilatation and torsion of the abomasum are very much less common than cases of left-sided displacement
Prognosis in cases of right-sided dilatations of the abomasum should be very guarded as often by the time veterinary advice is called for torsion has occurred with the cow in shock close to death.
Right-sided dilatations very frequently become torsions. Some cases do however resolve spontaneously.
If a torsion is suspected slaughter is the best option available. If dilation without actual torsion then surgical correction is worthwhile.
ABOMASAL ULCERATION
A condition of adult cattle and calves which may result in severe gastric bleeding sometimes accompanied by perforation which may be fatal, or, more commonly, a chronic syndrome with minimal bleeding and indigestion.
PREDISPOSING FACTORS
These have always been thought to be similar to those responsible for the development of displacement, dilatation and torsion of the abomasum, and this may be true for the chronic form. However, the acute form of the disease is seen in dairy cows at grass, mature bulls following transport and/or surgery, yearling feedlot cattle, and young (under 4 months) part-fed and single suckled calves. In young calves the problem appears to be related to the introduction of solid feed, and occasionally to the presence of abomasal hair-balls.
CLINICAL SIGNS
Acute haemorrhagic form In this form the animal may die within 24 hours of first becoming anorexic. The milk yield is drastically reduced, increased heart rate, ruminal stasis and blood in faeces are present. If the ulcer perforates and acute peritonitis develops, the animal goes into shock and dies rapidly.
Chronic form this form often follows a sub-acute haemorrhagic incident which lasts for about 5 days, with scant, blackish tarry faeces accompanying the other clinical signs of anorexia, reduced milk yield etc. Similarly few perforations are fatal as they are walled off by omental adhesions and localised peritoneal reaction. If perforation has occurred in the chronic form there is intermittent pyrexia, otherwise the clinical signs of chronic abomasal ulceration are reduced appetite, reduced milk yield and intermittent diarrhoea.
Many calves which have abomasal ulceration show no signs of illness.
DIAGNOSIS
The clinical signs and history together with the presence of blood in the faeces are usually sufficient in the bleeding cases. When blood is not in the faeces diagnosis can be difficult and other conditions need to be considered.
PROGNOSIS
The prognosis in the acute form is hopeless, and in the chronic form, although a transient improvement is sometimes seen following treatment, the animals usually relapse and are thus uneconomic to keep.
TREATMENT
In acute cases in valuable animals fluid therapy and blood transfusions may be attempted but the success rate is low
In chronic cases the use of oral kaolin and pectin together with magnesium oxide (to act as an antacid) are often used but the improvement seen is usually only transient.
Surgical removal is usually impractical as the ulcers are usually multiple and widespread.
PREVENTION OF ABOMASAL DISEASE
As most abomasal conditions are diet-related in high yielding dairy cattle the following are probably important in giving advice to farmers who have a problem.
1. Feed good quality roughage
2. Feed concentrates
3. Allow cows in early lactation sufficient exercise.
KETOSIS (Acetonaemia, Slow Fever)
A disease of ruminants which is the result of a failure to metabolise carbohydrate and volatile fatty acids, and characterised by high blood ketone and low blood glucose levels, and which is seen mainly in high producing dairy cattle in the first two months of lactation.
All high yielding dairy cows are in a negative energy balance in early lactation and are, therefore, biochemically if not clinically ketotic. This is biochemical ketosis can be readily made a clinical ketosis by relatively minor dietary or metabolic problems, when the demands for energy exceed that available from normal glucose and glycogen sources and liver gluceneogenesis results in a rise in ketone body formation which exceeds that normally tolerated.
Any increase in dietary protein intake will exacerbate the problem by using energy for its own metabolism and excretion.
Many theories have been put forward in an attempt to find causal factors. The conclusions reached are that ruminal flora are important and abnormal ruminal conditions may play a part in the development of clinical ketosis and that silage is potentially more ketogenic than hay.
EPIDEMIOLOGY
Ketosis is seen in dairy cattle especially during the winter housing period. The incidence in the UK is estimated to be between 1 and 5% of all dairy cows but the economic loss is probably underestimated because it is non-fatal, and there are production losses both during the disease itself and its effect on the subsequent yield in that lactation. The economic effect of subclinical ketosis may be almost as severe as that of the clinical disease.
In addition to the primary disease, ketosis may occur as a complication in some deficiency diseases, especially cobalt; and in other conditions where inappetence has resulted.
CLINICAL FINDINGS
1. The ‘wasting* form.
A gradual reduction in appetite with selective anorexia (concentrates refused, roughage eaten) and a concomitant reduction in milk yield over several days.
Weight loss may be quite dramatic over this period. Faeces are firm and dry, ruminal movements are reduced in frequency and intensity, and the cow appears depressed. Temperature, cardiovascular and respiratory parameters are all within the normal range. There is a smell of ketosis in the breath and in the urine. Sometimes the appetite becomes depraved and occasionally transient nervous signs (usually staggering) are seen. The wasting form will recover spontaneously without treatment but as this takes about 4 weeks the production losses are great and animals are treated as a matter of course.
2. The nervous form
The nervous signs are bizarre and of sudden onset, often occurring between periods of apparent normality. The cow appears delirious, walks in circles, crosses her legs, leans on objects and has licking and chewing mamas either involving herself or adjacent inanimate objects and can often be seen chewing concrete steps or tubular cubicle divisions. They also have a depraved appetite, make chewing movements and salivate profusely, become hyperaesthetic and very noisy when stimulated. Self-inflicted trauma is not uncommon in the nervous form of the disease.
DIAGNOSIS
Clinical signs and history, together with the exclusion of other conditions to which the ketosis might be secondary, e.g. left displacement of the abomasum are usually adequate. Blood tests can be useful.
TREATMENT
Intravenous glucose produces a rapid response in all cases and is essential in nervouscases, but unless repeated most cases will relapse. Oral glucogenic agents may be given e.g. propylene glycol or glycerine especially to the wasting* cases but ‘nervous* cases should be maintained on intravenous glucose until the nervous signs disappear.
Corticosteroids are of great value in maintaining the immediate response following intravenous glucose by stimulating gluconeogenesis, betamethasone and dexamethasone being the steroids of choice.
PREVENTION
1. Cows should be in the right condition at calving size - a body score of 3 to 3.5 is ideal.
2. Cows should not be steamed up, but fed once lactating at a slightly higher level than production, so called "lead feeding".
3. Good quality roughage should be fed and the protein content of the concentrate ration should not exceed 18%.
ACTINOBACILLOSIS (Wooden tongue)
DEFINITION
Actinobacillus lignieresi may cause lesions in the tongue, pharynx and its associated glands and in the stomach of cattle. Those in the tongue give rise to the syndrome "wooden tongue" in which inappetance and interference with swallowing occur.
INCIDENCE
Occurs sporadically, although several cases may occur on one farm in one year.
CLINICAL SIGN
It often appears to be of sudden onset, the affected animal has difficulty in swallowing and may be anorexic, excessive salivation is often seen. Swelling may be present under the jaw, particularly if the local lymph nodes are involved. Examination of the tongue is resented but if carried out, the base of the tongue is found to be thickened and fibrous. If inspection is possible, small discharging ulcers or swellings may be seen along the sides of the tongue. In chronic cases the tongue is shrunken and immobile and marked loss of condition occurs. In chronic cases lymph nodes may rupture to discharge thin yellowish pus.
Ulcers and nodules discharging pus have been recorded on the skin and infection within the rumen may give rise to abdominal pain or ruminal tympany.
EPIDEMIOLOGY
As A.lignieresi is part of the normal flora of the bovine body the initiating factor of the infection is important. Rough grasses, twigs or barley stalks may initiate the disease. Transmission to other cattle may occur if discharges from wounds contaminate pasture.
DIAGNOSIS
The clinical signs are fairly distinctive, but examination for foreign bodies and other causes of excessive salivation should be carried out. The cervical lymphadenitis is more difficult to differentiate, especially from other bacterial infections of these lymph nodes.
TREATMENT
Sodium iodide, sulphonamides e.g. sulphadimidine sodium, penicillin, streptomycin and tetracyclines can also be used and maybe more convenient, particularly in non-lactating animals. Five daily, intramuscular, doses of streptomycin is probably the commonest and most effective treatment.
CONTROL
Isolate animals with discharging lesions in order to prevent the contamination of feed with the discharges.
ACTINOMYCOSIS (Lumpy jaw)
DEFINITION
Infection with Actinomyces bovis most frequently occurs in the bones of the jaw to give "lumpy jaw". The resulting lesion may interfere with eating and eventually cause death by starvation. Infection may occur elsewhere in the gastrointestinal tract.
INCIDENCE
The disease is most common in mature cattle.
CLINICAL SIGNS
Most lesions are first noticed as a hard, painless swelling on the jaw bone level with the first molar or premolar teeth. They may enlarge rapidly in which case considerable pain may be present on palpation or grow only slowly. Soft tissue swelling may accompany the lesion. Lesions on the medial surface of the mandible may first be detected as a result of this swelling. Sinuses may erupt through the skin and discharge yellowish pus with hard ‘sulphur granules*. Enlargement of the lesions may lead to difficulty eating and breathing and progressive emaciation over a period of months.
DIAGNOSIS
The bony lesions are characteristic and diagnosis of lesions on the exterior of the jaw bone is easy. Medial lesions and the accompanying swelling must be differentiated from the reaction to material jammed in the teeth and other causes of lymphadenitis. When discharging sinuses are present, smears will confirm the cause but the organism may be difficult to isolate.
TREATMENT
Penicillin therapy repeated daily for 3-5 days may be effective as may the use of other antibiotics and the iodine treatment. Large lesions may require prolonged treatment and the bony changes may never resolve. In early cases complete remodelling of bone may occur and no trace of the lesion may remain. Many cases, especially those with secondary dental problems (tooth loss or loosening etc.) frequently lose weight rapidly and never respond to treatment.
CONTROL
The attention of stockmen should be drawn to the detection of early lesions.
ACUTE BRACKEN POISONING
Bracken fern (Pteridium aquilinum) contains a radiomimetic toxin and ingestion of the plant by cattle produces a syndrome characterised by haemorrhage, dullness and fever which is usually fatal.
PREVALENCE
The disease occurs sporadically, associated with a low morbidity, but high mortality. Except in calves under six months of age, in which the disease is unusual, acute bracken poisoning occurs in all ages of cattle, although the peak incidence is in young cattle aged between 1 and 3 years.
There is seasonal incidence of the disease with the majority of cases occurring in the early summer (late June - mid July) and in the autumn (late August - end of October), the disease being linked to the availability of adequate pasture. However situations do arise in which acute bracken poisoning can occur at other times in the year under certain managemental systems, e.g. where bracken is cut and used as bedding material as is the case in some areas of Wales and the Lake District
AETIOLOGY AND PATHOGENESIS
Acute bracken poisoning is caused by ingestion of large quantities of bracken fern (Pteridium aquilinum). Both the fronds and the rhizomes are toxic, whilst growing or when cut, and it also retains its toxicity when dried. The disease does not usually appear until the animals have been on bracken infested pasture for at least a month.
CLINICAL SIGNS
The clinical picture of acute bracken poisoning is dominated by three signs, ie. haemorrhage, dullness and fever.
Occasionally, among a group of animals acute bracken poisoning may present as a sudden death, but usually they present as extremely dull animals. The disease is characterised by multiple haemorrhages, especially in the intestinal and urinary tracts. Often frank blood clots appear in the faeces and at the nostrils. Blood in the urine is common. Severely affected animals are weak and may have a staggery gait. There is a high fever usually with complete ruminal stasis and inappetance. If treated roughly, subcutaneous bruising often appears. Death occurs within a week in untreated animals.
DIAGNOSIS
Diagnosis is based on the clinical signs and history of grazing bracken infested pasture. Blood tests are extremely useful when there is any doubt as to the diagnosis.
TREATMENT
Treatment is often ineffective and the prognosis is poor. Affected animals should be given high doses of antibiotics (penicillin, streptomycin) over a prolonged period, in an attempt to limit or prevent the secondary septicaemia from which many of the animals die. They should be handled gently and removed if possible, from the bracken pasture. If not, then their diet should be supplemented with hay/concentrates. Blood transfusions may be carried out on individual animals, but are seldom successful. Many other treatment regimes have been proposed, but are either useless or of extremely doubtful efficacy.
CONTROL
- Avoid use of bracken infested pastures at time of greatest risk, i.e. when grazing is in short supply.
- Feed supplements (hay/concentrates) when grazing of bare-infested pasture is unavoidable.
- Avoid overstocking of infested pastures.
- Reduce the level of bracken contamination by cutting or burning. However regrowth in the next season will occur and it does nothing to eradicate the plant.
- Spray bracken with a selective herbicide. Unfortunately this method of eradication can be quite expensive and costs will vary, depending on the method of application. Also, the kill out of the plant is not 100% and in order to give complete control repeat treatments in the following two or three years of those areas which, have survived the initial spraying are necessary (possibly only by knapsack spraying). If these small surviving areas are not treated complete regrowth will occur over a period of years.
- Avoid using bracken as bedding material.
ACUTE MYCOTOXOCOSIS
A number of differing clinical syndromes are attributed to the ingestion of mycotoxins by cattle from a variety of feedstuffs, these include neurological conditions, haemorrhagic syndromes and fever with dermatitis. The condition usually affects adult cattle.
AETIOLOGY
Under certain conditions some fungi will produce potentially harmful toxins. This has been well demonstrated for a number of fungi.
EPIDEMIOLOGY
The conditions of feed storage under which production of mycotoxins may occur are not well understood, but appear to be widely variable. Some of the mycotoxins elaborated by fungi in grains e.g. maize are the result of overheating, whereas mycotoxin production in silage and brewers grains in Britain may be the result of cold weather conditions. Cases are usually restricted to cattle eating the particular feedstuff that is incriminated, although the problem may present as a mixture of the various clinical syndromes on the same farm.
CLINICAL SIGNS
1. The haemorrhagic syndrome. The clinical signs are dullness, decreased appetite, reduced milk yield, occasional hair loss, bloody diarrhoea and multiple small haemorrhages of the gums. The usual outcome is death.
2. The fever-itch-dermatitis syndrome. This is usually associated with silage feeding, although some cases may be seen in hay-fed cattle. There is a widespread dermatitis, which is often particularly severe over the head and neck, but can also involve all other regions. The animals are persistently fevered and there is no response to antibacterial therapy. Associated with the fever are increased heart and respiratory rate, and there may be widespread enlargement of the superficial glands. These animals may live for several weeks with a variable appetite, but there is a gradual loss of condition and many cases die. Complications inthis syndrome include mastitis, metritis and abortion. A milder form with localised hair loss over the head and neck and no fever has also been recorded, the animals usually recover.
3. Other syndromes heart problems, liver failure, neurological disorders and kidney problems have also been associated with incidents of suspected mycotoxicosis.
DIAGNOSIS
The demonstration of mycotoxins in feedstuffs is useful in diagnosis when suspicious clinical signs are seen. However, often the ‘toxic* feed has been consumed before sampling occurs, and the failure to demonstrate mycotoxins does not rule out the diagnosis.
BABESIOSIS (Red-Water)
A tick-borne disease of cattle caused in Britain by the protozoan Babesia divergens which penetrates and destroys red blood cells and is characterised clinically by fever, anaemia and red urine. Since the life cycle of Babesia divergens and the epidemiology of the disease are closely associated with the ecology of the tick, Ixodes ricinus.
Life Cycle and Ecology of Ixodes ricinusttle in Britain is Ixodes ricinus, and a constant high relative humidity such as is provided by rank matted vegetation is necessary for its survival. As this type of vegetation dies yearly it creates a dead matted structure which protects ticks from winter frost and summer desiccation. Such a bioclimate is only found in the rough hill and moorland grazing of the Borders, West Scotland, Wales, Ireland and S.W.England. Particularly suitable are areas of heather, tall grasses and fern.
I. ricinus has both anchoring and piercing mouthparts and all the stages, i.e., adults, nymphs and larvae, suck blood from a wide range of mammals and birds. In cattle, tick attachment occurs mainly in the region of the face, ears, axillae and inguinal regions.
Ixodes is a 3-host tick and the life cycle lasts 3 years. The adult female feeds for 14 days and drops to the ground to lay several thousand eggs after which she dies. The larvae which hatch from the eggs will feed for about 6 days in the following year; then they drop to the ground and moult to the nymphal stage. On the third year this stage feeds, again for about 6 days, drops off and becomes adult. All stages occur in the host simultaneously, with a predominance of larval stages in early spring and early autumn.
Although ticks may be found on livestock throughout the year two peak periods of activity occur, namely:
March-June - spring feeders*
August-November - ‘autumn feeders*
It is thought that ticks feed only once per annum and that there are two distinct populations of ticks, one active in spring and the other in autumn. In the Borders only spring feeders occur whereas in other tick areas, autumn feeders also occur.
Although the life cycle takes 3 years to complete, the larvae and nymph feed only for approximately 6 days and the adults for 14 days, i.e. a total of 26 days. Ixodes is thus a temporary parasite.
AETIOLOGY
The cause of bovine babesiosis in the U.K. is Babesia divergens. The life cycle of Babesia divergens may be divided into two distinct phases, in the tick and in cattle.
The infective stages from the feeding tick enter the bloodstream, penetrate blood cells and divide to produce organisms lying near the edge of the red cell. Rupture of the parasitised blood cells follows and the released parasites enter other red cells and divide again.
PATHOGENESIS
The incubation period is usually between one and two weeks. During this period the parasitised blood cells are destroyed and anaemia develops. However, the subsequent anaemia is worsen by further destruction of affected blood cells by the bodies own immune system.
EPIDEMIOLOGY AND IMMUNITY
The epidemiology of outbreaks of babesiosis is related to: The availability of suitable tick habitats and the seasonal activity of ticks discussed earlier. Also important are the percentage of ticks infected and the immune status of the cattle.
The percentage of ticks infected under natural conditions is usually low but ticks will pass infection to their offspring resulting in a massive increase of infected larvae the next season.
The immune status of the host will vary according to age and previous exposure. Cattle brought into an endemic area are most at risk from the disease.
Young cattle born in endemic areas and infected as calves develop a parasitaemia but do not usually show clinical signs. The reason for this is not definitely known but may be due in part to antibodies absorbed from the cow through colostrum.In adult stock reared in endemic areas the immunity acquired as calves may be maintained either by a latent low grade infection or by repeated challenge which can lead to immunity with elimination of the parasite.
Where clinical babesiosis does occur in adult stock born and reared in endemic areas, this can be attributed to a breakdown in immunity due to massive challenge by infected ticks, stress, e.g. calving, intercurrent diseaseor a failure to develop immunity due to early treatment of a previous infection.
In summary, outbreaks of babesiosis are most likely to occur in areas of suitable bioclimate for ticks, i.e. hill or moorland grazing, at times of maximum tick feeding activity, i.e. spring or autumn; and stock over 2 years of age are principally affected.
CLINICAL SIGNS
The severe form of the disease which occurs in adults (over 2 years old) is characterised by sudden onset dullness, anorexia, reduced milk yield and ‘redwater*. On clinical examination there is fever, reduced or totally absent stomach movements, and anaemia. Haemoglobin released from the blood cells may be excreted in the urine and can colour it red. The severity of the anaemia may result in an impairment of cardiovascular function.
Other characteristic clinical findings are the ‘pipe-stem* faeces, caused by spasm of the anal sphincter in the early stages although constipation occurs later in the disease. Pregnant animals often abort. In animals in which the early stages of the disease are not recognised, recumbency is rapidly followed by death.
In yearlings the clinical signs are similar to those in adults but less severe and recumbency and death are rare.
In calves the condition often goes unrecognised as this age of animal often shows only vague inappetance and dullness and a transient fever.
DIAGNOSIS
This may be based on area, season, clinical signs and where necessary blood smear examination for presence of parasites.
TREATMENT
Currently in UK the only drug available for the treatment and prevention of bovine babesiosis is Imidocarb diproprionate, and there are special restrictions related to its use which must be observed. Where treatment is carried out early the prognosis is good. The haemoglobinuria should clear in 24 hours and if it persists treatment should be repeated.
PROPHYLAXIS
Apart from the prophylactic use of Imidocarb, this is based mainly on adequate tick control.
This may be accomplished by:
1) Pasture improvement to reduce the area suitable for tick habitations.
2) The application of acaricides to sheep and cattle at the time the ticks are feeding.
BACTERIAL ENDOCARDITIS
DEFINITION
An acute or chronic infection involving one or more of the heart valves and usually giving rise to heart failure spread of infection.
AETIOLOGY
Bacterial endocarditis very probably arises as the result of spread from infections elsewhere in the body.
Bacterial endocarditis is usually a disease of mature cattle.
CLINICAL SIGNS
The signs are those of heart failure, dull, inappetant animals, heart murmur, distension of the neck veins. Occassionally pneumonia or joint infections from the spread of infection. Fever is usually present.
Most cases of endocarditis die or are culled as poor prognosis cases within two weeks of first being seen to be ill. A small number may undergo a long duration illness associated with polyarthritis, intermittent dullness, fever and weight-loss.
DIAGNOSIS
Based upon clinical signs.
TREATMENT
None.
BLACKLEG (Blackquarter)
DEFINITION
Blackleg is an acute fatal disease of young cattle characterised by the development of swelling in the upper muscle masses of one or more limbs.
AETIOLOGY
Blackleg is caused by Clostridium chaevuoei.
PREVALENCE
This disease commonly occurs in Britain and throughout the world. It most frequently affects animals aged 6-24 months. The disease has a sporadic occurrence and in enzootic areas it may fail to occur for several years even when vaccination has been neglected.
EPIDEMIOLOGY
The condition is world wide in its distribution but tends to appear in definite areas, some of which may be localised to particular fields. The incidence in Britain can be quite high in certain areas where vaccination is not carried out. The disease most commonly occurs on permanent pastures during the summer and autumn months. It does not always require contaminated pasture and the disease can occur in housed animals. In areas where the disease has not been known to exist soil disturbances such as soil excavation or drainage can suddenly initiate outbreaks, probably by turning up, or by creating the conditions necessary for activation of latent spores.
The peak age incidence would appear to be 6-24 months, but younger animals or adults can be affected. Where Blackleg occurs in adult animals it is usually in areas of high incidence. The animals affected are frequently those in good condition and on a high plane of nutrition.
In untreated and unvaccinated groups of animals the mortality during an outbreak can be 10-25%.
CLINICAL SIGNS
At the beginning of an outbreak animals, frequently in good condition, may be found dead or severely ill with obvious subcutaneous swellings.
Affected animals are severely depressed and completely anorexic. Hot, painful swellings develop rapidly on the hindquarters, shoulders and neck, with the result that the animal becomes acutely lame. These swellings quickly become cold and painless. Later the overlying skin develops a parchment-like texture and on palpation, emphysema and crepitations can often be heard or felt. Frequently these lesions develop in the upper muscle masses of one limb only, but more than one limb may be affected. These signs are accompanied by a marked fever, an increased hearrt rate, and an increased respiratory rate. There is also a complete cessation of rumination.
Untreated, the disease is of short duration lasting only 12-36 hours and death usually occurs in less than 48 hours. Terminally the animal may collapse and exhibit muscle tremors or even convulsions. At this stage the temperature is likely to be subnormal. Treated animals which recover are often permanently lame and are culled because they are uneconomic.
PATHOGENESIS
Infection occurs by ingestion of the spores from contaminated pasture. Spores are absorbed passively through the gut wail and accumulate in the tissues where they remain dormant. Germination of resting spores occurs when the oxygen level of the tissues falls - as a result of injections, bruising, or, in fat animals, after heavy exertion resulting in muscle breakdown. The bacteria produce proteolytic enzymes and ferment carbohydrates to produce gas and acetic and butyric acids which give the lesions its characteristic appearance. Death results from the effects of bacterial toxins on the heart.
DIAGNOSIS
The clinical signs are sufficiently characteristic to allow an accurate clinical diagnosis, but can be confirmed by laboratory diagnosis.
PASTURE BLOAT
DEFINITION
This condition results from overdistension of the rumen by the normal gases of fermentation, which become trapped in the rumen contents and form a stable proteinaceous foam. Clinical signs develop soon after susceptible animals have been introduced to lush, legume-dominated pasture and severely affected individuals may be found dead.
AETIOLOGY
Pasture bloat occurs when the gas, which is normally produced by rumen fermentation, becomes trapped in the liquid contents. Foam does not stimulate the cardia to open and, consequently, gas does not pass into the oesophagus to be discharge by burping.
Substances which increase the viscosity of the rumen contents might result in gas bubbles being trapped in a viscous matrix and so slow down their rate of coalescence. Particulate matter (leaf fragments, chloraplasts, micro-organisms) is thought to be most important in this context. Soluble plant proteins are thought to be the major part of the surface active complex and all act as foaming agents. Tannins combine with and precipitate the proteins and there is a strong positive correlation between the absence of protein precipitants, e.g. tannins, and the tendency for a pasture to cause bloat. Recently in New Zealand, it has been claimed that low sodium in the herbage, giving a high potassium/low sodium ratio, increases the incidence of bloat.
EPIDEMIOLOGY
There is a high risk of bloat developing when cattle are given unrestricted access to pasture containing more than 50 per cent of bloat-inducing forage legumes. The bloat producing forage legumes include alfalfa (lucerne) and the clovers (red, white, sweet, alsike).
The peak incidence of disease occurs in the spring before flowering and on aftermath because it is the young growing plant that is most dangerous. However, alfalfa hay can still induce bloat, particularly if cattle are also being fed cereals. Jerseys are said to be more susceptible than Friesians or Ayrshires. The incidence of disease is higher in young cattle than in adults and those in good condition appear to be most susceptible.
CLINICAL SIGNS
Bloat usually develops from 2 to 3 days after initial exposure to a bloat-inducing forage. Because of the sudden onset of clinical signs and the relatively short course of the disease, susceptible individuals may be found dead. Initially, affected animals stand alone and look uneasy and uncomfortable; they may lie down, attempt to roil, stand up and bellow. At this stage there is obvious ruminal distension which quickly progresses to obvious abdominal distension with the drooling of saliva and mouth-breathing. Death usually occurs several minutes after the animal falls down.
The morbidity can be almost 100 per cent with up to 30 per cent severely affected with the others having abdominal distension. The mortality rate is low - less than 10 per cent.
DIAGNOSIS
This disease should be suspected when hungry cattle given unrestricted access to a lush pasture develop abdominal distension. In an animal which has been ~found dead3 the confirmation of frothy bloat is difficult and, consequently, other conditions, such as grass staggers, must be considered.
TREATMENT
Antifoaming agents reduce the surface tension of the rumen contents and allow the gas bubbles to coalesce and to escape by eructation. The drugs of choice are polyoxypropylene~polyoxyethylene (PPE) polymers which are water soluble, non-ionic and are not degraded in the rumen. When they are given by mouth, or preferably by stomach tube, they provide rapid relief and protection persists for about 12 hours. In Britain, poloxalene (Bloat Guard, *Agrimin) is given at the rate of 30-6Omls. Other treatments include vegetable and mineral oils (500m1), fats and synthetic detergents. Vegetable oils are degraded more quickly than mineral oils or detergents and will act for a shorter time unless given in large amounts.
PREVENTION
This is best attempted by the administration of anti-foaming agents or by pasture management.
Poloxalene at 10-12 g/day/adult should be given either in the food or in the water. When the risk of bloat is high, the dose should be halved and given twice daily. Oils can also be used either by oral dosing in the parlour, or by spraying on to the grass. However, relatively large quantities must be used because they are rapidly degraded.
Grass mixtures should have less than 50 per cent legumes and only non-bloating species should be used in high risk situations. Strip grazing and the feeding of supplementary roughage can also help to reduce the risk of pasture bloat.
GRAIN BLOAT
Grain bloat is associated with the feeding of large amounts (80% weight) of finely milled grain and small amounts of roughage. Occurs in beef and dairy cattle in feedlots.
Treatment is with Poloxalene - Oils.
FREE-GAS BLOAT
This is caused by an obstruction in the oesophageal lumen e.g. foreign body, or pressure from outside e.g. neoplastic lymph node which prevents burping of gas produced within the rumen. Inflammation of the rumen (chronic reticulitis) can also interfere with the normal rumenal contractions. Treatment is by stomach tubing to release the gas or by use of a trochar and cannula.
BOVINE PAPULAR STOMATITIS (BPS)
This condition, caused by a parapoxvirus is very common in Britain and other countries. It is characterised by lesions on the nose and in the mouth, and occasionally on the skin. Most cases have minor lesions which do not have any systemic effect on the animal, but in some debilitated animals, lesions in the mouth can become widespread and are then important in differential diagnosis from other diseases. All ages are affected but the young more commonly.
INCUBATION PERIOD
Uncertain. A calf can develop lesions by 7 days of age.
TRANSMISSION AND EPIDEMIOLOGY
Virus has been demonstrated simultaneously in pseudo-cowpox lesions on a cow*s teats, and in BPS lesions in the mouths of calves suckling the infected teats. Lesions have occurred in calves several months old which have had no direct contact with older animals, implying that infection might remain dormant in a calf for long periods. The condition is common where there is no contact with sheep, but it seems possible that an off infection might sometimes be the cause of BPS lesions.
INCIDENCE
The condition is very common and affects mainly calves but is by no means rare in older animals. Adult cows tend to have teat lesions rather than mouth lesions, but they may have both simultaneously or have mouth lesions alone. On examining a group of calves on one occasion it is likely that a small proportion will show lesions. If, however, the animals are examined repeatedly over a long period of time most are likely to show lesions at some time or other. On a farm where calves are seen to be affected it is very likely that some of the dairy cows will have teat lesions.
Individual minor mouth lesions are visible for a period of around 1-2 weeks. The mouth may be clear in that time but in a minority of cases successive crops of lesions may last for one to two months. Lesions may recur in an individual animal months or years later.
CLINICAL SIGNS
1. Mild cases
Lesions are confined to nose and mouth with very occasional involvement of the teats and there are no systemic signs of disturbance. Lesions can occur anywhere in the mouth but are more frequent in close proximity to teeth.
They are rounded or oval lesions, a few millimetres up to 1.5 cm in diameter with a peripheral red zone of congestion. Within the red zone is a narrow grey/white, often slightly raised, zone. The three zones do not always take a ring form but may be linear alongside the line of the molar teeth. In other sites lesions may not develop in a symmetrical circular form but an arc may extend and in such cases there may be no obvious central necrotic zone.
2. Severe cases
These are much less common than the mild form but they tend to occur when an animal is very debilitated from some intercurrent disease, e.g. parasitism in a calf. It is possible that they contribute to death of some animals, but it is impossible to estimate this accurately. Severe lesions tend to be diffuse and irregular in shape, slightly raised slightly roughened and of a yellow or grey colour. When they are most severe there is marked diphtheresis and some consideration may have to be given in a systemically ill animal to differential diagnosis from mucosal disease, foot-and-mouth disease and in some countries, rinderpest. On inspection of BPS cases it may be possible to find a discrete pathognomonic lesion away from the major lesions, and if the animal survives the mouth lesions regress, and it is then often possible to see an underlying basic circular form which may have been obscured a few days previously. Sometimes lesions become complicated by a secondary Fusobacterium necrophorum infection. Severe lesions are associated with wetness around the lips and the tongue may be tender to touch.
Circumscribed erosions and ulcers have been found in the skin between the hooves.
DIAGNOSIS
Many of the lesions are characteristic. It is not necessary to confirm diagnosis in mild cases, but in severe cases it may be important to do so.
BOVINE SPONGIFORM ENCEPHALOPATHY
DEFINITION
Bovine spongiform encephalopathy (BSE) is a recently recognised nervous condition of adult cattle. It was first recorded in the South of England in 1985 but has since been identified in all parts of the UK. The disease has an insidious onset with a varied spectrum of behavioural and locomotor disturbances. The clinical signs are progressive and the disease is invariably fatal. In the summer of 1988 BSE was made a notiflable disease.
EPIDEMIOLOGY
The condition was originally recognised in the British Isles. The incubation period is 2.5 - 8 years. The disease occurs in adult cows with a peak incidence between four and six years of age as a result of animals being exposed as calves. It has principally been identified in Friesian/Holstein cross cows, but this probably reflects the high numbers of this type of animal in the British dairy herd. It has also been identified in Ayrshires, Guernseys, Jerseys, Shorthorns and their crosses. There have been several cases in beef suckler cows. Pregnancy and lactation do not appear to influence the time of onset of clinical signs. The greater incidence in animals produced from the dairy sector is a reflection of concentrate feeding to the calves.
CLINICAL SIGNS
The disease has an insidious onset which usually begins with a subtle change in temperament. Increasingly abnormal behaviour, accompanied by progressive locomotor disturbances are characteristic of the disease.
Initially a farmer may notice that a previously quiet cow has become irritable and awkward to handle. For example the cow may be reluctant to enter the milking parlour and when it does it will often kick off the milk clusters. Abnormal behaviour includes repeated nostril licking, teeth grinding, attempts to scratch the head with hind cleats, rubbing against inanimate objects, aggression and general bullish behaviour. Locomotor disturbances include difficulty in rising, negotiating steps, tight corners or slippery surfaces. Ataxia, stiffness, paddling of the feet and hindleg hypermetria have also been recorded. Any attempts to handle or confine these animals e.g. by putting in a cattle crush usually amplify the clinical signs. There is usually evidence of trauma where cases have fallen over or rubbed themselves. Initially affected animals are often bright and eat well but latterly there is loss of condition and death is inevitable.
LABORATORY DIAGNOSIS
There is no laboratory test to confirm a diagnosis in the live animal. Laboratory investigations are only useful to rule out other possible diagnoses.
DIAGNOSIS
Not all cases of BSE will exhibit all the clinical features listed above, but as the disease is progressive, any clinical signs that are present will gradually become more marked. As such it may require more than one clinical examination to reach a provisional diagnosis of BSE.
The pathogenesis is still being investigated.
TREATMENT
There is no treatment and the disease is invariably fatal.
CONTROL
There is a compulsory slaughter policy in the U.K.
COLISEPTICAEMIA
This is a condition of colostrum deficient calves less than one week old. It has a sudden onset and affected calves almost invariably die.
AETIOLOGY
Particular serotypes of E.coli are associated with colisepticaemia.
INCIDENCE
The exact incidence of this condition is unknown, but the majority of calves which die during the neonatal period (i.e. during the first four weeks of life) die during the first two weeks of life, either as a result of colisepticaemia, or diarrhoea.
CLINICAL SIGNS
Many cases of colisepticaemia are said to be ‘sudden deaths", as when last observed the calf was seen to be well. However, careful stockmen will generally have noticed that the calf was dull, stiff and reluctant to rise and feed. Rapid deterioration and collapse then follow. Fever (1050F-40.50C) is frequently present but rapidly drops to sub-normal values as the animal collapses. Diarrhoea if present at all is scanty and a terminal event. In some cases, enlarged, puffy joint capsules may be seen and the occasional calf displays signs of central nervous system disturbance due to meningitis. Death ensues within 12 hours of the onset of clinical signs.
A small proportion of cases do not die but many of these subsequently suffer from arthritic lesions (joint-ill) and/or abscesses in the body tissues and organs, umbilicus, and, on occasions, the central nervous system.
EPIDEMIOLOGY
This is the classic condition of the calf which has been deprived of colostrum or has not absorbed colostral immunoglobulins (see neonatal calf diarrhoea).
DIAGNOSIS
Relatively sudden death in calves less than one week old which have a suitable epidemiological background, i.e. colostrum deficient and poor hygienic conditions may indicate a diagnosis of colisepticaemia.
TREATMENT
Because of the rapid onset and death of affected animals treatment is usually ineffective, even with massive doses of antibiotic.
CONTROL
This condition is easily controlled by increasing the concentrations of passively acquired colostral immunoglobulins in the serum of newborn calves.
NEONATAL CALF DIARRHOEA
Diarrhoea in calves during the neonatal period (i.e. the first four weeks of life) is very common. Various microbiological agents have been associated with the syndrome and the fate of affected calves is dependent on the severity of the biochemical changes. Diarrhoea caused by Salmonella is described under Salmonellosis.
AETIOLOGY
E.coli has been associated with neonatal calf diarrhoea since before the beginning of this century. Particular strains of E.coli are more effective than others at inducing disease. There are also numerous viruses and other microbiological agents that have been identified in diarrhoeic calf faeces; rotavirus, coronavirus, parvovirus, enterovirus, astrovirus, calicivirus, small cubic virus and a villous epithelial cell syncytia inducing virus. The two most important, and certainly most studied, viruses are rotavirus and coronavirus. Both these viruses will produce diarrhoea in colostrum-deprived calves, although strain differences do exist.
Among the other agents which have been associated with diarrhoea in neonatal calves, the small protozoan parasite of the genus Cryptosporidium is the most important.
The relative importance of E.coli, viruses and Cryptosporidium in the aetiology of neonatal calf diarrhoea has not been fully ascertained. E.coli are not often isolated from calves more than 10 days old, whereas rotavirus and coronavirus are mainly detected in the faeces of calves between 5 and 15 days old. These two viruses can be demonstrated in up to 60% of calves with diarrhoea.
INCIDENCE
Surveys of neonatal mortality are variable but figures of between 2% and 8% are not uncommon. It is suggested that approximately 50% of neonatal calf mortality is due to gastrointestinal associated conditions. This may represent 100,000 calves per annum being lost in the United Kingdom.
CLINICAL SIGNS
Only the clinical syndrome associated with E.coli is sufficiently distinct to enable an clinical diagnosis to be made with reasonable accuracy. Even then, confirmation by laboratory techniques would be required.
The syndrome produced by E.coli occurs in very young calves, usually less than 5 days of age and frequently as young as 24 hours old. The onset of the syndrome is very sudden, and the diarrhoea is very profuse, with a brownish-yellow colour. Affected calves can lose up to 15% of their bodyweight within 24 hours of the onset of diarrhoea. They quickly become dull, lethargic and dehydrated. Mortality rates can be very high among affected calves.
Generally, however, neonatal calf diarrhoea occurs mainly during the second and third weeks of life, but death occurs only in a proportion of affected calves. When death occurs it usually does so after three or four days of profuse diarrhoea, during which time there is marked loss of weight and increasing dullness. The faeces, which become progressively more fluid, rarely contain blood, and tend to impart a yellowish stain on the hindquarters and tail. If the diarrhoea continues calves become recumbent, or have great difficulty in rising and are very weak. Some calves become reluctant to feed early in the course of the condition, whereas others continue to take milk readily even after they become recumbent. Eventually, severely affected calves go into lateral recumbency and become comatose.
Cases which ultimately recover rarely reach the stage of recumbency although weakness, dullness and loss of weight are common. Although many such calves are diarrhoeic for several days, the faeces are usually less fluid than those of calves which ultimately die. In calves which recover, it is common to find that the hair is lost in those regions where faecal staining has occurred. Many calves which apparently recover from neonatal calf diarrhoea fail to grow as well as animals which have not been affected, and also appear to be more susceptible to pneumonia.
Calves which have died as a result of severe diarrhoea are severely dehydrated. If the illness has lasted for several days they are also very thin and have little perirenal fat. Many have a grossly distended urinary bladder, presumably due to the fact that calves do not urinate while recumbent.
PATHOGENESIS
The cause of death in severe neonatal calf diarrhoea is the severe depletion of fluid and electrolytes resulting from the diarrhoea. Briefly, in calves which are fed milk until death, diarrhoea results in a fall in plasma sodium and bicarbonate concentrations and in blood pH, whereas a rise is found in plasma urea and chloride concentrations. Plasma potassium concentrations are variable, but frequently are raised and myocardial potassium concentrations are consistently low. There is a fall in the plasma volume.
It is postulated that the diarrhoea results in metabolic acidosis which results in rapid respiration. As a result of acidosis, potassium is withdrawn from the heart muscle which results in terminal cardiac failure.
EPIDEMIOLOGY
Several major facts have emerged from epidemiological studies of calf mortality both in this country and North America, the most important of which is that although the feeding of colostrum to newborn calves does not guarantee survival, colostrum deprivation invariably results in death. Dairy calves first obtaining colostrum from a bucket have a higher mortality rate than similar calves which first ingest colostrum by suckling their dams. Calves born in byres have a much higher mortality rate than calves born in either yards, boxes or in the field. The mortality rate is highest in the first week of life and thereafter it decreases exponentially. The mortality rate in calves in a particular calf-house is directly proportional to the length of time that the building has been occupied by young calves. The mortality rate in dairy calves is at its highest between January and April each year. Ayrshire and Channel Island calves appear to be less resistant to neonatal disease than are Friesians. As the size of the adult cow herd increases, the mortality rate among the calves also increases. The mortality is higher, and the seasonal mortality pattern is much more marked, in Scotland than elsewhere in Great Britain.
Little is known about the situation in bought-in calves although it is known that currently at least one million calves are sold for rearing each year. Many such calves have to be freighted long distances to reach the rearing (i.e. northern and eastern) parts of the country and this entails frequent mixing of individuals during transit and at markets and holding centres. It has been shown that the mortality rate in these calves reaches a peak one week after arriving at their destination and that the mortality rate increases as calves travel northwards. However, it must be stressed again that no detailed investigation has studied the disease situation in these calves. The fact that many of them are two or three weeks of age when sold probably would tend to reduce the incidence of neonatal calf diarrhoea and other conditions such as salmonellosis and respiratory disease must obviously also be considered as possible causes of death.
IMMUNOLOGY
Precolostral calf serum is devoid of immunoglobulins and calves are dependent upon acquiring these immunoglobulins from colostrum which is usually a particularly rich source. After a feed of colostrum, immunoglobulins together with other whey proteins are absorbed through the intestinal epithelial cells of a calf*s intestine. Macromolecular absorption in newborn calves is remarkable for the speed and extent at which it proceeds, but the efficiency of absorption rapidly decreases after birth. The factors responsible for the cessation of macromolecular absorption in calves are not fully understood.
It has been found that wide variations exist in the serum immunoglobulin concentrations of colostrum-fed calves. Moreover, a direct correlation exists between a calf*s serum immunoglobulin concentration and that calf*s chances of survival. Many calves with little or no serum immunoglobulins die during the neonatal period, many of them from colisepticaemia, the rest from the effects of diarrhoea. With slightly higher concentrations colisepticaemia does not occur although deaths are still common as a result of diarrhoea. With higher serum immunoglobulin concentrations diarrhoea can occur but calves rarely die.
A very profound seasonal variation in the serum immunoglobulin concentrations of dairy bull and heifer calves has been found to occur in the west of Scotland with low mean values occurring between November and April of each year and high mean values between May and October. This seasonal variation is due to the different management techniques that summer and winter-born dairy calves are subjected to in this area. In the winter, most dairy calves are born in the byre and first obtain colostrum from a bucket whereas in the summer, most calves are born in the fields and first obtain colostrum by suckling their dams. Dairy calves which first obtain colostrum by suckling their dams usually absorb greater amounts of colostral immunoglobulins than do bucket-fed calves, hence the latter*s higher mortality rates.
The amount of immunoglobulin absorbed by a calf has been shown to be a function of first, the age when fed and second, the mass of immunoglobulin presented. The cessation of immunoglobulin absorption is now known to occur progressively from birth not suddenly at 24-30 hours after birth. This makes the timing of the first feed critical and the value of subsequent feeds of colostrum apparently of only marginal importance in relation to serum immunoglobulin levels.
DIAGNOSIS
In all outbreaks of neonatal diarrhoea, steps must be taken to eliminate the possibility of salmonellosis. Confirmation of one or other of the possible microbiological agents can be readily carried out by diagnostic laboratories
TREATMENT
Almost every available chemotherapeutic agent/antibiotic has been used in the treatment of neonatal calf diarrhoea at some time or other and most with very limited success. Most of the trials which have been carried out have been uncontrolled and few have considered the immune status of the call. The most frequently used treatment regimes consist of antibiotic therapy, combined with some form of food withdrawal and/or fluid replacement.
Fluid therapy has often been used in conjunction with antibiotics. It is clear that the electrolyte and fluid imbalance associated with neonatal calf diarrhoea is a complex disaster resulting in acidosis which, in turn, is probably responsible for death in that it initiates cardiac failure by depleting myocardial potassium. Any attempt at fluid therapy should be based upon a knowledge of the fluid and electrolyte status of a calf and should be administered under conditions of intensive care. Particular care is required in the correction of acidosis in the scouring calf.
The withdrawal of milk is frequently advocated as an adjunct to the treatment of diarrhoea. Certain proprietary preparations for oral replacement therapy contain appropriate ions and substances such as glycine, glucose and citrate to assist absorption of the electrolytes and are claimed to be of value.
CONTROL
The use of prophylactic antibiotics to control diarrhoea in home-bred calves can be expensive and frequently is not successful. It is the only course open to people purchasing calves for rearing although much of the trouble in these units can be prevented by delaying the purchase of calves until they are about one month old.
The control and subsequent prevention of disease in homebred dairy calves in a closed unit which is experiencing trouble should be based on those factors mentioned previously - reducing pathogen challenge and increasing the resistance of the calf.
Attempts should be made to increase the amounts of colostral immunoglobulin absorbed by each calf. In view of the fact that wide individual and possibly breed variations exist in colostral concentrations of antibody it is essential to feed as large a volume of colostrum as possible, which has no lasting ill effects on newborn calves. It is necessary to ensure that indoor calvings during winter occur in loose boxes or yards.In any case, the stockman must convince himself that a newborn calf has suckled to satiation (this may take 20 minutes) as early as possible.
Occasionally, despite precautions it is found that a calf with low serum imnmunoglobulin concentration has been produced. This is not due to an inability to absorb colostrum but is a result of either delayed feeding or ingestion of only a small quantity of colostrum. Some dams produce low volumes or concentrations of globulin and "pre-milking" or dripping markedly reduces the concentration of globulin from these quarters. The odd calf with a low serum immunoglobulin level is unlikely to experience diarrhoea if it is mixed with calves with much higher serum levels.
If, for some reason, box calving is not possible, then very large amounts of colostrum should be fed to calves as soon as possible after birth. It is usually possible to feed calves at one hour of age with up to five pints of colostrum. It is suggested that the stockman should be urged to feed up to six pints of colostrum as soon as possible after birth, but at least within the first 4 hours of life. This will not harm the calves although a transient diarrhoea and dullness will occur a few hours after ingesting such amounts. Even in such calves, the absorption of colostral immunoglobulin is very significantly increased if the calves are mothered.
Infection build-up cannot be ignored. Therefore, periodic disinfection should be practiced and calves should be kept in fairly small self-contained groups wherever possible. Obviously, bought-in calves constitute a major hazard to homebred animals and this practice is never consistent with the continued good health of homebred animals.
Other management factors should also be considered here. Newborn dairy calves probably thrive best at an ambient temperature in excess of 13C (550F). Single penning is desirable, not because it limits disease spread, but because the stockman tending the calves gets to know individual animals much more quickly. Successful calf rearing is a time consuming job demanding considerable expertise.
In order to increase the concentrations of specific antibodies to the microbiological agents associated with calf diarrhoea vaccination of the dams in the last few weeks of gestation has been investigated. Rotavec K99 is a vaccine currently available in the U.K. It raises antibody levels in colostrum against both E.coli and bovine rotavirus. Although still dependent on colostral transfer this vaccine gives good results if used appropriately.
However, it is the failure or partial failure in the transfer of colostral immunoglobulins from the cow to the calf that is a major contributory factor to the severity of neonatal calf diarrhoea. Thus increasing the level of specific antibodies in the colostrum is of limited value to a calf which fails to receive sufficient colostrum, at a time when its ability to absorb that colostrum is at a maximum.
SALMONELLOSIS
Infection with a number of serotypes of Salmonella spp. may give rise to a syndrome in which fever, diarrhoea (frequently with dysentery) and deaths occur in both calves and adults but, on occasions, in pregnant cows abortion may be the only overt clinical sign. The disease in cattle is a source of infection for man.
AETIOLOGY
S.dublin and S.typhimurium are the most common causes of bovine salmonellosis in Britain. Many other serotypes can cause disease. It should be remembered that all salmonellae may become pathogenic under the right conditions.
INCIDENCE
Salmonellosis is an important disease of cattle in Britain and throughout the world. The cost to the agricultural industry is not known but it has been claimed to be of major importance to calf rearers and is currently the second most commonly diagnosed cause of bovine abortion.
CLINICAL SIGNS
Salmonellosis can affect cattle of all ages but it is most frequently seen in adult cows and calves. The clinical signs for all serotypes are similar.
Adult cattle: Initially, in acute salmonellosis, there is rapid onset dullness and marked fever (40-41.50C) with inappetance and a dramatic drop in the milk yield of affected (dairy) cows. A severe diarrhoea ensues with foetid watery faeces which may contain blood, mucus and shreds or casts of necrotic bowel epithelium. Presumably as a result of this latter feature, abdominal pain is often noticed. Some
Calves: Calves of any age can be affected but it most frequently occurs between 2-8 weeks of age. The median age for S.dublin outbreaks is 4 weeks and for S.typhimurium it is 3 weeks.
Clinically the affected calves are very dull with marked lethargy. Unlike calves affected by colibacillosis which may continue to consume milk even when recumbent, calves with salmonellosis are usually completely inappetent. There is a marked fever, often as high as 41.50C with a profuse, evil-smelling diarrhoea. There may or may not be dysentery. Affected calves rapidly lose condition, become very weak, unable to stand and emaciated. Death occurs within 2-3 days of the development of clinical signs and the mortality can be as high as 30% and occasionally higher. In non-treated survivors the diarrhoea may persist for up to 2 weeks.
Following infection with S.dublin the development of gangrene-like lesions and osteitis of the extremities has been described with sloughing of the ear-edges, the tip of the tail and even the distal extremities of the limbs.
PATHOGENESIS
Infection usually occurs by the oral route. The source of organism is usually the faeces of an infected animal, whether clinically affected or a faecal carrier, although infected milk, uterine discharges and products of abortion may be important where infection occurs in adult cattle. Following ingestion, the organism may multiply within the gut. The organisms multiply within the gut wall and from there disseminate to the systemic circulation. Multiplication in the liver and blood stream gives rise to a septicaemia. The ability of Salmonella spp. to produce diarrhoea is largely associated with the invasion of the gut wall and the inflammatory reaction. In recovery the organism may become localised in joints, the foetus to give abortion, in the gall bladder or in other organs. Adult animals which have recovered from S.dublin infection may continue to excrete the organism in the faeces for several months (perhaps for life). Those which have recovered from S. typhinurium infection cease excreting organism after 6-14 weeks. Calves which have recovered normally cease to excrete the organism after a few weeks.
It is suggested that intercurrent disease such as fascioliasis (liver fluke) may predispose to infection.
EPIDEMIOLOGY
Host range. S.dublin infection does occur in species other than cattle but is primarily an infection of cattle. S.typhimurium can infect a wide variety of species and infections may originate from any of these including wild life.
SOURCES OF INFECTION
Although there are many possible ways by which susceptible cattle may acquire salmonella infection, the overwhelming evidence suggests that infection is most often acquired from other cattle which are excreting the organisms. For clinical disease to be established in cattle it would seem that challenge has to be relatively high.
1) Infection from other cattle. As stated above this is the most important source of infection with S.dublin and S.typhimurium. Infection may be introduced into a population of cattle either by the purchase of an adult carrier or by mixing, in market or in transit, with clinical or pre-clinical cases. Infection may pass from adults in a herd down to the calves or vice versa. Congenital infection of calves born at full-term does not appear to occur, but those calves born to cows which are faecal excretors almost invariably become infected either at parturition or soon after birth. Intensive husbandry systems, especially loose housing, have facilitated the spread of salmonella infection.
2) Infection from contaminated foodstuffs and water. Although the infection rate of cattle food constituents (e.g. bone, meat and blood meals and milk powders) can be high, surveys of the end-products (cattle and calf cakes or pellets) have shown a low incidence of infection and low counts of organisms.
The change to loose-housing has been associated with an increase in the volume of slurry for disposal. S.dublin may survive for up to 30 weeks in winter slurry, but the survival time on grass after being spread is much shorter. Survival in soil cores may be as long as 24 weeks. The recommendation to reduce the risk of spread of infection via slurry is: (1) storage of slurry for a minimum of 4 weeks; (2) pasture should not be grazed until 4 weeks after slurry spreading. There is at least one recorded outbreak of salmonellosis due to S.typhimurium occurring after slurry was spread on fields at a much higher rate than normal.
Outbreaks of salmonellosis have been attributed to cattle drinking contaminated water, effluent from knackeries, contamination of fields due to sewage overflow, or sewage sludge.
3) Infection from other domestic animals (and man). Few instances are recorded and often the primary source of infection is unknown. However, it is recorded that on a few occasions, Salmonella typhimurium infection has passed to cattle from chickens, ducks, geese, pigs and humans.
4) Infection from wild animals. Rats may allow a farm infection of S.typhimurium to persist. Only low infection rates in British farm rats have been recorded although in one case infected rat droppings in old hay were found to be the source of infection for beef cattle. Sparrows, starlings and seabirds have also been found to S.typhimurium rarely remain infected for any length of time and excretion of the organism usually only occurs for a few weeks.
Some animals which have recovered from S.dublin infection may become intermittent excretors. Animals which merely ingest the organism and excrete it in the faeces without becoming infected are referred to as passive carriers.
DIAGNOSIS
In calves, time of onset (3-4 weeks of age), the clinical signs of the disease - fever, depression, diarrhoea, sometimes with the presence of blood, the post-mortem findings and a history of recent purchase through markets may suggest a diagnosis of salmonellosis. In adults the clinical signs are also suggestive. Diagnosis must, however, be confirmed by the isolation of the organism.
TREATMENT
Affected animals should be treated by both the parenteral and oral routes with an antimicrobial drug. This is possible in calves but in adult ruminants many such drugs may disturb rumen flora if given orally. The same drug or class of drug e.g. an aminoglycoside should be given parenterally and by mouth as far as possible. Ampicillin, trimethoprim/ sulphonamide combination, neomycin, spectinomycin, enrofloxacin and sulphonamides are all available in injectable and oral forms. With drugs which can be absorbed from the gut, injections need only be given initially. Compounds available for oral dosing also include furazolidone and may be given as boluses, from oral dosers, or as soluble products for administration in drinking water or milk.
The drug of choice may be ampicillin, amoxycillin, enrofloxacin, trimethoprim/ sulphonamide (destroyed in functioning rumens) neomycin or furazolidone in that order. Antibiotic sensitivities of the salmonellae involved should be taken into account if treatment is unsuccessful or in continued outbreaks.
Calves do not usually become carriers following treatment but adults may, and disposal of adult cases to a secure rendering plant should be considered.
Careful nursing and management of individual calves is of great importance and the animals should be kept under lamps, turned regularly and fed several times daily until they improve. It is important to impress upon the person in charge of infected animals, adults or calves, the possibility of spread occurring to himself and his family and strict hygiene measures must be observed.
Prophylactic (oral) use of antibiotics should be discouraged as in most cases low levels of antibiotics have no effect on the excretion pattern of salmonellae. Indeed it has been shown in man that with non-invasive salmonellosis, antibiotics significantly increase the excretion period of the organism in the faeces.
CONTROL
Vaccines
Currently only multicomponent dead vaccines are available in the U.K. e.g. Bovivac (Hoechst). High serum concentrations of absorbed colostral immunoglobulins aid survival and reduce the severity of alimentary disturbance in calves with salmonellosis but, unless specific antibody to Salmonella is present cannot prevent infection.
Control measures which should be instituted during an outbreak of salmonellosis
Isolation of clinical cases to reduce the weight of contamination.
Recovered animals should be retained in isolation for at least 2 weeks after the cessation of diarrhoea.
Carcasses of fatal cases should be sent to knackeries capable of producing salmonella-free products.
Ideally, adult clinical cases of S.dublin infection should be slaughtered as recovered animals invariably remain persistent excretors.
Clinical cases should never be sent for emergency slaughter intended for human consumption.
Treatment of effluent in such a way as to minimise contamination of environment.
Following an outbreak the premises should be thoroughly cleaned and disinfected.
Restrict movement of animals either on to or off farm until final disinfection has been carried out.
FASCIOLIOSIS (liver fluke)
Fascioliosis in cattle occurs in the wetter western areas of the country but only in very wet years. The reason for the difference in severity of the disease between sheep and cattle would appear to lie basically in the fact that unlike sheep, cattle which have been previously infected with Fasciola hepatica acquire a degree of resistance to reinfection and also that the bovine liver appears to be able to tolerate the presence of very large numbers of developing immature parasites without the occurrence of the severe pathogenic effects seen in sheep. Outbreaks of acute and sub-acute Fascioliosis comparable to those seen in the sheep are therefore rare.
Bovine Fascioliosis is mainly a chronic disease, usually of calves or yearlings, which have spent their first autumn on infected pasture. Adult stock which have had previous experience of the parasite acquire an immunity and can withstand a heavy challenge from infected pastures without showing clinical disease. They may however harbour a small population of F.hepatica which could impair productivity.
The clinical signs are very similar to those seen in chronic Fascioliosis in sheep, namely loss of condition, marked anaemia and in severe cases submandibular oedema. Diarrhoea is not found in cases of chronic bovine fascioliosis unless they are complicated by the presence of Ostertagia spp, and this results in a different syndrome, the Fascioliosis-Ostertagiosis F/O Complex.
Treatment with triclabendazole, nitroxynil or oxyclozanide is usually successful. In the case of lactating animals milk has to be discarded for several days except where oxyclozanide is used. It is important to establish whether Ostertagia is a complicating factor in order that combined treatment for F.hepatica or O.ostertagi may be instituted. A combination product containing ivermectin and clorsulon, which is effective against adult flukes, could be used in the treatment of the F/O complex.
For control in normal years, cattle, whether housed or outwintered can be dosed prophylactically in December or January, with a drug effective against adult stages. Since triclabendazole is the only compound effective against most of the migratory stages in the liver it is the drug of choice for treatment at housing. In wet springs a second dose may be given to outwintered stock in May to remove infections acquired during winter and so minimise pasture contamination with eggs.
The economics of Fascioiosis in cattle are concerned mainly with losses in productivity rather than fatalities and it has been suggested that even a low level infection (approximately 100 F.hepatica) can result in an 8% loss in production while heavy infections (250 F.hepatica) can be responsible for a 20% loss in productivity.
FASCIOLOSIS
A parasitic condition of sheep and cattle caused by the migration and feeding habits of Fasciola hepatica in the liver tissue and bile ducts. Part of the life cycle is spent in a mud snail, Lymnaea truncatula and outbreaks in areas suitable for snail colonisation, usually occur in autumn and winter. These are characterised by weight loss, anaemia and hypoproteinaemia and in heavy infections of sheep sudden death may occur.
AETIOLOGY
The adult F.hepatica, or liver fluke, is leaf-shaped and is up to 3.5 cms. in length; it is situated in the bile ducts where the eggs are shed and subsequently passed in the faeces. These eggs then develop and hatch intomotile ciliated miracidia; this takes 9 days at the optimal temperature of 22-260C but at lower temperatures requires longer and no development occurs below 100C.
The adult F.hepatica, or liver fluke, is leaf-shaped and is up to 3.5 cms. in length; it is situated in the bile ducts where the eggs are shed and subsequently passed in the faeces. These eggs then develop and hatch into motile ciliated miracidia; this takes 9 days at the optimal temperature of 22-260C but at lower temperatures requires longer and no development occurs below 100C.
The liberated miracidia have a short life span and must contact the snail intermediate host, L.truncatula, within 3 hours if successful penetration of the latter is to occur. In infected snails development proceeds through sporocyst and rediae stages to the final snail stage, the cercariae; the latter are shed from the snail as motile forms which attach themselves to surfaces, such as grass blades, and encyst there to form the infective metacercariae. It takes a minimum of 6 to 7 weeks for completion of development from miracidia to metacercariae although under un-favourable circumstances a period of several months is required. Infection of a single snail with one miracidium can produce over 600 metacercariae.
Metacercariae ingested by the final host excyst in the small intestine, migrate through the gut wail, cross the peritoneum and penetrate the liver capsule. The young flukes tunnel through the parenchyma for 6 to 8 weeks then enter the bile ducts where they mature and migrate to the larger ducts and gall bladder in about 4 weeks. The period from ingestion of metacercariae to the presence of fluke eggs in the faeces is 10-12 weeks.
The minimal period for completion of one entire life cycle of F.hepalica is therefore 17-18 weeks.
ECOLOGY AND LIFE HISTORY OF L.truncatula
L.truncatula is a small snail, the adults being about 1 cm in length. The shell is usually dark brown and has a turreted appearance, i.e. coiled in a spiral form; the aperture is approximately half the total length of the snail and is on the right hand side.
L.truncatula snails are amphibious; they require moisture for normal activity but breathe atmospheric oxygen. Thus although they may spend hours in shallow water they may periodically emerge. They are capable of withstanding drought or freezing by respectively aestivating or hibernating in the mud. Optimal conditions include a slightly acid pH environment and a slowly moving water medium to carry away waste products. They feed mostly on algae.
The optimum temperature range for development is 18-220C and at this temperature egg masses will develop to adult snails in 3 weeks. L.truncatula is hermaphrodite and one snail is capable of producing, in a 3 month breeding season, up to 100,000 descendants.
EPIDEMIOLOGY
There are 3 main factors influencing the availability of the large numbers of metacercariae necessary for outbreaks of fasciolosis. These are:
1. Availability of suitable snail habitats
L.truncatula prefers wet mud to free water and permanent habitats include the banks of ditches or streams and the edge of small ponds. Following heavy rainfall or flooding temporary habitats may be provided by hoof marks, wheel ruts or rain ponds. Fields with clumps of rushes are often suspect sites, these having a slightly acid pH environment; although the latter pH is considered to be optimal, excessive pH levels are detrimental, e.g., as in peat bogs and areas of sphagnum moss.
2. Moisture
The ideal moisture conditions for snail breeding and also for F. hepatica development within the snails are provided when rainfall exceeds transpiration, i.e. when field capacity in terms of saturation is reached. Such conditions are also particularly advantageous for the development and hatching of Fasicola eggs for miracidia searching for snails and for the dispersal of cercariae after shedding from snails.
3. Temperature
A mean day night temperature of 100C or above is necessary for snails to breed and for development of F. hepatica within the snail to proceed. It is also the critical temperature for the development and hatching of fluke eggs. As the mean day night temperature increases during late spring and early summer so the developmental cycles of liver fluke, outside of the final host, become shorter, reaching a minimum of 5 weeks in midsummer.
The minimal temperature requirements for development of the extra-final host stages of F.hepatica only prevail from April to October in the southern half of Britain; farther north the necessary temperature is only present from May to September. Annual variations in these temperature conditions are minor and the main factor influencing the incidence of snail populations and therefore of fasciolosis is summer rainfall.
The number of annual cycles of snail breeding varies in different regions of the country, e.g. in West Scotland the minimal temperatures for snail breeding are present in May through September and the annual rainfall varies from 1,000 to 1,500 mm. In this region snails which hibernate over the winter commence to lay eggs in May; these egg masses hatch to young snails in June which reach maturity in late July to lay egg masses again on the pasture. With the failing temperatures in autumn this second generation is not completed until the following spring, i.e. there is only one generation per annum. Obviously farther south in Britain the period suitable for development is longer and an extra generation is possible.
As a result of studies on snail populations, climatic data and disease incidence in the UK, two annual cycles of infection in fasciolosis were described. The first, and most important, involved infection of the intermediate host snail in summer by miracidia developed from eggs deposited in spring and early summer by infected animals; this infection took at least 5 weeks to develop to the cercarial stage and resulted in an increase in pasture levels of metacercariae from late August onwards. This is the summer infection of snails. It is important to remember that the metacercariae produced by this infection, if not ingested in the autumn, are capable of over-wintering and initiating infection in animals in the following spring; any surviving metacercariae appear to die off by mid-summer.
The second, involved infection of snails in the autumn by miracidia developed from eggs deposited in the late summer; development of this infection in the snail ceased during the winter and was completed in the following spring resulting in an increase in pasture levels of metacercariae around mid-summer. This is the winter infection of snails and is thought to be of less importance in Britain than the summer infection. This is possibly due to a selective mortality of infected snails during the winter.
In the last few years further studies on the seasonal prevalence of fasciolosis have been made using parasite-free stock to monitor the seasonal availability of metacercariae on pasture and outbreaks of disease. These studies have underlined the importance of the summer infection of snails which produces the autumnal flush in pasture levels of metacercariae. Ingestion of the latter results in the clinical disease known to occur in sheep from October onwards and in cattle during the winter.
Although there is no evidence, that under field conditions sheep become immune to reinfection with Fasicola, the migration of flukes in animals previously exposed to the parasite is delayed; this results in a prolonged pre-patent period. Thus in previously exposed animals the period between the acquisition of infection and the onset of clinical disease may be longer than one would expect from a knowledge of the life cycle. Also, following treatment of carrier animals, the period between re-infection and reappearance of eggs in the faeces again may be prolonged.
THE DISEASE IN SHEEP
Clinical fasciolosis in sheep can be divided into acute, sub-acute and chronic, according to the number and stage of development of parasites in the liver, but since any such classification is always arbitrary there will be considerable overlap between these categories. It should always be remembered that an outbreak of fasciolosis will be a flock problem even though only a few individuals may be showing typical clinical signs at any one time and therapy must always be considered on this basis.
Acute Fasciolosis
CLINICAL SIGNS
Outbreaks of acute fasciolosis are seen in late autumn and early winter. Acute disease is associated with the presence of large numbers of immature flukes in the liver of affected sheep. The large number of flukes developing in the liver at one time can be the result of the sheep ingesting large numbers of metacercariae over a short period from very heavily infected pasture; it may also be that in sheep which have been exposed to the parasite before, migration of the flukes through the liver may be prolonged and so allow the fluke population to accumulate. Cases of acute fasciolosis in the field are generally presented as sudden deaths in a flock of ewes. On examination of the remainder of the flock one may find ewes which are weak, with pale mucous membranes, breathing difficulties, and in some cases there may be a palpably enlarged liver with some abdominal pain. Abdominal fluid build up is also a common finding in these cases. Diarrhoea is not a feature.
Since the flukes are still immature no eggs are present in the faeces of affected sheep.The flukes recovered from cases of acute fasciolosis at post-mortem are small, only 4-8 mm long, indicating an infection of about 6-8 weeks duration and there may be in excess of 1,000 flukes in the affected liver.
DIAGNOSIS
Diagnosis is most accurately based on a good post-mortem examination confirmed where possible by clinical examination of the survivors. In some cases there may be a history of the flock grazing known infected pasture 6-8 weeks previously. Forecasts issued by the Ministry of Agriculture on the possible incidence of fasciolosis can be of use in indicating the severity of the disease expected in subsequent months.
TREATMENT
The drug of choice in the treatment of outbreaks of acute fasciolosis is triclabendazole. Two other compounds which have some activity against immature flukes are nitroxynil and closantel.
Sub-acute Fasciolosis
CLINICAL SIGNS
This also occurs in the late autumn and early winter but in these cases the disease is not so rapidly fatal and the affected sheep may show clinical signs for one or two weeks prior to death. Large numbers of flukes are again present in an infected liver but the numbers are somewhat reduced from those found in cases of acute fluke though the parasites have developed further and a substantial proportion of the fluke population is now present as adults in the major bile ducts. This form of the disease may develop where the sheep have ingested large numbers of metacercanae over a longer period or the number ingested at any one time has not been sufficient to cause the acute form of the disease.
Affected sheep lose condition rapidly, become markedly anaemic with obvious pallor of their mucous membranes and may have a palpably enlarged liver and resent abdominal palpation. Submandibular oedema and abdominal fluid may be present in some cases. Diarrhoea is not a feature.
F. hepatica eggs are present in the faeces.
The number of flukes recovered at post-mortem examination vanes between 500-1,500 and usually about half the population have developed into adult flukes. This type of fasciolosis usually occurs 12-20 weeks after ingestion of large numbers of metacercariae.
DIAGNOSIS
This is based on clinical signs, faecal egg counts, and a good post-mortem. Again a history of grazing infected pasture some months previously may be obtained.
TREATMENT
Triclabendazole is again the drug of choice but nitzoxynil and closantel are also effective.
Chronic Fasciolosis
Outbreaks of chronic fasciolosis are seen in the latter part of the winter and in early spring and this form of the disease is characterised by a progressive loss of condition and terminal emaciation, pallor of the mucous membranes, submandibular oedema and abdominal fluid. This form of the disease is the result of the infection picked up in the autumn and winter which is now present as adult flukes in the bile ducts and over the ensuing months these flukes remove more blood from the circulation than the sheep can replace and so the anaemia becomes progressively worse. In uncomplicated cases diarrhoea does not occur.
Eggs are usually found In the faeces.
DIAGNOSIS
This is again based on clinical signs, faeces examination and post-mortem findings.
TREATMENT
Triclabendazole is best but nitroxynil, closantel and oxyclozanide may also be used. Oxyclozanide has no milk withdrawal period in milking sheep, the others cannot be used. Albendazole also has activity against adult fluke in addition to anti-nematode activity. A number of combination products for fluke and nematodes are available.
PROPHYLAXIS OF FASCIOLOSIS
Severe outbreaks of fasciolosis only occur following wet springs and summers. The Ministry of Agriculture have therefore been able to develop a formula for forecasting the likely incidence and severity of fasciolosis based mainly on rainfall figures from the preceding months. In the case of the summer infection of snails responsible for outbreaks of acute fasciolosis, accurate forecasts can be made by the end of the summer; however an ‘early warning* can also be issued if May and June have been unduly wet.
Control of fasciolosis whether on a long term or on a short term basis in conjunction with the forecast system may be approached in two ways; first, by reducing populations of the intermediate snail host or secondly by using anthelmintics to limit the availability of F. hepatica eggs and therefore miracidia to surviving snail populations.
REDUCTION OF L.truncatula POPULATIONS
Before any scheme of snail control is undertaken a survey of the control area for snail habitats should be made as the latter may be localised or whole fields may be involved.
The best long-term method for reducing snail populations is drainage. It has been demonstrated that permanent destruction of snail habitats can be achieved by this method but many are often hesitant to undertake expensive drainage schemes.
When the area of snail colonisation is confined, a simple method of control is to fence off this area or treat with a molluscicide such as copper sulphate. Although more efficient molluscicides have been developed these are expensive and none have proved to be a practical solution in fluke control in Britain.
USE OF ANTHELMINTICS
The prophylactic use of fluke anthelmintics is aimed at reducing pasture contamination by F.hepatica eggs at a time most suitable for their development, i.e. April to August, and removing fluke populations at a time of heavy burden, i.e. October-December, or at a period of nutritional and pregnancy stress to the animal, i.e. January to April.
Based on these criteria the following control programme for sheep is recommended for years with normal or below average rainfall.
1. Late April/early May - dose all adult sheep. The fasciolicide used should be highly efficient against adult flukes. Triclabendazole, nitroxynil, closantel, oxyclozanide or combination products can be used.
2. October - dose all sheep. Use a drug effective against parenchymal stages, eg. triclabendazole.
3. January - dose all sheep. Any recommended flukicidal drug such as triclabendazole, nitroxynil or closantel may be used.
In wet years 2 further doses with a flukicidal drug should be used as follows:
June (4-6 weeks after the May dose) - dose all sheep with triclabendazole, nitroxynil, closantel or oxyclozanide
October/November (4 weeks after early October dose) - dose all sheep with a drug effective against parenchymal stages - triclabendazole.
The exact timing of the spring and autumn treatments will depend on lambing and tupping dates.
OSTERTAGIOSIS
Ostertagia ostertagi is the most common cause of parasitic gastritis in cattle. The disease, ostertagiosis, is characterised by weight loss and diarrhoea and typically affects young cattle during their first grazing season, although herd outbreaks and sporadic individual cases have also been reported in adult cattle.
LIFE CYCLE
O.ostertagi has a direct life cycle. The eggs are passed in the faeces and develop within the faecal pat to the infective third stage. When moist conditions prevail the larvae migrate from the faeces onto the herbage.
After ingestion the larvae develop in the lumen of an abomasal gland before they emerge from the gland to become mature on the mucosal surface.
The entire parasitic life cycle usually takes three weeks but under certain circumstances many of the ingested larvae become inhibited in development for periods of up to six months.
The presence of O.ostertagi in the abomasum in sufficient numbers gives rise to extensive pathological and biochemical changes and severe clinical signs. These changes are maximal about 18 days after infection but it may be delayed for several months when arrested larval development occurs.
In heavy infections of 40,000 or more adult worms the principal effects of these changes are first, a reduction in the acidity of the abomasal fluid, the pH increasing from 2.0 up to 7.0. This results in a failure to activate pepsinogen to pepsin and to denature proteins. There is also a loss of bacteriostatic effect in the abomasum. Secondly, there is an enhanced permeability of the abomasal epithelium to macromolecules such as pepsinogen and plasma proteins. The results of these changes are a leakage of pepsinogen into the circulation leading to elevated plasma pepsinogen levels and the loss of plasma proteins into the gut lumen eventually leading to low blood protein levels. Clinically these consequences are reflected as inappetance, weight loss and diarrhoea and precise cause of the latter being unknown.
In lighter infections the main effects are sub-optimal weight gains.
CLINICAL SIGNS
Bovine ostertagiosis is known to occur in two clinical forms. In temperate climates with cold winters the seasonal occurrence of these is as follows.
The Type I disease is usually seen in calves grazed intensively during their first grazing season as the result of large numbers of larvae ingested 3-4 weeks previously; this normally occurs from mid-July onwards.
The Type II disease occurs in yearlings, usually in late winter or spring following their first grazing season and results from the maturation of larvae ingested during the previous autumn and subsequently inhibited in their development.
The main clinical sign in both Type I and Type II disease is a profuse diarrhoea and in Type I, where calves are at grass, this is usually persistent, watery and has a characteristic bright green colour. In contrast, in the majority of animals with Type II the diarrhoea is often intermittent and anorexia and thirst are usually present. The coats of affected animals in both syndromes are dull and the hind quarters heavily soiled with faeces.
In both forms of the disease the loss of body weight is considerable during the clinical phase and may reach 20% in 7-10 days. Carcass quality may also be affected since there is a reduction in total body solids relative to total body water.
In Type I disease, the morbidity is usually high, often exceeding 75%, but mortality is rare provided treatment is instituted within 2-3 days. In Type II disease only a proportion of animals in the group are affected but mortality in such animals is very high unless early treatment with an anthelmintic effective against both inhibited and developing larval stages is instituted.
EPIDEMIOLOGY
Dairy Herds
From epidemiological studies the following important facts have emerged:
1. A considerable number of larvae can survive the winter on pasture and in soil. Sometimes the numbers are sufficient to precipitate Type I disease in calves 3-4 weeks after they are turned out to graze in the spring. However, this is unusual, and the role of the surviving larvae is rather to infect calves at a level which produces patent sub-clinical infection which ensures contamination of the pasture for the rest of the grazing season.
2. A high mortality of overwintered larvae on the pasture occurs in spring and only negligible numbers can usually be detected by June. This mortality combined with the dilution effect of the rapidly growing herbage renders most pastures, not grazed in the spring, safe for grazing after mid-summer.
However, despite the mortality of larvae on the pasture it now appears that some can survive in the soil for at least another year and on occasion appear to migrate on to the herbage. Whether this is a common occurrence and whether the larvae migrate or are transported by terrestrial populations of earthworms or beetles is not definitely known but the occurrence of this apparent reservoir of larvae in soil may be important in relation to certain systems of control based on grazing management.
3. The eggs deposited in the spring develop slowly to larvae; this rate of development becomes more rapid towards mid-summer as temperatures increase, and as a result, the majority of eggs deposited during April, May and June all reach the infective stage from mid-July onwards. If sufficient numbers of these larvae are ingested the Type I disease occurs any time from July until October. Development from egg to larvae slows during the autumn and it is doubtful if many of the eggs deposited after September ever develop to larvae.
4. As autumn progresses and temperatures fall an increasing proportion (up to 80%) of the larvae ingested do not mature but become inhibited. In late autumn, calves can therefore harbour many thousands of larvae but few developing forms or adults. These infections are generally asymptomatic until maturation takes place during winter and early spring and if large numbers of these larvae develop synchronously, Type II disease occurs. Where maturation is not synchronous clinical signs may not occur but the adult worm burdens which develop can contribute to pasture contamination in the spring.
Two factors, one management and one climatic, appear to increase the prevalence of Type II ostertagiosis.
First, the practice of grazing calves from May until July on permanent pasture, then moving these to hay or silage aftermath before returning them to the original grazing in late autumn. In this system the accumulation of larvae on the original pasture will occur from mid-July i.e. after the calves have moved to aftermath. These larvae are still present on the pastures when the calves return in the late autumn and, when ingested, the majority will become inhibited and thus increase the potential for Type II disease.
Secondly, in dry summers the larvae are retained within the crusted faecal pat and cannot migrate on to the pasture until sufficient rainfall occurs to moisten the pat. If rainfall is delayed until late autumn many larvae liberated on to pasture will become inhibited following ingestion and so increase the chance of Type II disease. Indeed, epidemics of Type II ostertagiosis are typically preceded by dry summers.
Although primarily a disease of young dairy cattle, ostertagiosis can affect groups of older cattle, particularly if these have had no previous exposure to the parasite since there is no significant age immunity to infection. Also, acquired immunity in ostertagiosis is slow to develop and calves do not acquire a significant level of immunity until the end of their first grazing season. If they are then housed for thewinter and acquired immunity has waned by the following spring and yearlings turned out at that time are partially susceptible to reinfection and can contaminate the pasture with small numbers of eggs. However, immunity is rapidly reestablished and any clinical signs which occur are usually of a transient nature. During the second and third year of grazing a strong acquired immunity develops and adult stock in endemic areas are generally highly immune to reinfection. An exception to this rule occurs around the periparturient period when immunity wanes, particularly in heifers, and there are reports of clinical disease following calving. The reason is unknown but may be due to the development of larvae which were arrested in their development as a result of host immunity.
Beef Herds:
Although the basic epidemiology in beef herds is similar to dairy herds the influence of immune adult animals grazing alongside susceptible calves has to be considered. Thus in beef herds where calving takes place in the spring, ostertagiosis is uncommon since egg production by immune adults is low, and the spring mortality of the overwintered larvae occurs prior to the suckling calves ingesting significant quantities of grass. Consequently only low numbers of larvae become available on the pasture later in the year.
However, where calving takes place in the autumn or winter, ostertagiosis can be a problem in calves during the following grazing season after they are weaned. The epidemiology is then similar to that seen in dairy calves. Whether Type I or Type II disease subsequently occurs depends on the grazing management of the calves following weaning.
DIAGNOSIS
In older animals the clinical signs and history are similar but laboratory diagnosis is more difficult. A useful technique to employ in such situations is to carry out a pasture larval count on the field on which the animals had been grazing. Where the level of infection is more than 1,000 larvae per kg of dried herbage the daily larval intake of grazing cows is in excess of 10,000 larvae. This level is probably sufficient to cause clinical disease in susceptible adult animals or to upset the normal functioning of the gastric mucosa in immune cows.
TREATMENT
Type I disease responds well to treatment at the standard dosage rates with any of the modem benzimidazoles (albendazole, fenbendazole or oxfendazole), the probenzimidazoles, levamisole, or ivermectin. All of these drugs are effective against developing larvae and adult stages. Following treatment calves should be moved to pasture which has not been grazed by cattle in the same year. The field where the outbreak has originated may be grazed by sheep or rested until the following June.
For the successful treatment of Type II disease it is necessary to use drugs which are effective against inhibited larvae as well as developing larvae and adult stages. Only the modem benzimidazoles listed above or ivermectin are useful in the treatment of Type II disease when used at standard dosage levels although the probenzimidazoles are also effective at higher dose rates.
In young animals this decision is based on:
The clinical signs of inappetance, weight loss and diarrhoea
The season. For example, Type I occurs from July until September and Type II from March to May
The grazing history. In Type I disease, the calves have usually been set-stocked in one area for several months, in contrast, Type II disease often has a typical history of calves being grazed on a field from spring to mid-summer, before being moved and then brought back to the original field in the autumn. Affected farms usually also have a history of ostertagiosis in previous years.
Faecal egg counts. In Type I disease these can be more than 1,000 eggs per gram and are a useful aid to diagnosis; in Type II counts are highly variable, may even be negative and are of limited value.
Plasma pepsinogen levels. In clinically affected animals up to two years old these are usually raised.
Post-mortem examination
CONTROL
Traditionally, ostertagiosis has been prevented by routinely treating young cattle with anthelmintics over the period when pasture larval levels are increasing. For example, this involves one or two treatments usually in July and September and on many farms this prevented disease and produced acceptable growth rates. However, it has the disadvantage that since the calves are under continuous larval challenge their performance may be impaired. With this system effective anthelmintic treatment at housing is also necessary using a drug effective against inhibited larvae in order to prevent Type II disease. Today, it is accepted that the prevention of ostertagiosis by limiting exposure to infection is a more efficient method of control.
This may be done by grazing calves on new grass leys although it is doubtful if this should be recommended for replacement dairy heifers, as it would result in a pool of susceptible adult animals. A better policy is to permit young cattle sufficient exposure to larval infection to stimulate immunity but not sufficient to cause a loss in production. The provision of this ‘safe pasture* may be achieved in two ways:
First, by using anthelmintics to limit pasture contamination with eggs during periods when the climate is optimal for development of the free-living larval stages i.e. spring and summer.
Alternatively by resting pasture or grazing it with another host, such as sheep, which are not susceptible to O.ostertagi, until most of the existing larvae on the pasture have died out.
Sometimes a combination of these methods is employed.
Prophylactic Anthelmintic Medication
Since the crucial period of pasture contamination with O.ostertagi eggs is the period up to mid-July, one of the efficient modern anthelmintics may be given on two or three occasions between turnout in the spring and July to minimise the numbers of eggs deposited on the pasture. For calves going to pasture in early May two treatments, three and seven weeks later are used, whereas calves turned out in April require three treatments. With some anthelmintics which have a persistent effect and prevent infection for several weeks after administration, various regimens are recommended. For example ivermectin at 3, 8 and 13 weeks post turnout or doramectin at turnout and 8 weeks later.
Several rumen boluses have been developed which release in a sustained fashion or as programmed single ‘pulse* doses. When these boluses are administered to calves just prior to turn-out they prevent the development of infections acquired from overwintered larvae and so prevents the deposition of eggs during the spring. This in turn prevents the development of high levels of pasture contamination with larvae which are responsible for disease.
Anthelmintic prophylaxis has the advantage that animals can be grazed throughout the year on the same pasture and is particularly advantageous for the small heavily stocked farm where grazing is limited.
Anthelmintic treatment and move to safe pasture in mid-July
This is usually referred to as the ‘dose and move" system and is based on the knowledge that the annual increase of larvae occurs after mid-July. Therefore if calves grazed from early spring are given an anthelmintic treatment in early July and moved immediately to a second pasture such as silage or hay aftermath, the level of infection which develops on the second pasture will be low.
The one reservation with this technique is that in certain years the numbers of larvae which overwinter are sufficient to cause heavy infections in the spring and clinical ostertagiosis can occur in calves in April and May. However, once the ‘dose and move' system has operated for a few years this problem is unlikely to arise.
Alternate grazing of cattle and sheep
This system ideally utilises a three year rotation of cattle, sheep and crops. Since the effective life-span of most O.ostertagi larvae is under one year and cross infection between cattle and sheep in temperate areas is largely limited to Trichostrongylus axei, good control of bovine ostertagiosis should, in theory, be achieved. It is particularly applicable to farms with a high proportion of land suitable for cropping or grassland conservation and less so for marginal or upland areas, but in these areas good control has been reported using an annual rotation of beef cattle and sheep.
The drawback of alternate grazing systems is that they impose a rigorous and inflexible regimen on the use of land which the farmer may find impractical. Furthermore, in warmer climates where Haemonchus is prevalent this system can prove dangerous since this very pathogenic worm establishes in both sheep and cattle, but is not a problem in Scotland.
CALF DIPHTHERIA
DEFINITION
A infection of the oral cavity or, less frequently, the larynx and pharynx, of calves and young cattle resulting in swelling of the affected area, fever, depression and reluctance to eat or drink. Fusobacterium necrophorum is often involved.
INCIDENCE
The condition is common and may affect groups of calves or young cattle in a particular building or repeatedly on a particular farm.
AETIOLOGY
F.necrophorum is present in the lesions and its elimination by treatment usually cures the condition. It is, however, probably a secondary invader following damage to the oral cavity in animals suffering from intercurrent disease the commonest of which is bovine papular stomatitis.
CLINICAL SIGNS
Calves with calf diphtheria frequently have a swelling of the cheeks, throat, foetid or rancid breath, purulent discharge from the nose and may salivate excessively. A moist, painful cough, breathing difficulty, pain on swallowing and fever may be seen in more than one animal in a group. Depression and death may result in the absence of treatment. Local necrotic infections or ulcers in other parts of the oral cavity may produce a similar picture. Infected material may be inhaled and this can result in a severe pneumonia.
EPIDEMIOLOGY
The infection appears to spread by contact on dirty milk pails amongst groups of calves. The disease may also result from damage associated with rough feed and the eruption of teeth or from secondary infection of BPS lesions.
DIAGNOSIS
The clinical and pathological findings are characteristic. In particular the smell of the breath and the appearance of the lesions. It should be borne in mind that this condition may be secondary to other diseases affecting the oral cavity.
TREATMENT
Sulphonamides, penicillin or the tetracyclines are usually effective.
CONTROL
Disinfection of milk pails etc. coupled with improved hygiene is of value.
RESPIRATORY DISEASES OF CALVES LESS THAN ONE MONTH OLD
Respiratory diseases are not common in this age of calf and when they do occur, they usually involve the lower respiratory tract. The following specific disorders can be recognised.
NEONATAL ACUTE RESPIRATORY DISTRESS SYNDROME
This uncommon condition is thought to result when a calf is born too early, before its surfactant producing type 11 pneumonocyte cells in the lungs are mature. Affected individuals are born prematurely and are usually unable to stand. They have severe difficulty breathing. Severely affected cases die. Treatment will almost certainly be unsuccessful, although betamethasone, doxapram, clenbuterol and millophylline can be given.
RESPIRATORY SIGNS WITH SEVERE NEONATAL CALF DIARRHOEA
Calves with severe neonatal diarrhoea, particularly those which are recumbent, frequently have breathing problems. These signs are more likely to be the result of respiratory compensation for a metabolic acidosis following the neonatal diarrhoea rather than the result of an infectious pneumonia. However, calves with neonatal diarrhoea do sometimes develop acute exudative pneumonias and animals which have been in lateral recumbency for several days may develop the form referred to as hypostatic pneumonia.
ACUTE EXUDATIVE PNEUMONIA
It is usually considered that this syndrome is due to a primary bacterial infection of the lungs. Actinomyces pyogenes is the species most frequently isolated from these cases but Pasteurella species are also found, to a lesser degree. Calves which have suffered from severe neonatal diarrhoea seem to be particularly susceptible to this disorder. Prompt treatment with broad spectrum antibiotics usually produces a marked clinical improvement, but, in a small proportion of cases, recovery is incomplete and further episodes of pneumonia can occur. In a number of the latter cases chronic suppurative pneumonia develops.
ASPIRATION PNEUMONIA
This condition develops when a calf aspirates milk into the lower respiratory tract when being forced to drink milk from a bucket. Careless drenching of a sick animal, particularly when there is a degree of respiratory distress, can also produce the same syndrome. If the amount of fluid inhaled is small prompt antibiotic therapy will produce a clinical recovery. If a large amount has been inhaled and the animal does not die, it is likely to remain unthrifty because of the development of chronic pulmonary abscesses. This condition can be prevented by patiently coaxing calves to drink from a bucket.
LUNG ABSCESSES
These can follow incomplete recovery from one or more episodes of an acute exudative pneumonia. They can also arise as part of a septicaemia following navel ill, when they are usually multiple and in several lobes of the lungs.
CONGENITAL CARDIAC DISEASE
Complex congenital cardiac lesions may present with respiratory signs due to defective pulmonary circulation. Frequently, however, the respiratory signs are due to or exacerbated by a co-existing acute exudative pneumonia of an infectious nature. These animals may be smaller than normal and other congenital defects may also be present. At present, treatment is not possible for these cases.
PNEUMONIA IN HOUSED CALVES MORE THAN ONE MONTH OLD
DEFINITION
Respiratory diseases which are very common and economically very important in housed calves can develop suddenly or insidiously in individual animals as well as simultaneously in several animals within one group. While many infectious agents have been isolated from pneumonic calves, their individual importance is as yet unknown as is that of the many environmental factors which may affect the resistance of these calves.
INCIDENCE
The average mortality rate, in housed calves, resulting from pneumonia has been estimated at about 4 per cent. In many outbreaks, however, it can be considerably higher.
EPIDEMIOLOGY
Pneumonia in calves is important all over the United Kingdom. It occurs at all times of the year but there appears to be two specific peaks in incidence before Christmas and in the later winter/spring time. These increases in incidence could correspond to the periods of maximum numbers of susceptible calves.
AETIOLOGY/ PATHOGENESIS
A multitude of microbiological agents has been isolated from the lungs of pneumonic calves but their significance both individually and collectively has yet to be elucidated fully. It is possible that the infection rate and therefore the importance of the individual agents varies from year to year and from region to region. At present, the general view is that the mycoplasmas, parainfluenza virus (P13), respiratory syncytial virus (RSV), are the major pathogens. However, under certain circumstances, it is likely that many of the other agents frequently isolated from pneumonic calf lungs could exacerbate, if not initiate, respiratory disease since a large number of them can also be isolated from the healthy bovine lungs.
The inability of agents isolated from pneumonic lungs to produce clinical disease has led to the concept of a ‘multiple factor aetiology" for calf pneumonia. In this concept the effect of potential respiratory pathogens is modified by the "stress" of other diseases or by physical factors e.g. chilling, wide fluctuations in environmental temperature, overcrowding or the mixing of calves from various sources.
CLINICAL SIGNS
Large numbers of similarly aged dairy and dairy cross calves are generally housed together and consequently share the same air space. Therefore, it is not surprising that infectious respiratory disease is so often a group problem although initially, individuals only may appear to be affected.
The various respiratory syndromes will be described according to (a) the numbers of animals affected and (b) depending on the mode of onset of the clinical signs.
Chronic Pneumonia
Insidious onset, chronic pneumonia is a very common syndrome and there can be great variation in the severity of the disease in different groups of affected calves. In mild incidents, occasional coughing may be the only indications of the presence of respiratory disease. However, in severe outbreaks frequent bouts of coughing are common, almost all the calves in the group will have breathing difficulties with marked exercise intolerance when chased. Although affected animals are alert and maintain a good appetite, their growth rate is reduced and so an excessive difference in size develops between the calves.
The rectal temperature which can show daily fluctuations, is usually below 103F. In the severe incidents the morbidity rate is almost 100 per cent but fatalities are rare in uncomplicated cases. Secondary bacterial infections are probably responsible for exacerbating some of the cases. In animals with severe complications, lung damage may not resolve but give rise to chronic coughing and unthriftiness. Severe acute exudative bacterial pneumonias may then prove fatal.
Acute Pneumonia
Sudden onset acute pneumonia frequently referred to as "virus pneumonia* or "enzootic pneumonia", can occur as a primary outbreak or probably more frequently as a complication of an existing chronic pneumonia. These incidents frequently arise within a couple of weeks, often after a few days, of calves being stressed in some way, e.g. by being mixed with different groups in a new house, or by being sold and transported to another farm. The severity of the clinical disease within an affected group varies greatly. The morbidity rate is generally less than 50 per cent on self-contained units but this can vary greatly. The highest rates e.g. up to 90% affected, are usually seen on units into which dairy calves at around three weeks of age are purchased in large numbers to be reared for beef. Overall, the mortality rate is usually low (<5%) but it may reach 10 per cent or even higher in particularly severe incidents.
During their first winter housing period, several outbreaks of acute pneumonia can affect the one group of calves and it is often the same individuals which seem to be affected in these recurring outbreaks.
Individual Problems
Acute pneumonia can arise in individual animals either as a primary disease or as a complication of a chronic pneumonia. Recovered animals can suffer further pneumonic episodes and they eventually develop a severe chronic suppurative pneumonia. Affected individuals frequently die as a result of an acute exacerbation.
DIAGNOSIS
This is based upon the mode of onset of the clinical signs, the number of calves affected and the background history of the group.
The findings at the post-mortem examination of fatal cases of calf pneumonia are often not very helpful in establishing the precise cause of the disease, particularly if it has been of an infectious nature. This is because firstly, the primary agent may have disappeared, or secondly, so few organisms may be present that they are unable to be detected by routine investigative procedures or thirdly there is almost invariably invasion by a number of secondary agents, especially bacteria. Even the isolation and identification of a known pathogen is not in itself absolute confirmation that it alone was the causal agent involved since many pathogens can exist in the lungs of healthy animals without necessarily producing disease.
The use of paired blood samples, the first taken in the acute phase of the disease and the second in the convalescent phase some 2-3 weeks later, can identify active respiratory infection within a group of calves. Ideally, all animals at risk should be sampled.
TREATMENT
Mild chronic pneumonias may not be sufficiently severe to require treatment. However, when treatment is indicated the drugs of choice are long acting preparations of oxytetracycine and amoxycillin or tilmicosin.
The treatment of calves suffering from acute respiratory disease must be undertaken promptly and, in virtually every incidence, without knowing the precise cause. Since it is usually assumed that severe clinical signs are the result of secondary bacterial infections, a course of drug therapy is usually begun; this almost invariably consists of the administration of a broad spectrum antibiotic. However, it must be borne in mind, that antibiotics do not have an inhibitory effect on viral multiplication.
Recovery from acute pneumonia has considerably increased and the long-term damage to the lung has reduced by the use of flunixin.
It is also beneficial for a pneumonic individual to be isolated in airy accommodation until it has recovered.
CONTROL
The following recommendations have been used successfully on several self contained dairy units to reduce to a minimal level, but not eradicate, the dual problems of calf scour and pneumonia:
i) thorough cleansing and gas fumigation of the calf house
ii) ensure every calf gets the maximum amount (up to 6 pints) of colostrum within six hours of birth
iii) rear in groups of max 20-25 for as long as possible without moving the calves
iv) early wean and feed ad-lib.
If an outbreak of pneumonia develops, the calves born subsequently should be reared in a separate house as it is inadvisable to allow newly-born individuals to share the same air-space as animals suffering from obvious respiratory disease.
In beef units into which calves are introduced regularly, the prevention of respiratory disease can be very difficult to achieve even when routine disease control measures are fully implemented. It has been claimed that when the incidence and mortality from respiratory disease threatens the financial viability of the enterprise, the only measure which will significantly reduce incidence of disease is a course of antibiotics given to every purchased calf during its first three days in the unit. However, it must be emphasised that this is the final step to be taken only after all other measures have been tried and have failed and it should not be considered as the first step in the control of calf respiratory disease.
Unless the pneumonia is occurring at a very early age it is possible, and recommended to vaccinate the calves. Ask your veterinary surgeon for advice.
PNEUMONIC PASTEURELLOSIS (Transit Fever)
This disease is a pneumonia caused by Pasteurella species. Weaned suckled calves are usually affected soon after they have been housed.
AETIOLOGY
Pasteurella haemolytica biotype A serotype 1 (Al) represents about 75 per cent of the organisms isolated from cases in Britain although P.haemolytica A2 (10%) and P.multocida (10%) have also been found in the respiratory tracts of pneumonic animals.
EPIDEMIOLOGY
The incidence is highest in newly purchased, weaned, suckled calves from September to December when the majority of the calf sales occur. Consequently, the disease is seen predominantly in the northern and eastern areas of Britain on fattening beef farms. However, severe outbreaks with fatalities have also been confirmed in homebred, suckling beef calves housed with their dams as well as in milk fed and weaned dairy cross calves. Respiratory signs almost invariably develop within 4 weeks of suckled calves being housed (75% within 14 days) and, once the initial incident has passed, further group pneumonic episodes are uncommon.
CLINICAL SIGNS
Many outbreaks are called ‘transit fever* because they develop in cattle which have only been on the farm for a short time. Individuals are first seen to be standing alone and not eating. In severe incidents, the food intake of the whole group can suddenly decrease markedly. Occasional coughing may be heard, but frequent coughing is rare. Breathing difficulty and a nasal discharge may be common in the group, conjunctivitis and ocular discharge have only been seen when IBR is also involved.
The morbidity and mortality rates vary greatly from group to group and from year to year. In a study involving 2026 weaned suckled calves the morbidity rate was found to be 11 per cent and the mortality rate less than 1 per cent.
DIAGNOSIS
The epidemiological findings and the clinical signs are usually sufficient although post mortem findings, when available, will confirm the diagnosis. In early stages of the disease, Pasteurellae species can frequently be isolated in pure culture from nasopharyngeal swabs.
TREATMENT
P.haemolytica is susceptible to the penicillins, oxytetracycline and trimethoprimsulphonamide and other broad-spectrum antibiotics. P.multocida has a similar susceptibility pattern. Long acting antibiotic preparations are very useful since they obviate the need for daily handling.
The prognosis is good provided treatment is given during the early stages of the disease.
CONTROL
It is not possible to prevent the development of pneumonic pasteurellosis but physical stress factors should be minimised in newly purchased, weaned, suckled calves. If such animals are kept outside for as long as possible (at least 2 weeks) before being housed, then the prevalence and severity of the disease should be less. On some units, an injection of long-acting penicillin is given when the calves are housed and it has been claimed that this reduces the severity of the disease. Vaccination can be considered.
INFECTIOUS BOVINE RHINOTRACHEITIS
This disease is caused by bovine herpesvirus 1 and is characterised by reduced appetite, dullness, fever, nasal discharge, and ocular discharge with conjunctivitis. Clinical signs often develop soon after the arrival of newly purchased animals. The course of the illness is usually short, the morbidity is high and the mortality is low.
AETIOLOGY
IBR results from infection of the respiratory tract with bovine herpesvirus 1 (BHV1).
The most common route of viral transmission is by air, but because close contact between infective and susceptible individuals is necessary, the spread of infection is comparatively slow. Consequently, in a large group of susceptible animals, clinical cases may continue to arise for several weeks.
Two to three days after infection fever, conjunctivitis, dullness, reduced appetite and coughing develop. In mild cases, recovery will have taken place after 7 to 10 days although affected individuals can continue coughing for a couple of weeks.
The reasons for the sudden appearance of a severe form of IBR in Britain are not known, but there is circumstantial evidence to suggest that a "new" strain of virus may have been imported into Europe from North America, probably in latently-infected Holstein cattle.
EPIDEMIOLOGY
Following the initial diagnosis of the disease in Britain in 1962, mild incidents of IBR were recorded sporadically throughout the country. During the 1977-78 winter a severe form of IBR was recognised in Scotland and, since then, this form of the disease has spread nationwide
The incidence of disease is highest in fattening beef cattle and in dairy cows although beef cows and young calves can also be affected. In many outbreaks, the source of infection has been animals which have been on the farm for only a short time, often less than 4 weeks after purchase from a market. For this reason, IBR has been particularly prevalent on beef farms in northern and eastern Britain. In contrast, the incidence of disease has been greater in dairy animals in the south and west of the country because, in these areas, replacement heifers are mostly bought-in whereas, in other regions, they are usually home-bred. In addition, infection can also be introduced into a self-contained herd by individual animals returning from livestock shows having been infected by virus excreted from neighbouring, recovered animals.
Although IBR can occur in grazing cattle, severe incidents have only been confirmed during the winter housing period. It appears that "stress" factors such as weaning, mixing, overcrowding as well as the fear and fatigue associated with being sold, contribute significantly to the severity of the field disease. It is thought that those factors are largely responsible for the high morbidity and mortality in animals kept under intensive conditions.
CLINICAL SIGNS
Cattle which have been purchased from a market and have been on the farm less than 4 weeks are frequently those in which clinical signs are first seen. Initially, affected animals are dull with a reduction in appetite, which may be confined to roughage only, a serous nasal and ocular discharge and frequent coughing. In lactating dairy cows, there is a sudden reduction in milk yield.
In mild cases, recovery can take place within 7-10 days without treatment. However, in a small proportion of cases, the clinical signs become progressively more severe.
In the acute stage of the disease, beef cattle can lose up to 30 kg bodyweight and, during the convalescent period, they may fail to put on weight for up to 8 weeks although they have a normal appetite. The milk yield of dairy cows is reduced for several days or for several weeks if they have been severely affected. Pregnant cows often abort as a result of foetal death either within a few days of being infected or even after a delay of several months.
The morbidity rate is usually greater than 50 per cent and, in many outbreaks, it is over 90 per cent. In the majority of incidents, fatalities do not occur. However, up to 7 per cent of severely affected cases may die or have to be culled in outbreaks involving large numbers of purchased, intensively-managed, beef animals. It is on these latter units that IBR is seen at its most severe and where there is a regular high turnover of purchased animals, IBR can become endemic. Within a susceptible group or herd, it takes from 3 to 5 weeks from the time the first case has been seen until clinical signs regress completely.
DIAGNOSIS
The clinical picture is characteristic and differential diagnosis is seldom a problem. Nevertheless, the following conditions should be considered: foot and mouth disease, pneumonic pasteurellosis, malignant catarrhal fever, photosensitisation and infectious bovine keratoconjunctivitis.
TREATMENT
During the early stages of the disease, it has been shown that the severity of the clinical signs can be minimised by the daily administration of a broad spectrum antibiotic until the animals temperature returns to normal. However the treatment of severely ill animals with antibiotics, even for a prolonged period, does not invariably result in a complete clinical recovery.
CONTROL
Susceptible cattle should be vaccinated whenever there is a high risk of exposure to BHV1. At present, there are several vaccines available:
These vaccines, which are given on one occasion, have the advantage that (i) they give almost immediate protection and significant immunity within 48-96 hours, (ii) they do not produce abortion and (iii) they can be used to protect non-infected, in-contact animals even after disease has been confirmed within a group.
All ages of cattle can be vaccinated and, when the challenge is likely to be great, annual revaccination may be desirable.
CEREBROCORTICAL NECROSIS (CCN)
(Polioencephalomalacia)
DEFINITION
This is a sporadic, sudden onset nervous disease of ruminants in which affected individuals are staggering, blind and quickly become recumbent. The syndrome is due an aberration of thiamine metabolism.
AETIOLOGY
In ruminants, the requirement for the B vitamins is largely met by synthesis in the guts. CCN is considered to be caused by a thiamine deficiency because of the rapid response to thiamine treatment and tissue thiamine levels are lower synthesised (low dietary roughage), an inability to utilise the amounts produced (reduced absorption, impaired phosphorylation, increased rate of excretion), thiamine inhibitors (thiaminase), thiamine analogues acting as anti-metabolites, or simply an increased demand. It has been shown that rapidly growing cattle do have an increased requirement for thiamine and the diet which is usually fed to achieve maximum growth rates is a high cereal, low roughage one. When there is a high cereal intake, lactic acidosis develops and, as the pH falls, the following changes take place: firstly, the microflora in the gut changes from predominantly gram-negative to predominantly gram-positive species with an increase in the proportion of bacilli, secondly there is a decrease in the quantity of thiamine produced, thirdly thiaminase producing bacteria flourish, and fourthly, there is an accumulation of histamine and structurally similar bases which can act as potent thiaminase activators.
It has also been suggested that, even in the absence of effective concentrations of thiaminase 1, a deficiency of cobalt may predispose cattle to CCN. This could arise either by following a decrease in the activity of the rumen microorganisms responsible for thiamine synthesis, or by inducing liver damage, which is one of the effects of a prolonged deficiency of cobalt.
EPIDEMIOLOGY
CCN occurs worldwide not only in cattle, but in almost every farm ruminant species. The incidence is highest in cattle from 6 to 12 months which are being fed large quantities of concentrates and minimal amounts of roughage ie. feedlot conditions. Occasionally, grazing animals may be affected. Usually only single animals develop clinical signs, but group outbreaks can occur (up to 25% affected). The mortality rate varies according to the delay before treatment has begun, but it is of the order of 30 per cent.
CLINICAL SIGNS
This is a sudden onset disease in which the initial signs are dullness, aimless wandering, disorientation, apparent blindness, staggering gait and muscle tremors, particularly of the head. After several hours, the affected individual collapses and goes into lateral recumbency. They can develop convulsions although their legs can be stopped from paddling relatively easily. The rumen continues to cycle, there may be a history of diarrhoea or the animal may be diarrhoeic, and the temperature is usually within the normal range. Clinical signs tend to be more severe the younger the animal affected. Untreated cases will die after an illness of from 2 to 6 days duration.
DIAGNOSIS
CCN should be suspected when a young fast growing bovine on a high cereal diet is seen to be wandering aimlessly, or standing alone and apparently blind, or is found in lateral recumbency.
TREATMENT
Thiamine (Vitamin Bl injection) at 10 mg/kg bodyweight usually repeated after 12 and 24 hours (Vitamin Bl injection). In cases given thiamine immediately after the onset of clinical signs, a beneficial clinical response can often be noticed within 12 hours and there may be an apparently complete clinical recovery after 24 hours. When treatment is delayed, several days may pass before any clinical improvement becomes apparent; such cases firstly begin to eat, then mental awareness returns and, finally, the ability to see returns. However, a few cases remain blind although otherwise they appear to have recovered completely.
CONTROL
Since CCN is a problem almost wholly associated with young cattle being fed on a high cereal - low roughage diet, the most obvious measure is to increase the proportion of roughage. While this does reduce the danger from CCN, it is probably uneconomic to do so in a feedlot-type operation. Therefore, where CCN has been a problem, supplementary thiamine should be added so that the total dietary intake is about 25 mg/kg dry feed.
CHRONIC RUMINAL DISTENSION
DEFINITION
This condition is associated with progressive abdominal enlargement due to ruminal distension, weight-loss and a variable degree of diarrhoea.
INCIDENCE
Chronic ruminal distension is a syndrome and may arise as the result of several different and unrelated events. As a syndrome it is, however, most common in weaned beef and dairy calves (particularly if they are weaned on to a high concentrate diet) and elderly cows.
AETIOLOGY
In cattle, aged less than one year, the condition usually occurs in the absence of other obvious abnormalities and it is usually assumed to be due to a primary defect in rumenal function, under certain circumstances this has been shown to be due to low fibre in the diet. Occasionally the condition may arise as a sequel to another disorder.
In mature cattle, chronic rurninal distension usually occurs as a sequel to some other abnormality.
CLINICAL SIGNS
Calves: There is usually a history of the problem being obvious soon after weaning but never being severe enough to warrant a special consultation. Affected animals are usually bright, afebrile and apparently maintaining a reasonable appetite. They are, however, either losing weight or also failing to keep up with the others in the group. Abdominal pain is not a feature. The abdomen is often greatly enlarged and fluid sounds may be easily elicited on ballottement of either flank. Left-flank tympany is usually present and this, in combination with the distension ventrally, gives rise to a very characteristic shape which is most obvious when the subject is viewed from behind. Diarrhoea is usually present but rarely profuse.
NB. When chronic rumenal distension arises as the result of thymic lymphosarcoma, a sound diagnosis of this latter condition is usually possible following first examination.
Mature Cattle: The above description will suffice for many adult cattle with chronic ruminal distension. However there are several additional factors which are worth mentioning. First, it is possible to carry out rectal examination in these animals and therefore it is possible to confirm that the abdominal distension is due to an enlarged rumen in this way and not merely the fact that other demonstrable lesions are usually associated with this disorder in adult cattle means that a full clinical examination is much more commonly helpful in adults. Thus, in some (but unfortunately not many) cases where the problem has arisen following reticular adhesions, there may be a history suggestive of an earlier traumatic reticulitis or else abdominal pain may still be present; in other cases where distension is due to upper alimentary tract cancer, questions as to the type of cow, farm of origin, quality of grazing, access to bracken, presence of oral papillomata and any other signs suggestive of such cancer should also be considered.
TREATMENT
Clearly the approach to treatment must depend on the age of the affected animal.
Spontaneous recovery may occur in calves but there is little doubt that this may be hastened or calves may be saved by either the surgical formation of a small ruminal fistula or else the insertion of an in-dwelling rumen cannula. If the latter procedures are followed in calves without any other clinical abnormalities, the prognosis is generally good. In contrast, the prognosis for adult cattle with definite chronic ruminal distension is always bad. So often they either deteriorate due to an extension or worsening of the underlying cause of the problem (e.g., in the case of upper alimentary tract cancer) or else they reach a stage of sub-optimal health with impaired productivity (e.g. in the case of chronic reticular adhesions). Hence, early slaughter should be advised for all cases unless there is a good case to consider some other approach and any surgical manoeuvre must be carried out on the strict understanding that the prognosis is likely to be very poor.
CHRONIC SUPPURATIVE PULMONARY DISEASE
This is a common condition affecting cattle of all ages but particularly housed calves and adults. The main clinical signs are weight loss and coughing which may be present for a period of weeks or months and may have developed following one or more acute pneumonic episodes.
INCIDENCE
This was found to be one of the most common single respiratory conditions of adult cattle in a six year survey. Considerable losses also occur as a result of chronic suppurative pulmonary disease in intensively reared, housed calves; probably up to 50% of the losses are due to this disease.
AETIOLOGY
Chronic suppurative pulmonary disease is bacterial in origin but probably develops following either incomplete recovery from an acute pneumonia which may be viral or bacterial in origin or as a complication of a chronic pneumonia and bronchitis caused by mycoplasmas.
EPIDEMIOLOGY
This disease is particularly common in housed intensively reared calves and in adults but it occurs in cattle of all ages, both housed and at grass kept under beef and dairying systems. Animals with chronic suppurative pulmonary disease frequently develop an acute exacerbation following stress e.g. calving.
CLINICAL SIGNS
Typical cases are dull, thin and only intermittently fevered. Frequent, sometimes productive, coughing is present. Chest pain may be obvious at rest or occasionally detectable and sometimes even localised on percussion; during this procedure it is quite common to precipitate coughing although areas of dullness are rarely detectable. Affected calves sometimes have a mucoid nasal discharge, lose weight, have a variable appetite and frequently become pot-bellied.
DIAGNOSIS
Clinical signs - weight loss and coughing over several weeks with variable appetite, pyrexia and dullness. The post-mortem findings are characterisitic.
TREATMENT
In the main, these cases will show very little if any clinical response to antibiotic therapy although this may be required following an acute exacerbation in order to prolong the animal*s life. As chronic weight loss occurs it is best to cull affected individuals as soon as possible.
COCCIDIOSIS
Bovine coccidiosis is primarily a disease of calves under 6 months old which are kept under crowded unhygienic conditions. It is characterised clinically by a watery and sometimes blood-stained diarrhoea.
CLINICAL SIGNS
Clinical signs usually occur about 21 days after initial infection. In mild cases the faeces are watery with no blood apparent but in more severe infections the faeces contain blood. Straining is a characteristic clinical sign and dehydration and loss of condition proceeds rapidly. Clinical coccidiosis is usually presented as a sudden outbreak of dysentery among calves kept under crowded unhygienic conditions, e.g. as may occur in loose boxes, cattle courts or in feed lot systems.
EPIDEMIOLOGY
The life cycle of bovine coccidia takes 17 to 21 days.
Most outbreaks of bovine coccidiosis can be attributed to a build up of resistant oocysts on pasture or bedding.
Animals infected with coccidia develop immunity but information on the duration of this immunity is lacking; certainly low numbers of coccidia oocysts can frequently be detected in bovine faeces and may act as a source of infection for susceptible calves.
TREATMENT AND CONTROL
Treatment over 3-5 days with sulphadimidine or amprolium is recommended. In farms where the disease is a problem the infected premises should be thoroughly cleaned and disinfected and bedding should be kept dry. When the disease occurs at pasture, alternative grazing should be provided and the contaminated area avoided for at least one year. Prevention is based on good management practices to avoid heavy build up of oocysts, for example moving feed trough regularly.
Anticoccidial feed supplements can be used if necessary.
"ACUTE" COPPER POISONING
Chronic ingestion of copper results in the breakdown of blood cells which produces the main clinical sign of blood staining in the urine.
PREVALENCE
The incidence of copper poisoning in cattle is very low and most cases occur in young animals.
AETIOLOGY AND PATHOGENESIS
Adult cattle appear to be able to tolerate the continuous intake of relatively large amounts of copper without ill effects. However young cattle, particularly young calves are more susceptible to the effects of ‘chronic copper poisoning*. Large amounts of copper can be retained in the liver but eventually a point is reached when a large proportion of this stored copper is released into the bloodstream producing a massive breakdown of red blood cells. Although the condition is due to ingestion of excess amounts of copper over a prolonged period the clinical disease presents as an acute syndrome. Most cases arise due to environmental contamination but occasionally cases occur when copper supplemented food (e.g. concentrates prepared for pigs) is fed.
CLINICAL SIGNS
These are of sudden onset. Affected animals are dull and anorexic. Red stained urine and marked jaundice are seen. Fever is not a feature. Deaths usually occur within a few days. Recovery has been reported. It would appear that stress, e.g. weaning, can precipitate the onset of clinical signs.
TREATMENT
There is no specific treatment. The source of copper should be eliminated.
DIFFUSE FIBROSING ALVEOLITIS (DFA)
DEFINITION
DFA is a disease characterised by increased respiratory rate and depth of breathing and frequent coughing in bright, old, thin cows.
INCIDENCE
This is one of the two common chronic respiratory diseases of adult cattle, the other being chronic suppurative pneumonia.
AETIOLOGY
In many cases the precise cause of this syndrome cannot be determined but it is likely that DFA represents the end stage of several different disease processes, one of which maybe farmer*s lung.
CLINICAL SIGNS
A thin, bright cow that is eating well, with an increased respiratory rate and depth at rest. Coughing is frequent, harsh and non-productive. Breathing difficulty commonly develops after exercise and this may be the presenting sign. Terminally, severe cases become dull and develop congestive heart failure; they then become dull and develop other signs of congestive cardiac failure.
ENZOOTIC HAEMATURIA
Bovine enzootic haematuria has been recognised as a distinct clinical entity since 1834, when it was described as a chronic haematuric condition of adult cattle confined to upland and rough grazing. Haematuria is a term used to describe blood in the urine.
GEOGRAPHICAL DISTRIBUTION AND PREVALENCE
Enzootic haematuria has a worldwide distribution, although it tends to be confined to localised areas in which cattle are grazing on rough, unimproved, bracken infested pasture. Within the British Isles, enzootic haematuria occurs in Scotland, Wales and North West England.
Generally, the disease is sporadic in occurrence but, in some herds, many animals may become affected over a period of years. The disease is one of mature cattle, cases in animals of less than three years of age being extremely rare. In Scotland, the vast majority of affected animals are aged six years or older. Male and female cattle are equally affected.
CLINICAL SIGNS
The clinical picture varies according to the duration and severity of haematuria. Initially many animals have intermittent bouts of mild haematuria, lasting only a few days, with remissions of weeks or even months. During this period, which can last for months or years, there is no loss of condition and the animal appears otherwise healthy. However, most eventually become increasingly haematuric with shorter remissions until haematuria is continuous. Some animals appear to have continuous haematuria from the outset.
As the severity increases and remissions become shorter then further clinical signs develop. There is loss of condition and fall in milk yield although the animal does remain bright. Urination, occasionally accompanied by straining, becomes more frequent and the urine often contains large clots of blood. Due to this blood loss, the gums become pale and occasionally anaemia is so severe that cardiovascular abnormalities develop. Usually, on rectal examination there are no abnormalities detectable, but in approximately 20% of cases a bladder mass can be palpated. Clinically a co-existing pyelonephritis complicates approximately 15% of cases and in these enlargement of the left kidney is detected per rectum.
In Scotland, 50% of enzootic haematuria cases have clinically detectable oral papillomata.
The course of the disease is extremely variable depending, as do the clinical signs, on the duration and severity of haematuria. In general, the course is between three months and three years. Death is usually due to haemorrhagic anaemia, but in some cases may be attributed to complications such as pyelonephritis.
AETIOLOGY
It appears that the lesions described represent a spectrum of changes which may be induced by the same aetiological agents. In general, the lesions of enzootic haematuria may be regarded as the response of the bladder to an irritant which presumably arrives in the urine.
For many years, bracken has been suggested as the aetiological agent in bovine enzootic haematuria and indeed, the condition has been reproduced in cattle experimentally, including induction of bladder tumours, by longterm feeding of bracken. Also, bracken is a known carcinogen for laboratory animals, e.g. it will induce bladder tumours in guinea pigs.
TREATMENT AND CONTROL
No known treatment is of any use in this disease and affected animals should be fattened for slaughter.
Control measures would include pasture improvement.
PYELONEPHRITIS
The precise definition of pyelonephritis is inflammation of the kidney. Normally secondary to infection.
AETIOLOGY AND PREVALENCE
In cattle, pyelonephritis is a common condition, although sporadic in occurrence, which is almost entirely confined to mature cattle, particularly cows, and is caused by Corynebacterium renale. Occasionally the initial, acute, episode is severe enough to lead to renal failure but more commonly it is a chronic, relapsing condition and the acute phase may pass unnoticed. The economic importance of the disease at present is unknown.
It is generally agreed that pyelonephritis is basically an infectious and contagious disease but that there are subsidiary aetiological factors since intact and healthy urinary tract relatively resistant to infection. These subsidiary factors may include trauma (e.g. service, calving) or a degree of urinary obstruction.
CLINICAL SIGNS
There are two forms of the disease, i.e. acute and chronic:
Acute pyelonephritis
Abdominal pain is one of the major features of acute pyelonephritis. The animal is dull, anorexic, stands with its back arched, frequently shifts its stance, and may periodically kick at its abdomen. There is straining and frequent passing of small quantities of urine which is discoloured, containing blood, pus and tissue debris. Fever is common.
Chronic pyelonephritis
If the animal does not die in the acute phase then it may progress to the chronic form of pyelonephritis. Chronic pyelonephritis can, however, develop without any apparent acute phase.
In chronic pyelonephritis there is loss of condition and a fall in milk yield over a period of weeks, during which there are bouts of fever and inappetance. The frequency of urination is increased and may be accompanied by straining. The urine is turbid, containing pus, tissue debris and frequently small clots of blood.
DIAGNOSIS
Confirmation of diagnosis in early cases is based on examination of the turbid, blood-stained urine from which the organisms may be isolated. In later cases, the enlarged kidneys, distended ureters and thickened bladder may be recognised per rectum. The post mortem findings are characteristic.
TREATMENT
The use of large doses of penicillin for a week or more have been said to produce complete cures in some cases. Usually, however, there is irreparable kidney damage when the condition is diagnosed and, although treatment can produce a temporary improvement, relapse is the rule. Also, it should be remembered that remission does occur in untreated animals.
CONTROL
Surveys of dairy herds have indicated that a percentage of apparently healthy cattle harbour C.renale in the vagina. This may be as high as 23% in herds where cases of pyelonephritis have been recognised. There is evidence to suggest there is dissemination of the organism to close neighbours in tethered cattle. C.renale has also been isolated from the urine of healthy cattle and the penile sheath of bulls.
Control measures would include general hygiene and removal of clinical cases.
FARMER'S LUNG
Farmer's Lung is an extrinsic allergy which develops in housed adult cattle following their repeated exposure to mouldy hay dust containing fungal allergens. Two clinical forms have been recognised: a sudden onset form in which only individual animals are ill and an insidious onset form in which several animals within a herd may be affected simultaneously.
INCIDENCE
This is the most common respiratory disease of housed adult cattle in Britain, particularly when climatic conditions mean that bad hay has been made.
AETIOLOGY
The inhalation of mouldy hay dust containing antigens can result in an animal becoming sensitised and developing precipitating antibodies. When a sensitised individual inhales antigens, clinical signs develop after several hours and consequently, a hypersensitivity reaction occurs. Recent evidence has shown that dust particles alone can trigger off the condition.
PATHOGENESIS
When hay with a moisture content of 30-40% is baled, the temperature within the bale can rise to around 650C and the thermophilic microflora which then develops is dominated by the actinomycetes, in particular Mfaeni and T. vulgaris. After bales of mouldy hay have been opened and shaken, up to 1,500 million actinomycete spores may be present per cubic metre of air. These actinomycete spores are able to penetrate down to the lungs. The temperature within the lungs is sufficiently high for germination to begin and the enzyme-like substances produced induce the formation of precipitating antibodies. Afterwards, when these enzyme-like substances are inhaled preformed on plant and dust particles, a hypersensitivity reaction may result in the development of obvious signs of respiratory disease 6-10 hours later.
CLINICAL SIGNS
Sudden onset form - Individual animals. Mild to moderate attacks are unlikely to be noticed. Severe attack - sudden onset difficulty breathing in an alert animal. Milk drop is invariably present in lactating dairy cows and anorexia is a common feature.
Insidious onset form - Individuals or Group Disease. Obvious rapid breathing and frequent coughing in a bright cow. Weight loss. Decreased milk yield.
EPIDEMIOLOGY
This disease is most common m the western mainly upland areas of south-west Scotland, the Lake District of England and Wales; these areas enjoy a regular rainfall during the hay making season. Dairy cows are more often affected because they are housed for longer periods. Older cows tend to develop obvious clinical signs towards the beginning of the winter (November, December, January) whereas younger cows are usually first seen to be ill towards the end of winter (February, March, April).
DIAGNOSIS
Farmer*s lung has only been confirmed in cattle being fed mouldy hay. Even severely affected individuals are bright. After appropriate treatment, recovery time is short.
TREATMENT
Betamethasone for two days. NB. This can produce abortion in pregnant cows. Antibiotics should probably be given. Removal of affected individual from source of antigens. Etamiphylline and frusemide if in cor pulmonale. (N.B. Not all products containing etamiphylline are licensed for food-producing animals).
CONTROL
The only way to avoid the development of this disease in areas where the hay is regularly mouldy is not to make hay.
Change to silage feeding
Artificial drying of baled hay
Install fans - practical and cheap.
If farmers lung is confirmed in cattle then the farmer/cattle-man should be asked whether he himself suffers any respiratory trouble or has developed a flu-like respiratory illness which has proven difficult to shake off. If so, then the seeking of medical advice should be advised.
THE FAT COW SYNDROME
A condition caused by excessive energy intake in dairy cattle in late lactation and the dry period which is exacerbated by a low protein intake over the same period.
These cows become over-fat, with excessive subcutaneous fat depots which are mobilised to the liver at the time of greatest demand i.e. post-calving and early lactation, and the subsequent deposition of fat in the liver results in metabolic problems e.g. hypocalcaemia, acetonaemia and an increase in periparturient infections e.g. mastitis.
The condition is an exacerbation of what is known to happen in more than 70% of apparently normal high-yielding dairy cattle in the U.K. as they change from a state of positive energy balance to one of negative energy balance at parturition.
CLINICAL SIGNS
Cows that are very fat during the dry period and at calving have an increased incidence of periparturient problems e.g. hypocalcaemia etc. which are unusually resistant to treatment. The severely affected cases have reduced appetites eventually becoming totally anorexic and subsequently ketotic although there is no response to treatment. These severe cases usually die or are culled within 10 days. In less severe cases milk yields are dramatically reduced, metritis, mastitis, lameness are common as incidental findings, and in animals which are kept the body condition suddenly deteriorates 3-4 weeks after calving. Anoestrus and suboestrus are a problem and lactation is usually severely curtailed.
DIAGNOSIS
Usually a group problem but may affect individuals e.g. show cows or dominant cows in a herd. If the above clinical signs are present then a diagnosis can be made using a mathematical calculation involving blood glucose, AST and free fatty acid levels as an estimate of fatty infiltration of the liver. Liver biopsy can be used to confirm this condition.
TREATMENT
Treatment of over-fat pregnant cows is of little value and affected cases should be slaughtered.
Cases not diagnosed till after calving usually prove resistant to treatment and are also probably better culled as they prove to be economic disasters if kept.
CONTROL
Dairy cows should be prevented from becoming over-fat during late lactation and the dry period by keeping energy intake down and maintaining a balanced ration.
Feeding should be closely monitored to ensure that cows are not over-fed and dairy cows should be ‘lead-fed* and not steamed-up.
FASCIOLIOSIS (liver fluke)
Fascioliosis in cattle occurs in the wetter western areas of the country but only in very wet years. The reason for the difference in severity of the disease between sheep and cattle would appear to lie basically in the fact that unlike sheep, cattle which have been previously infected with Fasciola hepatica acquire a degree of resistance to reinfection and also that the bovine liver appears to be able to tolerate the presence of very large numbers of developing immature parasites without the occurrence of the severe pathogenic effects seen in sheep. Outbreaks of acute and sub-acute Fascioliosis comparable to those seen in the sheep are therefore rare.
Bovine Fascioliosis is mainly a chronic disease, usually of calves or yearlings, which have spent their first autumn on infected pasture. Adult stock which have had previous experience of the parasite acquire an immunity and can withstand a heavy challenge from infected pastures without showing clinical disease. They may however harbour a small population of F.hepatica which could impair productivity.
The clinical signs are very similar to those seen in chronic Fascioliosis in sheep, namely loss of condition, marked anaemia and in severe cases submandibular oedema. Diarrhoea is not found in cases of chronic bovine fascioliosis unless they are complicated by the presence of Ostertagia spp, and this results in a different syndrome, the Fascioliosis-Ostertagiosis F/O Complex.
Treatment with triclabendazole, nitroxynil or oxyclozanide is usually successful. In the case of lactating animals milk has to be discarded for several days except where oxyclozanide is used. It is important to establish whether Ostertagia is a complicating factor in order that combined treatment for F.hepatica or O.ostertagi may be instituted. A combination product containing ivermectin and clorsulon, which is effective against adult flukes, could be used in the treatment of the F/O complex.
For control in normal years, cattle, whether housed or outwintered can be dosed prophylactically in December or January, with a drug effective against adult stages. Since triclabendazole is the only compound effective against most of the migratory stages in the liver it is the drug of choice for treatment at housing. In wet springs a second dose may be given to outwintered stock in May to remove infections acquired during winter and so minimise pasture contamination with eggs.
The economics of Fascioiosis in cattle are concerned mainly with losses in productivity rather than fatalities and it has been suggested that even a low level infection (approximately 100 F.hepatica) can result in an 8% loss in production while heavy infections (250 F.hepatica) can be responsible for a 20% loss in productivity.
FASCIOLOSIS
A parasitic condition of sheep and cattle caused by the migration and feeding habits of Fasciola hepatica in the liver tissue and bile ducts. Part of the life cycle is spent in a mud snail, Lymnaea truncatula and outbreaks in areas suitable for snail colonisation, usually occur in autumn and winter. These are characterised by weight loss, anaemia and hypoproteinaemia and in heavy infections of sheep sudden death may occur.
AETIOLOGY
The adult F.hepatica, or liver fluke, is leaf-shaped and is up to 3.5 cms. in length; it is situated in the bile ducts where the eggs are shed and subsequently passed in the faeces. These eggs then develop and hatch intomotile ciliated miracidia; this takes 9 days at the optimal temperature of 22-260C but at lower temperatures requires longer and no development occurs below 100C.
The adult F.hepatica, or liver fluke, is leaf-shaped and is up to 3.5 cms. in length; it is situated in the bile ducts where the eggs are shed and subsequently passed in the faeces. These eggs then develop and hatch into motile ciliated miracidia; this takes 9 days at the optimal temperature of 22-260C but at lower temperatures requires longer and no development occurs below 100C.
The liberated miracidia have a short life span and must contact the snail intermediate host, L.truncatula, within 3 hours if successful penetration of the latter is to occur. In infected snails development proceeds through sporocyst and rediae stages to the final snail stage, the cercariae; the latter are shed from the snail as motile forms which attach themselves to surfaces, such as grass blades, and encyst there to form the infective metacercariae. It takes a minimum of 6 to 7 weeks for completion of development from miracidia to metacercariae although under un-favourable circumstances a period of several months is required. Infection of a single snail with one miracidium can produce over 600 metacercariae.
Metacercariae ingested by the final host excyst in the small intestine, migrate through the gut wail, cross the peritoneum and penetrate the liver capsule. The young flukes tunnel through the parenchyma for 6 to 8 weeks then enter the bile ducts where they mature and migrate to the larger ducts and gall bladder in about 4 weeks. The period from ingestion of metacercariae to the presence of fluke eggs in the faeces is 10-12 weeks.
The minimal period for completion of one entire life cycle of F.hepalica is therefore 17-18 weeks.
ECOLOGY AND LIFE HISTORY OF L.truncatula
L.truncatula is a small snail, the adults being about 1 cm in length. The shell is usually dark brown and has a turreted appearance, i.e. coiled in a spiral form; the aperture is approximately half the total length of the snail and is on the right hand side.
L.truncatula snails are amphibious; they require moisture for normal activity but breathe atmospheric oxygen. Thus although they may spend hours in shallow water they may periodically emerge. They are capable of withstanding drought or freezing by respectively aestivating or hibernating in the mud. Optimal conditions include a slightly acid pH environment and a slowly moving water medium to carry away waste products. They feed mostly on algae.
The optimum temperature range for development is 18-220C and at this temperature egg masses will develop to adult snails in 3 weeks. L.truncatula is hermaphrodite and one snail is capable of producing, in a 3 month breeding season, up to 100,000 descendants.
EPIDEMIOLOGY
There are 3 main factors influencing the availability of the large numbers of metacercariae necessary for outbreaks of fasciolosis. These are:
1. Availability of suitable snail habitats
L.truncatula prefers wet mud to free water and permanent habitats include the banks of ditches or streams and the edge of small ponds. Following heavy rainfall or flooding temporary habitats may be provided by hoof marks, wheel ruts or rain ponds. Fields with clumps of rushes are often suspect sites, these having a slightly acid pH environment; although the latter pH is considered to be optimal, excessive pH levels are detrimental, e.g., as in peat bogs and areas of sphagnum moss.
2. Moisture
The ideal moisture conditions for snail breeding and also for F. hepatica development within the snails are provided when rainfall exceeds transpiration, i.e. when field capacity in terms of saturation is reached. Such conditions are also particularly advantageous for the development and hatching of Fasicola eggs for miracidia searching for snails and for the dispersal of cercariae after shedding from snails.
3. Temperature
A mean day night temperature of 100C or above is necessary for snails to breed and for development of F. hepatica within the snail to proceed. It is also the critical temperature for the development and hatching of fluke eggs. As the mean day night temperature increases during late spring and early summer so the developmental cycles of liver fluke, outside of the final host, become shorter, reaching a minimum of 5 weeks in midsummer.
The minimal temperature requirements for development of the extra-final host stages of F.hepatica only prevail from April to October in the southern half of Britain; farther north the necessary temperature is only present from May to September. Annual variations in these temperature conditions are minor and the main factor influencing the incidence of snail populations and therefore of fasciolosis is summer rainfall.
The number of annual cycles of snail breeding varies in different regions of the country, e.g. in West Scotland the minimal temperatures for snail breeding are present in May through September and the annual rainfall varies from 1,000 to 1,500 mm. In this region snails which hibernate over the winter commence to lay eggs in May; these egg masses hatch to young snails in June which reach maturity in late July to lay egg masses again on the pasture. With the failing temperatures in autumn this second generation is not completed until the following spring, i.e. there is only one generation per annum. Obviously farther south in Britain the period suitable for development is longer and an extra generation is possible.
As a result of studies on snail populations, climatic data and disease incidence in the UK, two annual cycles of infection in fasciolosis were described. The first, and most important, involved infection of the intermediate host snail in summer by miracidia developed from eggs deposited in spring and early summer by infected animals; this infection took at least 5 weeks to develop to the cercarial stage and resulted in an increase in pasture levels of metacercariae from late August onwards. This is the summer infection of snails. It is important to remember that the metacercariae produced by this infection, if not ingested in the autumn, are capable of over-wintering and initiating infection in animals in the following spring; any surviving metacercariae appear to die off by mid-summer.
The second, involved infection of snails in the autumn by miracidia developed from eggs deposited in the late summer; development of this infection in the snail ceased during the winter and was completed in the following spring resulting in an increase in pasture levels of metacercariae around mid-summer. This is the winter infection of snails and is thought to be of less importance in Britain than the summer infection. This is possibly due to a selective mortality of infected snails during the winter.
In the last few years further studies on the seasonal prevalence of fasciolosis have been made using parasite-free stock to monitor the seasonal availability of metacercariae on pasture and outbreaks of disease. These studies have underlined the importance of the summer infection of snails which produces the autumnal flush in pasture levels of metacercariae. Ingestion of the latter results in the clinical disease known to occur in sheep from October onwards and in cattle during the winter.
Although there is no evidence, that under field conditions sheep become immune to reinfection with Fasicola, the migration of flukes in animals previously exposed to the parasite is delayed; this results in a prolonged pre-patent period. Thus in previously exposed animals the period between the acquisition of infection and the onset of clinical disease may be longer than one would expect from a knowledge of the life cycle. Also, following treatment of carrier animals, the period between re-infection and reappearance of eggs in the faeces again may be prolonged.
THE DISEASE IN SHEEP
Clinical fasciolosis in sheep can be divided into acute, sub-acute and chronic, according to the number and stage of development of parasites in the liver, but since any such classification is always arbitrary there will be considerable overlap between these categories. It should always be remembered that an outbreak of fasciolosis will be a flock problem even though only a few individuals may be showing typical clinical signs at any one time and therapy must always be considered on this basis.
Acute Fasciolosis
CLINICAL SIGNS
Outbreaks of acute fasciolosis are seen in late autumn and early winter. Acute disease is associated with the presence of large numbers of immature flukes in the liver of affected sheep. The large number of flukes developing in the liver at one time can be the result of the sheep ingesting large numbers of metacercariae over a short period from very heavily infected pasture; it may also be that in sheep which have been exposed to the parasite before, migration of the flukes through the liver may be prolonged and so allow the fluke population to accumulate. Cases of acute fasciolosis in the field are generally presented as sudden deaths in a flock of ewes. On examination of the remainder of the flock one may find ewes which are weak, with pale mucous membranes, breathing difficulties, and in some cases there may be a palpably enlarged liver with some abdominal pain. Abdominal fluid build up is also a common finding in these cases. Diarrhoea is not a feature.
Since the flukes are still immature no eggs are present in the faeces of affected sheep.The flukes recovered from cases of acute fasciolosis at post-mortem are small, only 4-8 mm long, indicating an infection of about 6-8 weeks duration and there may be in excess of 1,000 flukes in the affected liver.
DIAGNOSIS
Diagnosis is most accurately based on a good post-mortem examination confirmed where possible by clinical examination of the survivors. In some cases there may be a history of the flock grazing known infected pasture 6-8 weeks previously. Forecasts issued by the Ministry of Agriculture on the possible incidence of fasciolosis can be of use in indicating the severity of the disease expected in subsequent months.
TREATMENT
The drug of choice in the treatment of outbreaks of acute fasciolosis is triclabendazole. Two other compounds which have some activity against immature flukes are nitroxynil and closantel.
Sub-acute Fasciolosis
CLINICAL SIGNS
This also occurs in the late autumn and early winter but in these cases the disease is not so rapidly fatal and the affected sheep may show clinical signs for one or two weeks prior to death. Large numbers of flukes are again present in an infected liver but the numbers are somewhat reduced from those found in cases of acute fluke though the parasites have developed further and a substantial proportion of the fluke population is now present as adults in the major bile ducts. This form of the disease may develop where the sheep have ingested large numbers of metacercanae over a longer period or the number ingested at any one time has not been sufficient to cause the acute form of the disease.
Affected sheep lose condition rapidly, become markedly anaemic with obvious pallor of their mucous membranes and may have a palpably enlarged liver and resent abdominal palpation. Submandibular oedema and abdominal fluid may be present in some cases. Diarrhoea is not a feature.
F. hepatica eggs are present in the faeces.
The number of flukes recovered at post-mortem examination vanes between 500-1,500 and usually about half the population have developed into adult flukes. This type of fasciolosis usually occurs 12-20 weeks after ingestion of large numbers of metacercariae.
DIAGNOSIS
This is based on clinical signs, faecal egg counts, and a good post-mortem. Again a history of grazing infected pasture some months previously may be obtained.
TREATMENT
Triclabendazole is again the drug of choice but nitzoxynil and closantel are also effective.
Chronic Fasciolosis
Outbreaks of chronic fasciolosis are seen in the latter part of the winter and in early spring and this form of the disease is characterised by a progressive loss of condition and terminal emaciation, pallor of the mucous membranes, submandibular oedema and abdominal fluid. This form of the disease is the result of the infection picked up in the autumn and winter which is now present as adult flukes in the bile ducts and over the ensuing months these flukes remove more blood from the circulation than the sheep can replace and so the anaemia becomes progressively worse. In uncomplicated cases diarrhoea does not occur.
Eggs are usually found In the faeces.
DIAGNOSIS
This is again based on clinical signs, faeces examination and post-mortem findings.
TREATMENT
Triclabendazole is best but nitroxynil, closantel and oxyclozanide may also be used. Oxyclozanide has no milk withdrawal period in milking sheep, the others cannot be used. Albendazole also has activity against adult fluke in addition to anti-nematode activity. A number of combination products for fluke and nematodes are available.
PROPHYLAXIS OF FASCIOLOSIS
Severe outbreaks of fasciolosis only occur following wet springs and summers. The Ministry of Agriculture have therefore been able to develop a formula for forecasting the likely incidence and severity of fasciolosis based mainly on rainfall figures from the preceding months. In the case of the summer infection of snails responsible for outbreaks of acute fasciolosis, accurate forecasts can be made by the end of the summer; however an ‘early warning* can also be issued if May and June have been unduly wet.
Control of fasciolosis whether on a long term or on a short term basis in conjunction with the forecast system may be approached in two ways; first, by reducing populations of the intermediate snail host or secondly by using anthelmintics to limit the availability of F. hepatica eggs and therefore miracidia to surviving snail populations.
REDUCTION OF L.truncatula POPULATIONS
Before any scheme of snail control is undertaken a survey of the control area for snail habitats should be made as the latter may be localised or whole fields may be involved.
The best long-term method for reducing snail populations is drainage. It has been demonstrated that permanent destruction of snail habitats can be achieved by this method but many are often hesitant to undertake expensive drainage schemes.
When the area of snail colonisation is confined, a simple method of control is to fence off this area or treat with a molluscicide such as copper sulphate. Although more efficient molluscicides have been developed these are expensive and none have proved to be a practical solution in fluke control in Britain.
USE OF ANTHELMINTICS
The prophylactic use of fluke anthelmintics is aimed at reducing pasture contamination by F.hepatica eggs at a time most suitable for their development, i.e. April to August, and removing fluke populations at a time of heavy burden, i.e. October-December, or at a period of nutritional and pregnancy stress to the animal, i.e. January to April.
Based on these criteria the following control programme for sheep is recommended for years with normal or below average rainfall.
1. Late April/early May - dose all adult sheep. The fasciolicide used should be highly efficient against adult flukes. Triclabendazole, nitroxynil, closantel, oxyclozanide or combination products can be used.
2. October - dose all sheep. Use a drug effective against parenchymal stages, eg. triclabendazole.
3. January - dose all sheep. Any recommended flukicidal drug such as triclabendazole, nitroxynil or closantel may be used.
In wet years 2 further doses with a flukicidal drug should be used as follows:
June (4-6 weeks after the May dose) - dose all sheep with triclabendazole, nitroxynil, closantel or oxyclozanide
October/November (4 weeks after early October dose) - dose all sheep with a drug effective against parenchymal stages - triclabendazole.
The exact timing of the spring and autumn treatments will depend on lambing and tupping dates.
OSTERTAGIOSIS
Ostertagia ostertagi is the most common cause of parasitic gastritis in cattle. The disease, ostertagiosis, is characterised by weight loss and diarrhoea and typically affects young cattle during their first grazing season, although herd outbreaks and sporadic individual cases have also been reported in adult cattle.
LIFE CYCLE
O.ostertagi has a direct life cycle. The eggs are passed in the faeces and develop within the faecal pat to the infective third stage. When moist conditions prevail the larvae migrate from the faeces onto the herbage.
After ingestion the larvae develop in the lumen of an abomasal gland before they emerge from the gland to become mature on the mucosal surface.
The entire parasitic life cycle usually takes three weeks but under certain circumstances many of the ingested larvae become inhibited in development for periods of up to six months.
The presence of O.ostertagi in the abomasum in sufficient numbers gives rise to extensive pathological and biochemical changes and severe clinical signs. These changes are maximal about 18 days after infection but it may be delayed for several months when arrested larval development occurs.
In heavy infections of 40,000 or more adult worms the principal effects of these changes are first, a reduction in the acidity of the abomasal fluid, the pH increasing from 2.0 up to 7.0. This results in a failure to activate pepsinogen to pepsin and to denature proteins. There is also a loss of bacteriostatic effect in the abomasum. Secondly, there is an enhanced permeability of the abomasal epithelium to macromolecules such as pepsinogen and plasma proteins. The results of these changes are a leakage of pepsinogen into the circulation leading to elevated plasma pepsinogen levels and the loss of plasma proteins into the gut lumen eventually leading to low blood protein levels. Clinically these consequences are reflected as inappetance, weight loss and diarrhoea and precise cause of the latter being unknown.
In lighter infections the main effects are sub-optimal weight gains.
CLINICAL SIGNS
Bovine ostertagiosis is known to occur in two clinical forms. In temperate climates with cold winters the seasonal occurrence of these is as follows.
The Type I disease is usually seen in calves grazed intensively during their first grazing season as the result of large numbers of larvae ingested 3-4 weeks previously; this normally occurs from mid-July onwards.
The Type II disease occurs in yearlings, usually in late winter or spring following their first grazing season and results from the maturation of larvae ingested during the previous autumn and subsequently inhibited in their development.
The main clinical sign in both Type I and Type II disease is a profuse diarrhoea and in Type I, where calves are at grass, this is usually persistent, watery and has a characteristic bright green colour. In contrast, in the majority of animals with Type II the diarrhoea is often intermittent and anorexia and thirst are usually present. The coats of affected animals in both syndromes are dull and the hind quarters heavily soiled with faeces.
In both forms of the disease the loss of body weight is considerable during the clinical phase and may reach 20% in 7-10 days. Carcass quality may also be affected since there is a reduction in total body solids relative to total body water.
In Type I disease, the morbidity is usually high, often exceeding 75%, but mortality is rare provided treatment is instituted within 2-3 days. In Type II disease only a proportion of animals in the group are affected but mortality in such animals is very high unless early treatment with an anthelmintic effective against both inhibited and developing larval stages is instituted.
EPIDEMIOLOGY
Dairy Herds
From epidemiological studies the following important facts have emerged:
1. A considerable number of larvae can survive the winter on pasture and in soil. Sometimes the numbers are sufficient to precipitate Type I disease in calves 3-4 weeks after they are turned out to graze in the spring. However, this is unusual, and the role of the surviving larvae is rather to infect calves at a level which produces patent sub-clinical infection which ensures contamination of the pasture for the rest of the grazing season.
2. A high mortality of overwintered larvae on the pasture occurs in spring and only negligible numbers can usually be detected by June. This mortality combined with the dilution effect of the rapidly growing herbage renders most pastures, not grazed in the spring, safe for grazing after mid-summer.
However, despite the mortality of larvae on the pasture it now appears that some can survive in the soil for at least another year and on occasion appear to migrate on to the herbage. Whether this is a common occurrence and whether the larvae migrate or are transported by terrestrial populations of earthworms or beetles is not definitely known but the occurrence of this apparent reservoir of larvae in soil may be important in relation to certain systems of control based on grazing management.
3. The eggs deposited in the spring develop slowly to larvae; this rate of development becomes more rapid towards mid-summer as temperatures increase, and as a result, the majority of eggs deposited during April, May and June all reach the infective stage from mid-July onwards. If sufficient numbers of these larvae are ingested the Type I disease occurs any time from July until October. Development from egg to larvae slows during the autumn and it is doubtful if many of the eggs deposited after September ever develop to larvae.
4. As autumn progresses and temperatures fall an increasing proportion (up to 80%) of the larvae ingested do not mature but become inhibited. In late autumn, calves can therefore harbour many thousands of larvae but few developing forms or adults. These infections are generally asymptomatic until maturation takes place during winter and early spring and if large numbers of these larvae develop synchronously, Type II disease occurs. Where maturation is not synchronous clinical signs may not occur but the adult worm burdens which develop can contribute to pasture contamination in the spring.
Two factors, one management and one climatic, appear to increase the prevalence of Type II ostertagiosis.
First, the practice of grazing calves from May until July on permanent pasture, then moving these to hay or silage aftermath before returning them to the original grazing in late autumn. In this system the accumulation of larvae on the original pasture will occur from mid-July i.e. after the calves have moved to aftermath. These larvae are still present on the pastures when the calves return in the late autumn and, when ingested, the majority will become inhibited and thus increase the potential for Type II disease.
Secondly, in dry summers the larvae are retained within the crusted faecal pat and cannot migrate on to the pasture until sufficient rainfall occurs to moisten the pat. If rainfall is delayed until late autumn many larvae liberated on to pasture will become inhibited following ingestion and so increase the chance of Type II disease. Indeed, epidemics of Type II ostertagiosis are typically preceded by dry summers.
Although primarily a disease of young dairy cattle, ostertagiosis can affect groups of older cattle, particularly if these have had no previous exposure to the parasite since there is no significant age immunity to infection. Also, acquired immunity in ostertagiosis is slow to develop and calves do not acquire a significant level of immunity until the end of their first grazing season. If they are then housed for thewinter and acquired immunity has waned by the following spring and yearlings turned out at that time are partially susceptible to reinfection and can contaminate the pasture with small numbers of eggs. However, immunity is rapidly reestablished and any clinical signs which occur are usually of a transient nature. During the second and third year of grazing a strong acquired immunity develops and adult stock in endemic areas are generally highly immune to reinfection. An exception to this rule occurs around the periparturient period when immunity wanes, particularly in heifers, and there are reports of clinical disease following calving. The reason is unknown but may be due to the development of larvae which were arrested in their development as a result of host immunity.
Beef Herds:
Although the basic epidemiology in beef herds is similar to dairy herds the influence of immune adult animals grazing alongside susceptible calves has to be considered. Thus in beef herds where calving takes place in the spring, ostertagiosis is uncommon since egg production by immune adults is low, and the spring mortality of the overwintered larvae occurs prior to the suckling calves ingesting significant quantities of grass. Consequently only low numbers of larvae become available on the pasture later in the year.
However, where calving takes place in the autumn or winter, ostertagiosis can be a problem in calves during the following grazing season after they are weaned. The epidemiology is then similar to that seen in dairy calves. Whether Type I or Type II disease subsequently occurs depends on the grazing management of the calves following weaning.
DIAGNOSIS
In older animals the clinical signs and history are similar but laboratory diagnosis is more difficult. A useful technique to employ in such situations is to carry out a pasture larval count on the field on which the animals had been grazing. Where the level of infection is more than 1,000 larvae per kg of dried herbage the daily larval intake of grazing cows is in excess of 10,000 larvae. This level is probably sufficient to cause clinical disease in susceptible adult animals or to upset the normal functioning of the gastric mucosa in immune cows.
TREATMENT
Type I disease responds well to treatment at the standard dosage rates with any of the modem benzimidazoles (albendazole, fenbendazole or oxfendazole), the probenzimidazoles, levamisole, or ivermectin. All of these drugs are effective against developing larvae and adult stages. Following treatment calves should be moved to pasture which has not been grazed by cattle in the same year. The field where the outbreak has originated may be grazed by sheep or rested until the following June.
For the successful treatment of Type II disease it is necessary to use drugs which are effective against inhibited larvae as well as developing larvae and adult stages. Only the modem benzimidazoles listed above or ivermectin are useful in the treatment of Type II disease when used at standard dosage levels although the probenzimidazoles are also effective at higher dose rates.
In young animals this decision is based on:
The clinical signs of inappetance, weight loss and diarrhoea
The season. For example, Type I occurs from July until September and Type II from March to May
The grazing history. In Type I disease, the calves have usually been set-stocked in one area for several months, in contrast, Type II disease often has a typical history of calves being grazed on a field from spring to mid-summer, before being moved and then brought back to the original field in the autumn. Affected farms usually also have a history of ostertagiosis in previous years.
Faecal egg counts. In Type I disease these can be more than 1,000 eggs per gram and are a useful aid to diagnosis; in Type II counts are highly variable, may even be negative and are of limited value.
Plasma pepsinogen levels. In clinically affected animals up to two years old these are usually raised.
Post-mortem examination
CONTROL
Traditionally, ostertagiosis has been prevented by routinely treating young cattle with anthelmintics over the period when pasture larval levels are increasing. For example, this involves one or two treatments usually in July and September and on many farms this prevented disease and produced acceptable growth rates. However, it has the disadvantage that since the calves are under continuous larval challenge their performance may be impaired. With this system effective anthelmintic treatment at housing is also necessary using a drug effective against inhibited larvae in order to prevent Type II disease. Today, it is accepted that the prevention of ostertagiosis by limiting exposure to infection is a more efficient method of control.
This may be done by grazing calves on new grass leys although it is doubtful if this should be recommended for replacement dairy heifers, as it would result in a pool of susceptible adult animals. A better policy is to permit young cattle sufficient exposure to larval infection to stimulate immunity but not sufficient to cause a loss in production. The provision of this ‘safe pasture* may be achieved in two ways:
First, by using anthelmintics to limit pasture contamination with eggs during periods when the climate is optimal for development of the free-living larval stages i.e. spring and summer.
Alternatively by resting pasture or grazing it with another host, such as sheep, which are not susceptible to O.ostertagi, until most of the existing larvae on the pasture have died out.
Sometimes a combination of these methods is employed.
Prophylactic Anthelmintic Medication
Since the crucial period of pasture contamination with O.ostertagi eggs is the period up to mid-July, one of the efficient modern anthelmintics may be given on two or three occasions between turnout in the spring and July to minimise the numbers of eggs deposited on the pasture. For calves going to pasture in early May two treatments, three and seven weeks later are used, whereas calves turned out in April require three treatments. With some anthelmintics which have a persistent effect and prevent infection for several weeks after administration, various regimens are recommended. For example ivermectin at 3, 8 and 13 weeks post turnout or doramectin at turnout and 8 weeks later.
Several rumen boluses have been developed which release in a sustained fashion or as programmed single ‘pulse* doses. When these boluses are administered to calves just prior to turn-out they prevent the development of infections acquired from overwintered larvae and so prevents the deposition of eggs during the spring. This in turn prevents the development of high levels of pasture contamination with larvae which are responsible for disease.
Anthelmintic prophylaxis has the advantage that animals can be grazed throughout the year on the same pasture and is particularly advantageous for the small heavily stocked farm where grazing is limited.
Anthelmintic treatment and move to safe pasture in mid-July
This is usually referred to as the ‘dose and move" system and is based on the knowledge that the annual increase of larvae occurs after mid-July. Therefore if calves grazed from early spring are given an anthelmintic treatment in early July and moved immediately to a second pasture such as silage or hay aftermath, the level of infection which develops on the second pasture will be low.
The one reservation with this technique is that in certain years the numbers of larvae which overwinter are sufficient to cause heavy infections in the spring and clinical ostertagiosis can occur in calves in April and May. However, once the ‘dose and move' system has operated for a few years this problem is unlikely to arise.
Alternate grazing of cattle and sheep
This system ideally utilises a three year rotation of cattle, sheep and crops. Since the effective life-span of most O.ostertagi larvae is under one year and cross infection between cattle and sheep in temperate areas is largely limited to Trichostrongylus axei, good control of bovine ostertagiosis should, in theory, be achieved. It is particularly applicable to farms with a high proportion of land suitable for cropping or grassland conservation and less so for marginal or upland areas, but in these areas good control has been reported using an annual rotation of beef cattle and sheep.
The drawback of alternate grazing systems is that they impose a rigorous and inflexible regimen on the use of land which the farmer may find impractical. Furthermore, in warmer climates where Haemonchus is prevalent this system can prove dangerous since this very pathogenic worm establishes in both sheep and cattle, but is not a problem in Scotland.
FOG FEVER
This is a sudden onset, respiratory distress syndrome with minimal coughing which occurs typically in hungry fat, beef-type cows, in the autumn, within two weeks of their being moved onto lush pasture.
AETIOLOGY
The cause of fog fever has still not been fully resolved but there is an increasing amount of circumstantial evidence to link the development of clinical signs with the ingestion of large amounts of the amino acid, L-tryptophan.
INCIDENCE
This is one of the most common respiratory diseases of grazing adult beef cows.
EPIDEMIOLOGY
This is a disease of adult (> two years old) beef suckler cows of which Hereford and Hereford cross animals appear to be particularly susceptible. The condition has been reported from all over the British Isles and there appears to be a positive relationship between the lushness of the grass and the severity of the clinical disease. Clinical signs usually develop within two weeks (4-10 days) of a sudden change to lush pasture and this is the reason for the highest incidence of disease occurring in the autumn.
PATHOGENESIS
Following the ingestion of lush grass in relatively large quantities, L-tryptophan is converted in the rumen into 3 methyl indole and indole acetic acid. Under experimental conditions, the feeding of comparatively large amounts of L-tryptophan and 3 methyl indole to cows can result in the development of respiratory distress and deaths several days later.
CLINICAL SIGNS
Fog fever is a group disease, although in many outbreaks, only one animal may be seen by the farmer to be ill initially.
Severe form/Early stage. Sudden onset respiratory distress which is often severe. When moved, mouth-breathing may develop. Dullness. Anorexia. Normal temperature. A high proportion of severe cases die (75%), especially if they are moved or excited in any way. Those which survive for three days usually recover.
Severe form/Late stage. The respiratory distress gradually becomes less obvious. They become brighter and begin eating again. Normally not more than 5% of the cows in an affected group are severely affected. However, the other 95% are likely to be suffering from a mild form of fog fever. Frequent coughing is not a feature of either the severe or the mild forms of the disease.
DIAGNOSIS
The clinical and epidemiological features of this disease are sufficiently characteristic to enable a diagnosis to be made quickly.
TREATMENT
Flunixin meglumine (Finadyne) and frusemide may be beneficial. Affected animals should be kept as quiet as possible and in those herds in which one or more cases have recently occurred, the cows should not be subjected to conditions calculated to cause excessive excitement or exertion e.g. being moved from one field to another, as further cases may be precipitated. However, if affected individuals survive the first three days of illness, they will almost certainly recover, although convalescence may be prolonged.
CONTROL
Avoid giving hungry beef cows unrestricted access to lush pasture. Strip-grazing, pre-feeding cows prior to changing pasture or allowing less susceptible stock to graze lush pasture first may decrease the risk of disease.
FOOT-AND-MOUTH DISEASE
Foot-and-Mouth disease (FMD) is a highly contagious viral disease affecting all ruminants, both domesticated and wild, and swine, in which it causes vesicles and ulcers in the mouth, on the udder and on the feet. While mortality is generally low, loss of production is severe. The disease is found in many areas of the world. South America, Africa, the middle East and Asia are endemic areas. Western Europe is normally free of the infection.
AETIOLOGY
Foot-and-mouth disease virus (FMDV) is an aphthovirus within the picornaviridae. Characteristics of the virus which are important in the epidemiology of the disease include the rapid growth cycle of the virus, the stability of the virus under a variety of conditions and the occurrence of serotypes.
Serotypes: There are 7 serotypes which are designated according to the geographical area where each was first recovered. Within each serotype there are several subtypes.
Disinfectants:
F- a region where foot-and-mouth disease frequently occurs, has increased dramatically in recent years with consequent increased risk of disease introduction.
The other route by which foot-and-mouth disease has gained entry to the UK is by windborne carnage from the continent and this is considered to have been the way disease spread from Brittany to Jersey and the Isle of Wight in 1981. Since the infection has been eradicated throughout the EU the most likely route by which - for cattle, sheep and pigs this is the respiratory tract. They can all be infected by inhaling doses in the range 10-25 infectious units. In contrast, the dose to infect cattle by the oral route is almost 1 million infectious units. Pigs can be infected by around 10 infectious units given orally. The dose to infect sheep by the alimentaiy route is not known.
Once one or more animals in a herd have been infected the quantity of virus in the environment will be greatly amplified and then transmission by several different routes will be possible. Resulting incubation periods will generally shorten as disease spreads through the herd.
The incubation period depends on the species, dose, route and strain of virus. In within-farm spread the incubation period can vary from 2-10 days but generally it can be expected to be 2-4 days for cattle, sheep and goats; 1 or 2 days longer for pigs. In between-farm spread by airborne route the incubation period can range from 4-14 days, depending on the infecting dose.
PATHOGENESIS
The usual route of virus entry is via the mucosae and lymphoid tissues of the pharyngeal/tonsillar region. Less frequently initial infection can occur through cuts in the mouth or on the feet as a result of abrasions and contact with contaminated materials. e.g. food stuffs (swill, meat) and fomites.
During the acute phase of disease (vesicles less than 1 week old), all body secretions and excretions of infected animals will contain high amounts of virus.
Post mortem the drop in pH associated with lactic and pyruvic acid formation during rigor mortis will inactivate FMD virus in skeletal muscles but virus will still persist in offal or bone marrow where such pH changes do not occur. It is for this reason that countries normally free of the disease which import carcase meat from endemic areas insist on the prior deboning of the meat amongst other measures.
Virus is also excreted from infected animals in aerosols of exhaled breath and in lymph from ruptured vesicles. The most important species in relation to airborne excretion is the pig. One infected pig can excrete around 4000 million infectious units per day.
Cattle, sheep and goats excrete much lower amounts of virus in breath; the highest recorded amount for these species is 10 infectious units per day. Therefore, as emitters of airborne virus, one infected pig is equivalent to around 3,000 infected cattle. For all species the excretion of airborne virus lasts for 4-5 days from the first development of vesicles.
Convalescent cattle, sheep and other ruminants, but not pigs, may carry the virus in their pharyngeal region for periods of many months. Vaccinated cattle can become carriers if exposed to infection without having developed clinical disease. There is some circumstantial evidence which suggests that transmission from carrier cattle may occur occasionally in the field but this has not been reproduced experimentally.
CLINICAL SIGNS
Cattle
Following contact exposure, lesions appear in 2-10 days. Some viral strains are associated with longer incubation periods than others. There is an early serous nasal discharge which often becomes muco-purulent. There may also be an ocular discharge.
Early lesions in the mouth generally appear as blanched, roughly circular areas on the tongue or dental pad. These become more prominent as fluid collects underneath until a vesicle is formed which stands out clearly from the normal surrounding epithelium. When viewed along its surface the tongue may appear corrugated. Vesicles on the tongue frequently reach several centimetres in diameter and are situated characteristically on the dorsum, but may be under the tip or on the sides of the tongue close to the molar teeth. Tongue lesions cause the animal much pain. In some cases stomatitis produces profuse salivation. Handling the tongue frequently results in large pieces of epithelium becoming detached, leaving deep, red ulcers with a ragged edge. Vesicles followed by ulcers also appear in other parts of the mouth particularly on the dental pad, hard palate, gums and inside the lips. The animal is anorexic.
In calves, vesicles and ulcers are less obvious and often difficult to find but deaths are not uncommon due to viral effects on heart muscle.
Healing of the ulcers on the tongue and other parts takes place surprisingly rapidly. Within 3-4 days the base of the ulcer becomes covered with a serofibrinous exudate and regeneration of the epithelium is complete within about 10 days unless secondary bacterial infection supervenes which leads to scarring.
Mortality in adult cattle very seldom exceeds 5% but may be much greater in calves. Cattle recovered from FMD are immune for about 2-5 years to clinical disease from that strain of the virus.
Pigs
Tongue lesions are much less dramatic than in cattle and heal much more rapidly. Vesicles occur as one or more raised white areas of about 0.5-1 cm diameter on the dorsum. They rupture readily to leave small ulcers. Frothy saliva may be present around the lips. Vesicles may also occur on the snout and on the lips and gums.
Foot lesions are generally prominent and lameness is marked. Vesicles and ulcers occur at the bulbs of the heels, around the coronary band and in the interdigital space. In piglets sloughing of the horns of the hooves and of the supernumary digits takes place readily leaving the sensitive laminae exposed.
There is depression, anorexia and loss of condition. Piglets frequently die suddenly.
Sheep and goats
Adult sheep and goats are not generally severely affected: indeed lesions in the mouth are often difficult to detect and those on the feet may be confused with foot-rot or abscesses. Vesicles and ulcers may develop on the tongue or particularly on the dental pad. They are usually small (1 cm). If foot lesions occur they usually do so at the coronary band or in the interdigital cleft and may cause marked lesions.
CARRIERS
Clinical recovery is the normal sequel to FMD but in ruminants virus is carried in the cells of the oesophagus and pharynx despite high levels of circulating antibody. Virus can also be recovered from oesophageal fluid samples of vaccinated ruminants following exposure to infection despite full clinical immunity.
Cattle may be carriers for up to 2 years; sheep for up to 9 months and goats for up to 2 months. Pigs are not known to be carriers.
PROPHYLAXIS
Inactivated FMD vaccines are widely used throughout the world and could only be used in this country in an emergency.
Following vaccination, cattle are immune to challenge infection after about 14 days. Antibody may be detected on primary vaccination as early as 3-7 days. Satisfactory immunity can only be guaranteed against the homologous strain for 4-6 months after primary vaccination and on revaccination cattle may be protected for 9 months to 1 year. Repeated annual vaccination not only gives satisfactory high levels of protection against the homologous strain but increases the range of strains against which protection is afforded.
Pigs are not as readily immunised as cattle and high concentrations of virus and different adjuvants are necessary. Recently pigs have been satisfactorily protected for up to 9 months with vaccines incorporating oil adjuvants.
Disadvantages of vaccination include the problem that symptomless carriers of the disease can occur following vaccination.
CONTROL OF FMD
Two approaches to the control of FMD are currently applied. In the UK a policy of "stamping out" of the disease has been traditionally followed which relies on a well developed state veterinary organisation for the early recognition of disease followed by slaughter, disinfection and strict movement control. This policy has proved successful over the years and is less costly than compulsory annual prophylactic vaccination. The policy is combined with vigorous attempts to prevent the introduction of virus by the control of animal and animal product importation.
The second approach, applied in endemic FMD areas, relies on systematic vaccination which may also be coupled with ‘stamping-out* in the event of an outbreak. This approach provided excellent control in western continental Europe where vaccination has eradicated the infection. However, the vaccine is costly and success depends on the existence of well developed veterinary services which can organise effective quality control of vaccines, adequate cover of susceptible livestock and good movement control. Where the organisational support is lacking vaccination alone cannot fully be relied upon to control the disease (e.g. areas of South America and Africa).
Between these two approaches many variations are practised notably strategic vaccination in the face of an outbreak where baffler or ring vaccination is applied (e.g. in some eastern European countries).
Control of FMD outbreaks in the United Kingdom
FMD is a notifiable disease so if the disease is suspected, the police or the Divisional Veterinary Officer (DVO) must be notified. Immediate restrictions are placed on the farm (Form A) to prevent movement of people, animals or things on or off the premises. The DVO inspects the farm. If positive or suspicious, Form C is served to prohibit movement of susceptible animals within 5 miles. Lesion material is sent to the World Reference Laboratory for FMD at Pirbright. If FMD is confirmed, movement restriction is extended to 10 miles around the infected place. An Infected Area Order is made and a Form D is served on premises which have been directly or indirectly in contact with the initial outbreak to restrict movement of animals for 21 days since exposure to infection.
Infected farm. All susceptible animals are valued, slaughtered and cremated or buried as soon as possible. There is immediate preliminary disinfection. Following disposal of animals, thorough disinfection takes place. Restocking is permitted 6 weeks alter slaughter or 4 weeks after disinfection, whichever is sooner, but depends on whether or not the disease has been brought under control in the area.
Infected areas. These areas are at least 10 miles around the infected farm. No animal may be moved, except to abattoir under licence. No markets may be held. Milk tankers may be fitted with filters and milk is heat treated before being fed to animals. No movement of slurry, litter or manure is permitted. There is no hunting, racing or shooting. The restrictions are lifted gradually; to 5 miles 14 days alter the last outbreak and then completely removed after a further 7 days.
Controlled areas. These are set up to allow tracing of animals and are usually of short duration. All animal movements require a licence. Markets are controlled. Disposal of manure and refuse from abattoirs is regulated. The hunting of deer is prohibited.
HAEMOPHILUS SOMNUS SEPTICAEMIA (Infectious meningoencephalitis, Sleeper Syndrome)
DEFINITION
This is an acute septicaemia due to Haemophilus somnus infection characterised clinically by nervous, joint and respiratory signs which can develop simultaneously or separately. The main pathological findings are vasculitis, thrombosis and infarction. This disorder is most common in beef cattle being fattened under feedlot conditions.
EPIDEMIOLOGY
This is primarily a disease of feedlot cattle (6-12 months old) although the disorder has been confirmed in cows and in cattle at pasture. The incidence is highest during the winter months with most cases occurring from 4-5 weeks after the animals have arrived. The morbidity rate is low (5 per cent), but the case fatality rate is high (up to 80%). This condition is second in incidence to CCN in feedlot animals. This disorder has been confirmed in North America and also in Europe including Britain.
Haemophilus somnus is also a specific cause of pneumonia in calves less than 4 months old, particularly those still sucking their dams, and this is said to be most common in the spring and summer months.
CLINICAL SIGNS
Haemophilus somnus is responsible for a condition which mainly affects the central nervous system, but signs referable to the locomotor system, respiratory system and reproductive tract have also been documented. In affected individuals, clinical signs referable to more than one system frequently develop.
Peracute syndrome. The first indication of an outbreak is often an animal found dead.
Acute syndrome. This is the most common form of the disease. Affected cattle are found dull, recumbent and fevered. They are usually blind. If they can get to their feet, they stagger, readily knuckle over at the fetlocks and quickly fall down after walking only a short distance.
Chronic syndrome. Up to 10 per cent of animals not affected by the nervous (acute) syndrome can become lame. Firm swellings around the joint can be detected several days after the onset of lameness and, although many joints are usually involved, those at the hock and stifle are the most obviously affected. This lameness can persist for weeks or months and can develop into chronic polyarthritis.
Respiratory signs which include laryngitis, tracheitis and pneumonia can develop in feedlot animals as part of the acute and chronic syndromes.
In young calves, the first indication of H.somnus infection may be a calf found dead and at post mortem, the only lesions are those of an acute pneumonia. Others in the group may subsequently develop signs of a non-specific pneumonia.
Haemophilus somnus can be isolated regularly from the apparently normal urogenital tract and it has been associated with a mucopurulent vaginal discharge from infected cows and purulent ejaculate from bulls. However, the exact role of H.somnus in bovine infertility is still unclear.
DIAGNOSIS
This depends on the isolation of H.somnus from the blood, cerebrospinal fluid or joints of suspected cases. At necropsy, the macroscopic appearance of the brain lesions is characteristic and microscopical examination would confirm the diagnosis. Other conditions which should be considered in the differential diagnosis include cerebrocortical necrosis, lead poisoning and listeriosis.
TREATMENT
This bacteria is sensitive to penicillin, ampicillin, the tetracyclines and the sulphonamides. Affected cattle will generally recover quickly if treated before they become recumbent otherwise, few recumbent animals ever get to their feet again.
CONTROL
Haemophilus somnus septicaemia is not common enough in Britain to warrant specific control measures although an effective vaccine is available in North America. There does not appear to be a positive correlation between the presence of high serum and antibody titres in individual animals and protection from reinfection. Other control measures include mass medication with in-feed antimicrobials.
HYPOMAGNESAEMIC TETANY (Staggers)
Hypomagnesaemia can occur under differing managemental systems and, although the syndromes are basically the same, they will be described individually. Firstly, the most common and important form of hypomagnesaemia affects recently calved dairy cows on lush fertilised grass in the spring - grass staggers. Secondly, newly calved beef cows on a high roughage diet in the late winter and spring and thirdly, fast growing calves being fed predominantly on milk. The condition grass staggers will be described in detail with the differences between it and the other disorders in beef cows and calves described later.
DEFINITION
This condition occurs in mature, lactating dairy cows usually within a few weeks of their being moved on to lush grass in the spring. The onset of clinical signs is associated with a sudden fall in the plasma magnesium and calcium concentrations and affected individuals may be found dead or in lateral recumbency.
AETIOLOGY
Within the body, about 40 per cent of the magnesium is in the soft tissues with the remainder being found in the skeleton which, in adults, is metabolically inert. Of the total body magnesium, only the 1 per cent in the extracellular fluid is available to satisfy immediate physiological needs. Because an effective homoeostatic mechanism for the control of magnesium has not yet been identified, adult cattle are totally dependent upon dietary sources to satisfy their day to day requirements and to meet any sudden increase in demand.
A lactating cow requires to ingest about 20g magnesium every day in order to absorb the 4g it needs. On typical winter rations, 30-35g magnesium is ingested per day compared with only 10-25g magnesium ingested when grazing lush grass in the summer. While there is a positive correlation between herbage and serum magnesium concentrations, the amount of magnesium ingested and its availability to the animal are dependent upon the complex interaction of a large number of environmental factors.
Factors which can result in a low herbage magnesium concentration include low soil magnesium, high soil potassium, high applications of artificial nitrogenous (ammonium) and/or potash fertilisers, the composition of the herbage and the age of the sward.
Factors which can reduce the intake of magnesium include absolute or relative starvation, low dry matter intake, unpalatable herb age and sudden onset, cold wet windy weather (acute cold stress reduces both magnesium and calcium plasma concentrations).
Herbage magnesium has an availability of about 30 per cent but, on some diets, this can fall to 5 per cent. The availability of herbage magnesium varies according to the composition of the sward, the amount of soluble carbohydrate in the diet and the amount of protein in the diet.
The major factor responsible for the sudden increase in demand for magnesium is increased milk production. Approximately 20 per cent of the total exchangeable magnesium is secreted daily into the digestive tract and, consequently, anything which significantly affects resorption by decreasing the passage time of the intestinal contents, eg. diarrhoea, will decrease the amount of magnesium resorbed.
EPIDEMIOLOGY
This is a relatively common disease although the incidence varies greatly from year to year, from area to area and is closely associated with managemental and climatic factors. Clinical signs usually develop in high yielding, dairy cows within the first two months of lactation, ie. around peak milk production, within a few weeks of their being put out in the spring to graze young, lush, fertilised grass. The incidence of disease is said to increase with age and, it has been suggested, that the incidence is highest in Ayrshires and lowest in the Channel Island breeds.
The condition can also occur in the autumn in newly calved dairy and beef cows particularly after a sudden cold spell and, in the case of the beef cows, before supplementary feeding has begun.
CLINICAL SIGNS
Many apparently healthy cattle can have hypomagnesaemia and the onset of clinical signs is frequently brought on by excitement following turning out, oestrus, collection or transport. Although the development of clinical signs can be divided into several progressive stages, only the per-acute stage (found dead) and the acute stage (lateral recumbency) are relevant in this situation.
In the per-acute stage, affected animals are found dead. This is one of the few conditions in which a cow can literally drop dead, ie. an actual cause of "sudden death".
The vast majority of cases are found in lateral recumbency with the ground torn up round about them. When lying still, they can rear the head back with with the neck extended and, if stimulated eg. by handling, they have convulsions and make determined paddling movements. They may also roar, froth at the mouth, defaecate, and breath irregularly. Consequently, on close examination, there is usually evidence of traumatic damage to head and limbs and the temperature is elevated. In untreated cases, death occurs relatively quickly, usually within hours of an animals becoming recumbent.
The morbidity rate is low but may reach 10 per cent. The mortality rate is difficult to assess accurately because a proportion are found dead, but probably about 20-30 per cent of treated cases die.
DIAGNOSIS
This is based almost wholly on the type of animal and its situation. Staggers should be suspected if a lactating dairy cow is found dead in the spring soon after being put out to grass and if hyperaesthesia and/or convulsions are seen in recently calved dairy cows which have been grazing lush grass for a short time particularly if there has been a sudden onset, cold, wet spell of weather.
TREATMENT
Since hypocalcaemia is thought to precipitate the onset of clinical signs, it may be beneficial to give initially a warmed solution of calcium borogluconate slowly intravenously. When giving a solution of magnesium sulphate (25%) it is advisable to give it subcutaneously, preferably at several sites, because of the risk of ventricular fibrillation.
However, it can be given intravenously but only VERY SLOWLY. Solutions containing soluble salts of both calcium and magnesium are claimed to result in improved recovery rates on certain farms.
Clinical signs will almost certainly recur unless an adequate amount of available magnesium is given in the diet because of the lack of a homoeostatic mechanism for the regulation of magnesium. Since all cows around peak lactation are likely to be hypomagnesaemic to a greater or lesser degree, control/preventive measures must be considered from the herd point of view.
CONTROL/PREVENTION
All control measures must be based on providing an adequate daily intake of magnesium in the ration. The most common method and the most practical is to feed concentrates with added magnesium. Also, magnesium oxide as calcined magnesite can be added directly to concentrates at a rate of 50g calcined magnesite per cow per day in the parlour. Dairy cows can also be given magnesium boluses prior to the period of maximum risk. These bullets supply l-2g of magnesium per day for about 28 days after which time the animal can be treated again if necessary. It is recommended that 2 bullets per cow are administered. Other methods of attempting to feed supplementary magnesium include feed blocks but they are considered to be of limited value because some cows never eat them. In situations where there is only a piped water supply, soluble magnesium salts can be introduced at a predetermined rate into the water supply. The pasture itself can also be treated either in the long term with magnesium limestone or calcined magnesite can be applied to acid soils as a fertiliser. Smaller quantities of calcined magnesite can also be dusted onto the herbage where it can act as a supplement during the following grazing period. This is most useful in intensive grazing situations. In future years it might be worth considering other measures such as putting potash fertiliser on during the summer and autumn and not in the spring and changing the composition of the sward by reducing the amount of grass and increasing the proportion of clovers and herbs.
HYPOMAGNESAEMIA IN SPRING CALVING BEEF COWS
Spring calving beef cows can develop hypomagnesaemic tetany in the late winter and spring after calving particularly if they have been on a high roughage (low available magnesium) diet. This type of feeding leads to a low grade, persistent hypomagnesaemia usually in the absence of any clinical signs. However, a small number of animals can develop prodromal signs and the sub-acute form of hypomagnesaemia may also be recognised. As the milk yield of the cow increases after calving, the demand for magnesium and particularly for calcium increases quickly. Consequently, any factor which leads to a sudden decrease in the plasma concentration eg. a sudden deterioration in the weather, can lead to the onset of tetany.
The prodromal stage can last for several days or weeks. Initially, there may only be a decreased appetite with mild hyperaesthesia and muscle tremors. Although these clinical signs will often resolve spontaneously, a proportion of animals will progress into the sub-acute stage in which the hyperaesthesia is more marked and the animal holds its head high. There may be exaggerated ear movements and affected individuals are restless and staggery. When excited, they may roar and gallop in a frenzied manner before falling down and taking convulsions (acute stage).
The treatment is basically the same as with grass staggers except that beef cows should not be separated from their young calves. The provision of supplementary feeding, particularly energy, prior to the period of maximum risk and also of shelter where appropriate are the best recommendations for preventing this condition. When the period of maximum risk can be accurately identified, the use of magnesium bullets are also worthwhile considering.
It should not be forgotten that both forms of grass staggers (tetany and sudden death) also occur in beef cows in the autumn, particularly in recently calved cows.
HYPOMAGNESAEMIA IN THE CALF
This is a condition of 2-4 month old calves fed predominantly on milk. It is still relatively common in fast growing, single suckled calves although the incidence has decreased markedly in bucket reared animals as a result of the popularity of early weaning systems and the use of supplemented milk substitutes.
The cause of the clinical signs in this type of animal is an absolute deficiency of magnesium due to the relatively low magnesium content of milk. The fall in the blood magnesium concentration is progressive because in the calf, skeletal magnesium is a depletable reserve. This drop in blood magnesium is exacerbated in fast growing animals and, as the calf gets older, not only does its requirement for magnesium increase but the efficiency of absorption from the alimentary tract decreases. The feeding of poor quality roughage also decreases the efficiency of absorption of magnesium.
The clinical signs are similar to those in dairy cows with grass staggers and frequently the onset of clinical signs is initiated by excitement eg. collecting cows and calves for routine examination. Calves are commonly found dead usually with some evidence of their having had convulsions.
The best method of prevention is to offer creep feeding as soon as possible. Where the period of maximum risk is easily identified, two sheep magnesium bullets can be given to young calves.
INFECTIOUS BOVINE KERATOCONJUNCTIVITIS (New forest disease; pink-eye)
DEFINITION
An infectious inflammatory disease of the cornea and conjunctivae particularly in young cattle, characterised by lacrimation, conjunctivitis and corneal ulceration.
INCIDENCE
The incidence varies from year to year, but spread within a group of animals is usually very rapid and the morbidity can be as high as 80%.
AETIOLOGY
Several microbiological agents have been recovered from cases of infectious bovine keratoconjunctivitis. Moraxella bovis is the bacterium most commonly isolated from affected eyes. Several species of Mycoplasma have also been associated with the disease.
CLINICAL SIGNS
Bilateral tear production and mild conjunctivitis are the first clinical signs noted. The eye is obviously painful. Within 1-2 days, a small greyish white opacity appears in the centre of the cornea. The grey opacity may enlarge to cover a large area of the cornea with a grey/white spot developing in the centre of the cornea. Occasionally in severe cases deep corneal ulceration may occur. Rarely complete perforation of cornea ensues. In the older lesion, many small blood vessels can be seen in the peripheral areas of the cornea. Healing of large ulcers is accompanied by extensive corneal vascularisation. The animal, if not blind in the affected eye, certainly suffers impaired vision.
Affected animals are usually dull, with a reduction in appetite and a resultant weight loss. Although adult dairy cows are rarely affected, there is a reduced milk yield in affected animals. Economically the disease is important because of the reduced weight gains in calves and fattening animals, up to 10% compared to unaffected animals in the same group.
EPIDEMIOLOGY
The disease is virtually confined to animals less than two years old but occasionally adult animals are affected. It occurs in most parts of the world and is most common in the summer and autumn months. Because the disease is more prevalent in the summer months, flies are considered to be important in the transmission of the disease. Carrier animals are thought to be responsible for the carry over of the disease from year to year. Severe outbreaks of infectious keratoconjunctivitis can occur during the winter especially where large number of animals are closely confined together.
DIAGNOSIS
Diagnosis in very early stages may present some difficulty, but if a group of young animals is showing excess lacrimation and conjunctivitis with no other signs of systemic or upper respiratory infection, it should be presumed to be infectious keratoconjunctivitis.
TREATMENT
In the majority of cases, the lesions of IBK will resolve following treatment with locally applied antibiotics and several methods of application are available.
Ointments. Special formulations are available which will maintain therapeutic concentrations for up to 48 hours when a repeat treatment should be used.
Subconjunctival injection. Will produce therapeutic concentrations in the eye for periods of 24-48 hours. Often effective but may require repeated dose and can produce local reactions.
Parenteral injection. Therapeutic concentrations can be attained following parenteral administration of oxytetracyclines, tylosin and sulphadimidine. Severely ulcerated eyes may also require surgical closure to save the eye.
CONTROL
The recommended method of controlling an outbreak of IBK is by prompt antibiotic treatment of affected animals. Little success has been achieved in eradication of infection from groups using local or parenteral antibiotics.
Vaccines have been described and used commercially in other countries but their efficacy has yet to be proved.
INFECTIOUS BOVINE RHINOTRACHEITIS
This disease is caused by bovine herpesvirus 1 and is characterised by reduced appetite, dullness, fever, nasal discharge, and ocular discharge with conjunctivitis. Clinical signs often develop soon after the arrival of newly purchased animals. The course of the illness is usually short, the morbidity is high and the mortality is low.
AETIOLOGY
IBR results from infection of the respiratory tract with bovine herpesvirus 1 (BHV1).
The most common route of viral transmission is by air, but because close contact between infective and susceptible individuals is necessary, the spread of infection is comparatively slow. Consequently, in a large group of susceptible animals, clinical cases may continue to arise for several weeks.
Two to three days after infection fever, conjunctivitis, dullness, reduced appetite and coughing develop. In mild cases, recovery will have taken place after 7 to 10 days although affected individuals can continue coughing for a couple of weeks.
The reasons for the sudden appearance of a severe form of IBR in Britain are not known, but there is circumstantial evidence to suggest that a "new" strain of virus may have been imported into Europe from North America, probably in latently-infected Holstein cattle.
EPIDEMIOLOGY
Following the initial diagnosis of the disease in Britain in 1962, mild incidents of IBR were recorded sporadically throughout the country. During the 1977-78 winter a severe form of IBR was recognised in Scotland and, since then, this form of the disease has spread nationwide
The incidence of disease is highest in fattening beef cattle and in dairy cows although beef cows and young calves can also be affected. In many outbreaks, the source of infection has been animals which have been on the farm for only a short time, often less than 4 weeks after purchase from a market. For this reason, IBR has been particularly prevalent on beef farms in northern and eastern Britain. In contrast, the incidence of disease has been greater in dairy animals in the south and west of the country because, in these areas, replacement heifers are mostly bought-in whereas, in other regions, they are usually home-bred. In addition, infection can also be introduced into a self-contained herd by individual animals returning from livestock shows having been infected by virus excreted from neighbouring, recovered animals.
Although IBR can occur in grazing cattle, severe incidents have only been confirmed during the winter housing period. It appears that "stress" factors such as weaning, mixing, overcrowding as well as the fear and fatigue associated with being sold, contribute significantly to the severity of the field disease. It is thought that those factors are largely responsible for the high morbidity and mortality in animals kept under intensive conditions.
CLINICAL SIGNS
Cattle which have been purchased from a market and have been on the farm less than 4 weeks are frequently those in which clinical signs are first seen. Initially, affected animals are dull with a reduction in appetite, which may be confined to roughage only, a serous nasal and ocular discharge and frequent coughing. In lactating dairy cows, there is a sudden reduction in milk yield.
In mild cases, recovery can take place within 7-10 days without treatment. However, in a small proportion of cases, the clinical signs become progressively more severe.
In the acute stage of the disease, beef cattle can lose up to 30 kg bodyweight and, during the convalescent period, they may fail to put on weight for up to 8 weeks although they have a normal appetite. The milk yield of dairy cows is reduced for several days or for several weeks if they have been severely affected. Pregnant cows often abort as a result of foetal death either within a few days of being infected or even after a delay of several months.
The morbidity rate is usually greater than 50 per cent and, in many outbreaks, it is over 90 per cent. In the majority of incidents, fatalities do not occur. However, up to 7 per cent of severely affected cases may die or have to be culled in outbreaks involving large numbers of purchased, intensively-managed, beef animals. It is on these latter units that IBR is seen at its most severe and where there is a regular high turnover of purchased animals, IBR can become endemic. Within a susceptible group or herd, it takes from 3 to 5 weeks from the time the first case has been seen until clinical signs regress completely.
DIAGNOSIS
The clinical picture is characteristic and differential diagnosis is seldom a problem. Nevertheless, the following conditions should be considered: foot and mouth disease, pneumonic pasteurellosis, malignant catarrhal fever, photosensitisation and infectious bovine keratoconjunctivitis.
TREATMENT
During the early stages of the disease, it has been shown that the severity of the clinical signs can be minimised by the daily administration of a broad spectrum antibiotic until the animals temperature returns to normal. However the treatment of severely ill animals with antibiotics, even for a prolonged period, does not invariably result in a complete clinical recovery.
CONTROL
Susceptible cattle should be vaccinated whenever there is a high risk of exposure to BHV1. At present, there are several vaccines available:
These vaccines, which are given on one occasion, have the advantage that (i) they give almost immediate protection and significant immunity within 48-96 hours, (ii) they do not produce abortion and (iii) they can be used to protect non-infected, in-contact animals even after disease has been confirmed within a group.
All ages of cattle can be vaccinated and, when the challenge is likely to be great, annual revaccination may be desirable.
BOVINE IRITIS (Silage eye)
DEFINITION
A distinct clinical disease primarily affecting the iris and manifesting itself by a marked inflammatory response. Seen in all ages of cattle, associated with silage feeding. Corneal ulceration is not a feature.
INCIDENCE
Very variable but up to 50% of adult dairy cattle during the winter period. Usually small numbers of adults sharing a common feeding system. Seen in animals as young as 10 weeks of age.
AETIOLOGY
The aetiology has yet to be determined, but may involve ocular infection with Listeria spp or other micro-organisms including Mycoplasma.
CLINICAL SIGNS
Cows normally present with a diffuse white or bluish opacity of the cornea, often with several large foci of yellow material visible deep to the cornea. Usually unilateral but occasionally both eyes are affected. Early cases show lacrimation and constriction of the pupil. There is no observed change in the conjunctiva and the animals are blind in the affected eye. As the iris produces an inflammatory response so the cornea begins to show changes. First, a bluish opacity which begins as a localised area then spreads over the whole cornea. Second, distinct white focal spots on the cornea which enlarge and become yellow later.
EPIDEMIOLOGY
A common factor in almost all cases is the feeding of big bale silage. This has usually been fed in ring feeders or feeders which allow the silage to contact the animals eyes.
DIAGNOSIS
This condition can be differentiated from IBK by the class of animal affected, the history and time of year, and by a thorough ophthalmic examination.
TREATMENT
This condition is very resistant or totally unresponsive to local antibiotic therapy. Systemic antibiotics however may aid in the resolution of lesions in very early cases. The use of atropine and corticosteroids to reduce the inflammatory response gives a very rapid regression of clinical signs in many cases. Subconjunctival injections of atropine (5mg) and dexamethasone (3mg) have been suggested. Beware corticosteroids in pregnant animals. Many cases resolve in 14-21 days with no permanent damage to the eye and a return to normal function.
JOHNE'S DISEASE
Johne*s Disease is an infectious disease of ruminants, characterised by a long incubation period and clinically by diarrhoea and weight loss. The disease is of economic importance only in cattle and sheep, with weight loss being the major clinical sign in sheep.
AETIOLOGY
The agent of Johne*s disease is Mycobacterium avium paratuberculosis
PREVALENCE
The exact incidence of the disease is unknown, and although slaughterhouse surveys have shown that about 11% of all cattle are infected the incidence of clinical cases is much lower with the overall incidence being less than 0.2% although in affected herds the incidence may be as high as 5%. The disease is sporadic and in an affected herd only one or two cows may be lost per year. As it has been shown that in the lactation prior to the establishment of clinical disease the milk yield may fall by several hundred gallons, culling for low yields has tended to reduce the incidence in dairy herds.
CLINICAL SIGNS
Since Johne*s disease has a long incubation period it is almost always seen in adult cows and bulls. Development of the clinical disease often follows a period of stress such as calving or around the time of peak lactation. Initially, the diarrhoea tends to be intermittent, accompanied by a slight weight loss and a slight decrease in milk yield. This period of intermittent diarrhoea may last for several weeks but gradually the diarrhoea becomes persistent with a dramatic drop in milk yield, and a marked loss of skeletal muscle, especially from the hindquarters. As a consequence of the reduced milk yield, the calves of affected beef-type suckler cows are small and stunted. Loss of coat pigmentation may also occur in a proportion of cases. Throughout the disease, however, the animal remains bright and continues to eat well. This may continue for several months but eventually if the animal is not slaughtered on economic grounds a point is reached where the animal becomes quite ill, anorexic and very dull. At this stage death usually supervenes within a day or two.
PATHOGENESIS
Under natural conditions, infection is by the oral route, following ingestion of the organism in contaminated water or feed. Transplacental infection can also occur. Infection occurs during the first month or two of life and the organism settles in the intestinal mucosa where multiplication occurs. These organisms stimulate a hypersensitivity which results in the thickening of the intestinal wall. The time taken for development of this lesion varies considerably from 15 months to several years. Obviously since there would appear to be a fairly high infection rate but a low incidence of clinical disease some animals must clear themselves of infection.
The thickening of the intestinal mucosa causes loss of surface area, malabsorption, and increased epithelial permeability with loss of plasma protein. Johne*s disease is thus an example of protein losing enteropathy, a significant loss of blood proteins occurs. The attempted maintenance of essential proteins occurs at the expense of less essential tissues especially skeletal muscle, which is noted clinically as weight loss.
EPIDEMIOLOGY
Johne*s Disease is widely distributed throughout most of the temperate areas of the world, especially Europe and North America. Poorly drained and acid soils deficient in phosphoric acid and calcium carbonate appear to favour the persistence of the disease.
The organism is shed in faeces and can survive and remain infective on pastures and in dried faeces for up to a year at least. Infection is acquired by ingestion of infected faeces or anything, water, grass, foodstuffs contaminated by infected faeces. Calves less than six months old are most susceptible to infection and adult animals are normally resistant to infection. It is the young calf which is most likely to be exposed to heavy infection if suckling the teats of a clinical case.
The length of time between exposure to infection and the development of clinical disease varies greatly from as short as 15 months to 3 years or more. Thus, although clinical disease can occur in animals as young as 2 years old the peak age incidence occurs at 4-6 years old. Occasionally an older animal may develop the clinical disease.
Although infected animals may not present as clinical cases until they are adults, it is likely that they have been excreting the organism in the faeces in increasing numbers from the time of infection, thus acting as a source of infection for other animals. The acquisition of an infected, excreting, but clinically normal animal is the most likely method of introducing infection to a previously uninfected herd.
DIAGNOSIS
This is based on the characteristic clinical signs and the results of laboratory tests.
TREATMENT
There is no effective treatment.
CONTROL
Control of the disease should be based on the slaughter of clinical cases and the prevention of infection.
Johne*s disease-free herds should attempt to maintain that status by avoiding the introduction of, or contact with, possible excretors.
Once a disease has become established in a herd, the most effective way of mitigating losses in the future is to cull severely on the basis of a dropped milk yield during lactation or a degree of weight loss, before diarrhoea has become clinically evident. In dairy herds which have a rigorous culling policy for poor milk yield it is unlikely that many clinical cases will develop.
Since the most susceptible period for infection is the first few months of life, separation of calves from the adult herd after the initial neonatal period will lower the incidence of the disease in dairy herds. Young animals should not be allowed to graze pastures, or have access to streams which may be heavily contaminated. This policy cannot of course be used on beef-suckler herds and here the early diagnosis and removal of clinical cases is imperative in order to reduce pasture contamination. Culling on the basics of poor weight gain in calves would be the equivalent of poor milk yield in dairy herds. While congenital infection has been demonstrated it has not been proved that these calves go on to develop clinical disease. Nonetheless it would seem prudent to ensure that the last calves of clinical cases are fattened for slaughter rather than kept for breeding.
VACCINATION
Vaccination can interfere with tuberculin testing and with the diagnostic tests required for importation of animals into certain countries. It is under the control of the Department for the Environment and Rural Affairs and is not available for routine use.
JOINT ILL
An infectious polyarthritis of young calves often associated with navel infection soon after birth.
Antibiotic sensitivity may be carried out on isolates but this increases the delay in treatment which should be started as promptly as possible. Drainage and drug irrigation of the joint is hazardous due to risk of increasing infection.
CONTROL
Ensure colostrum supply is adequate for all calves at risk. Maintain clean environment, especially bedding. Disinfect umbilicus within an hour of birth using tincture of iodine, a neutral iodophor (10,000 ppm) or neutral hypochlorite solution (50,000 ppm), and repeated on days 2 and 3 on farms where cases have previously occurred. Few cases develop in calves born outdoors.
COMMON DISEASES OF THE FOOT - Foul In the foot or Interdigital Necrobacillosis (loor, loo, foul, foot rot, claw ill)
This condition is an acute infection of interdigital skin and adjacent and underlying tissues. It is caused by an infection with Fusobacterium necrophorum and possibly in association Bacteroides melaninogenicus. These two organisms together appear to act synergistically to penetrate the epidermis (or enter through a traumatic skin lesion) and then produce cellulitis which leads to severe lameness.
A swelling of the coronary band is seen which forces the two claws apart. The interdigital skin then splits and there may be a discharge of pus and/or necrotic tissue debris. The important diagnostic feature is the split skin. Untreated cases will develop a progressive cellulitis which may track up the leg, infection may also enter the joints.
This condition is common in all ages of cattle but beware, it is over diagnosed by farmers. Treatment is simple in the majority of cases as they will respond to systemic antibiotics. Early cases may respond to a single dose of treatment, more severe cases will require a long acting product or a 3-5 day course of treatment. As these organisms tend to be very sensitive most products are effective e.g. oxytetracycline (especially long-acting preparations in non-lactating animals) Procaine penicillin, Tylosin (Tylan 200) Cephalexin (Ceporex) or Ceftiofur sodium (Excenel).
The milk withdrawal period is often the most important consideration when choosing a treatment for these cases.
Traumatic damage to the interdigital skin may lead to this condition so measures to reduce trauma can often reduce the incidence e.g. avoid stones, stubble, rape and kale, also keep feet as dry as possible improve bedding and remove slurry.
The prognosis for most cases is extremely good.
"Super Foul" probably better termed "Peracute Foul" has been seen as a problem in the U.K. over the last 1-2 years. It presents as a very severe rapidly progressive foul which doesn*t respond to conventional therapy. Work is continuing to determine how this condition differs from the normal Foul in the Foot. These cases require extremely prompt and very aggressive treatment.
Footbaths are often advocated for the control of foul in the foot (e.g. 5% formalin solutions). These need to be kept clean and changed frequently, some cases of "Super-Foul" have been associated with poorly maintained footbaths.
Interdigital Dermatitis (scald)
This condition is an inflammation of the interdigital skin without the cracking and fissuring seen in interdigital necrobacillosis. These lesions have a pronounced foetid smell, no fissures and in most cases respond to topical antibiotics.
It is suggested that the lesions are caused by F. necrophorum and Dichelobacter (Bacteroides) nodosua Although there are also now suggestions that it may be related to Digital Dermatitis (see below). The control and treatment of this condition is identical to that for Digital Dermatitis (DD).
Interdigital Skin Hyperplasia
(corn)
The skin adjacent to the lateral digit is most commonly affected. The hyperplasia is thought to be secondary to chronic irritation e.g. low grade interdigital infections. In some instances it may be an inherited condition common in Hereford bulls but also seen in other breeds.
Lameness is caused by the pinching of the interdigital mass or secondary infection leading to Necrobacillosis.
Small lesions will resolve spontaneously if excess horn from the axial wall is removed thus widening the axial space when the cow bears weight. Larger lesions require surgical removal with the application of a dressing. In all cases any secondary infection must be treated.
Digital Dermatitis
The condition is characterised by a moist, exudative lesion occurring in the skin at its junction with the horn of the heel usually midway between the two claws. Its surface is dark red - brown and the hair is erect and matted with exudate. Removing the surface debris reveals a red, raw area, usually circular and 1 to 2cm in diameter. The area is extremely painful and has a characteristic strong pungent smell. There is however no associated tissue swelling which helps in differentiation from "foul in the foot".
This condition has become one of the most common causes of lameness in the U.K. today.
Lesions respond rapidly to topical oxytetracycline aerosol spray. Herd treatment using tetracycline foot bathing is also successful providing the feet are cleaned before entering the bath. Various foot bath regimes are described for prophylaxis using 4g/l tetracycline at intervals of 3 to 4 weeks, and treatment lg/l for 4 to 5 days. Foot bathing in solutions 6g/l has been described in very severely affected herds. Lincospectin at a rate of 150g per 200 litres water has also been used. Topical application of lincospectin is also effective.
It must be remembered that this is an infectious condition, there is at least anecdotal evidence of farm to farm transmission.
Slurry heel (heel erosion)
This is a condition of housed cattle standing for long periods of time in corrosive slurry. The normal soft horn of the heel becomes worn away. This is important because it results in rotation of the foot backwards, and may result in a raised toe. Deep erosions may result in infected heels or white line lesions in the axial groove. Control is obtained by attention to the environment especially removing slurry and keeping feet clean and dry.
"Mud Fever"
This is similar to the condition seen in horses, and presents as swelling from the top of the hoof to above the fetlock. Skin becomes inflamed and thickened and hair crusted. Treat by cleaning and drying the area and apply an antiseptic cream.
As Dermatophilus infection is involved systemic antibiotics may also be required.
Laminitis
This condition is currently considered to be extremely important in the aetiology of many claw lesions as well as being a primary cause of lameness in its self.
Laminitis is inflammation of the corium arising from a systemic disorder due to a wide spectrum of largely interdependent aetiological factors. These include metabolic and digestive disorders often seen with rapid changes of diet especially from low energy forage diets to high concentrate diets. There is still much debate as to whether it is excess energy or protein which is the major problem. It is sufficient here simply to advise that cattle always have access to adequate long forage and to avoid sudden dietary changes. Calving or severe inflammatory processes e.g. metritis or mastitis may also lead to laminitis. Local influences within the hoof may also be important such as trauma and overload especially seen in recently housed cattle who do not readily use cubicles and thus have greatly reduced lying times.
Acute laminitis may be caused by one single factor such as acute rumen acidosis with a release of endotoxins. The acute condition is rare but is seen on occasions. Treatment is to remove the underlying cause, place the animal on soft conforming bed and give analgesics. Following an acute attack most cases become chronic, also chronic laminitis often occurs without any history of an acute attack. This "subclinical laminitis" is extremely common. Cows may develop laminitic rings as hoof wall growth is affected. The pedal bone often sinks within the foot resulting in pressure on the corium at the toe. Laminitis can result in any of the following:- Hoof overgrowth, soft horn especially at the white line, yellow discolouration of solar horn, blood in the horn, hardship lines i.e. horizontal grooves on the wall, soft powdery horn, pain and discomfort and gross claw overgrowth.
It can be seen from the above that laminitis is a complex multi-factorial disease which may pre-dispose the cow to many of the common claw lesions.
White line abscess
This is caused by the penetration of the white line by fragments of grit or stones. The white line has often been previously weakened by chronic laminitic changes. If the foreign body tracks to the corium it will form an extremely painful abscess. These can often be diagnosed using hoof testers. Treatment is to provide drainage and to trim away all under run horn. This may require the removal of a large part of the wall or sole. Never leave an area which could become impacted with debris.
Severe deep infections may require antibiotic treatment but this is not common. The prognosis is usually very good however some deep infections may track into joint structures.
The application of a block to the healthy digit will reduce the animals discomfort and also reduce the risk of further trauma to the affected digit.
Foreign body penetration of the sole
Although penetration of the white line is by far the most common site of foot penetration, any part of the sole can be damaged by a sharp object.
It is not sufficient to simply remove the foreign body, all under-run sole must be removed to leave only healthy tissue. The application of a dressing is optional. As a general rule most lesions will heal faster left open, the only real need for dressing is to control haemorrhage.
Solar ulcer
Solar ulcers typically occur on the lateral claw of the hind foot (the pedal bone in this claw rests partly on the sole) or less commonly on the medial claw of the front foot.
The proposed aetiology is that following laminitis the pedal bone drops and later pinches the corium over this site. This results in haemorrhage into the horn or severe impairment of horn production. The resultant horn defect is the ulcer which then becomes plugged with granulation tissue. Over growth of the toe and erosion of the heel will also rotate the pedal bone increasing pinching at this site. The solar ulcer is very often bilateral, it is good practice always to examine the other foot and perform corrective foot trimming when treating solar ulcer cases.
The ulcer is treated by removing all under-run horn and dishing out the sole so that there is no pressure on that site. The application of a block will greatly improve the cows gait and aid recovery.
Sole haemorrhage (bruising)
Haemorrhagic areas with softening and yellow discolouration of solar horn is all part of the subclinical laminitic syndrome, or may follow acute laminitis. This often does not require specific treatment but should be a warning that laniinitis is a problem within that animal or herd. Steps should then be taken to remove underlying factors leading to laminitis. This should be differentiated from areas of normal healthy pigmented horn when examining the sole.
Severe solar haemorrhage may result in under-running of the sole as the solar horn grows out. If found this should be treated by removing all the "false" sole to leave only healthy solar horn.
Horizontal Fissure
Horizontal cracks can go unnoticed until they have grown towards the toe and become unstable. They then become extremely painful and cause very severe lameness. They are caused by a severe illness in the past, often about 9-10 months previously. Common causes of this lesion are peracute toxic mastitis or severe metritis after calving.
The claw should be trimmed to at least reduce the movement and pinching of the underlying sensitive corium. Secondary infection should be treated and if possible a block used to support the other claw which is often similarly effected. It is common to see this lesion in all eight claws.
As this is an extremely painful condition which is likely to occur in more than one foot and which often presents in late lactation it may be more humane to consider culling some of these cows.
Fracture of the pedal bone
Classically associated with Fluorosis this fracture of the pedal bone can be seen following severe trauma e.g. running on hard ground or oestrus behaviour. Typically the medial claw of the front foot is involved and animals stand with a cross-legged stance. Affected animals show little or no heat or swelling of the foot. X rays can be used to confirm the diagnosis if required, the common fracture site is across the pedal joint to the solar surface of the bone. The hoof horn acts as a good splint and many cases will heal in 2-3 months if a block is placed on the other claw.
Deep Digital Sepsis
Deep infection of the foot usually follows other foot disease e.g. solar ulceration, white line disease or a puncture wound.
The infection can be localised to one structure or involve several e.g. septic pedal arthritis, septic navicular bursitis/osteomyelitis, tenosynovitis of the deep digital flexor tendon sheath or abscess in the heel involving the digital cushion. These lesions usually result in severe lameness, heat and swelling around the coronet and often discharging sinuses at the coronet
Treatment will not respond to antibiotics alone and requires radical drainage and curettage of infected or necrotic tissue. Many require amputation of the digit.
Spastic paresis
This is a progressive condition of unknown aetiology affecting one or usually both bind limbs. Shortening of the gastrocnemium and calcaenean tendon leads to severe over extension of the hock. Usually seen in calves 2-9 months of age. Treatment is by neurectomy of the tibeal nerve. Affected animals should not be used for breeding.
As well as the above causes of foot lameness there are also a number of neurological and orthopaedic conditions which must be considered. For example:
Joint ill
Hip dysplasia
Hypertrophic osteoartbropathy
Ankylosing spondylosis
Hip dislocation
Osteoporosis
Sacroiliac luxation or subluxation - post partuxn
Patellar luxation
Anterior cruciate rupture
Contracted tendons
Calcanean tendon rupture
Gastrocnemius muscle rupture
Haematoma
Tarsal cellulitis
Carpal hygroma
Radial paralysis
Suprascapular paralysis
Brachial plexus paralysis
Femoral paralysis
Obturator paralysis
Sciatic paralysis
Tibial paralysis
Osteochrondrosis
The Prevention of lameness
For many years nutrition was considered the main cause of laminitis and thus many lameness problems. It is true that ruminal acidosis can result in laminitis so every< 4.0), provide long fibre in diet and avoid sudden diet changes which may result in acidosis. The cows environment is now recognised as being extremely important in the development of lameness. Factors which effect "cow comfort" have a major influence on foot disease. Cows under normal pasture conditions will spend some 12-14 hours per day lying down. In poor cubicles this can be greatly reduced. Whatever the cubicle design adequate bedding is essential for comfort. Cubicles built in the 1960*s - 1970*s are commonly too small for today*s cows. In order to provide satisfactory "cow comfort" cubicles need to have sufficient length and width (8ft/2.4m x 4ft/ 1.2m for the average Friesian cow). They also require up to 1-1.2m of borrowing space to allow the cow to lunge forward on rising. A low kerb <6inches/ 15cm and a good bed is also important, as is sufficient numbers of cubicles.
Walkways need to be well maintained clean and free of slurry, concrete should be not too smooth nor too rough. Areas such as gateways and around water troughs must be well maintained. Tracks to the pasture areas need to be built with cow comfort in mind.
Routine foot trimming to prevent overgrowth will reduce the incidence of lameness, but beware as poor foot trimming is itself a risk factor.
Footbaths also have a place in the treatment and control of lameness.
LEAD POISONING
DEFINITION
This condition results from the ingestion of large amounts of lead-containing substances usually over a short period of time. Affected individuals may be found dead, or they may develop acute neurological signs, or they may appear blind.
AETIOLOGY
Lead poisoning in cattle occurs when large amounts of lead are ingested over a relatively short period of time. The most readily available sources of this heavy metal include old paint (doors, tins), metallic lead (batteries, shot) and also old engine oil, linoleum and felt. Forage can become contaminated by fall-out from smelters, by the application of sewage sludge, as a result of a high lead content in the soil and from the combustion of leaded petrol.
The susceptibility to lead poisoning depends upon the animal species, type of compound, age and diet. The incidence of disease is high in ruminants perhaps because particulate matter can remain in the stomach where it is converted to soluble lead acetate in the acid environment. Young cattle are more often affected than adults because firstly, they are more inquisitive and tend to lick everything secondly, their tolerance for lead is only about half that per unit body weight of adult cattle and thirdly, their absorptive efficiency is greater (x2). High dietary calcium and phosphorus decreases lead absorption whereas low dietary calcium has the opposite effect. The various forms of lead vary in their solubility with lead acetate being the most soluble. Only about 2% of inorganic lead is actually absorbed because insoluble complexes are formed in the alimentary tract and these are excreted in the faeces.
Although all ages can be affected, the prevalence is comparatively high in young animals because they are so inquisitive. Cases occur in housed and grazing animals, and, although only one or two animals are usually affected, the incidence of disease can occasionally be much higher eg. in cattle eating contaminated silage.
CLINICAL SIGNS
These are the result of firstly, acute central nervous system involvement because a large amount of lead has been ingested over a short time and secondly, intestinal tract involvement as a result of the caustic action of the lead salts on the gut. There is usually a delay of a few days following a toxic dose. Two forms of the disease are recognised in cattle.
Acute Form. This is most common in young animals. The signs develop suddenly and persist for only a short time (12-36 hours). Therefore, many cases are found dead (Sudden Death). Initially, individuals are blind, staggery, with muscle tremors especially of the head and neck. When stimulated, periods of intense excitement (rolling eyes, champing jaws, frothing at the mouth) are followed by depression and head-pressing. Eventually, the animal collapses, develops intermittent convulsions and soon dies because of respiratory failure.
Subacute Form. This is most common in adults. There is extreme dullness, anorexia, drooling of saliva and teeth-grinding. There are signs of abdominal pain, a cessation of ruminal contractions with constipation followed by a foul smelling diarrhoea. Such animals are reluctant to move and, when made to do so, they circle either way because of blindness. Death usually occurs after 3-4 days.
A syndrome characterised by poor growth rate and even weight loss has been recognised in growing cattle grazing over old lead workings. This can be considered to be chronic lead poisoning.
DIAGNOSIS
Lead poisoning should be suspected when cattle suddenly develop signs of severe nervous disease, or are found dead. In living animals if the blood lead concentration is in excess of 0.35 ppm. then they have been exposed to unusually high amounts of lead. In fatal cases, samples of liver and kidney should be taken; concentrations in excess of 10 ppm wet matter in liver and 25 ppm in wet kidney cortex are diagnostic.
TREATMENT
Many cases of acute lead poisoning die, irrespective of whether drug therapy is attempted.
The recommended drug is sodium calcium edetate given intravenously. This should be repeated daily for 2-3 days if considered necessary. Blood lead levels must be determined at least 7 days apart after 28 days has elapsed from full clinical recovery.
If the blood lead concentration is in excess of 1.0 ppm then the prognosis is bad. Recovery can take up to 2 weeks, during which time supportive therapy might be necessary. The blindness which usually persists for several days after a general recovery, can be permanent.
After treating the sick animals, the source of the lead should be looked for and if found, disposed of. In some cases, an obvious source may not be found.
PREVENTION
Cattle should be prevented from having access to potential sources of lead, e.g. rubbish dumps. Old painted doors should not be used to make calf pens.
LEPTOSPIROSIS
DEFINITION
Infection with Leptospira spp. can cause clinical signs which include fever, jaundice, anaemia, kidney infection and abortion. The majority of infections are subclinical. It is also a ZOONOSIS, and can infect man.
INCIDENCE
Infection is widespread in cattle in Britain. Serological evidence suggests that at least 70% of British cattle have been infected with one or more serotypes of Leptospira spp. Death from leptospirosis is rare in cattle in Britain. The occurrence of haemolytic anaemia due to Leptospira spp. is unknown but is probably rare.
CLINICAL SIGNS
Calves less than two months old, meningitis is the main clinical syndrome. Affected animals suffer severe depression with a greatly reduced appetite. There is marked fever. They exhibit neurological signs such as, muscle tremors and paddling when in lateral recumbency. Occasionally, they will exhibit extensor rigidity. Some calves may be blind.
In slightly older calves, around six months of age, the clinical signs are due to a septicaemia with anorexia, dullness and fever. Bleeding of the mucous membranes occurs and there is also an anaemia, with pallor and jaundice and blood in urine.
Infection of the adult milking cow in early lactation results in an acute syndrome, the milk drop syndrome in which there is a sudden drop in milk yield with a fever. Surprisingly, affected cows often continue to eat normally with no obvious abnormality in demeanour. The small amount of milk which is produced has an orange-yellow colour with a thick, sticky consistency which resembles colostrum. All four quarters are affected, but the udder itself is soft and flabby with no evidence of inflammation or hardness. The milk yield slowly returns to normal, with or without treatment. Very occasionally abortion will occur at this stage.
With chronic infection, following localisation in the kidneys and uterus, abortion occurs about 6-12 weeks after infection. Abortion can occur at any stage of gestation between four and nine months. Abortion tends to occur in the younger cows during their second or third pregnancy but also occur in the older cows. The incidence of abortion on individual farms, but in endemically infected herds an annual abortion rate of between 4-7% due to leptospirosis can occur.
Calves born alive in late gestation may be very weak, lethargic and even non viable.
It is also likely that the foetal membranes will be retained.
EPIDEMIOLOGY
Transmission occurs when the urine, aborted foetuses, or uterine discharges of an infected animal containing viable leptospirae reach a susceptible animal. Venereal and congenital transmission occurs but is less important. The source of infected urine may be a rodent, a dog or a cow. Cattle remain carriers of L.hardjo for up to 18 months. The organisms remain viable in damp soil or free surface water for periods of up to 6 months.
The most common method of transmission is in splashes of freshly-voided urine from other cattle. L.hardjo infection may be enzootic in a herd and transmission may occur between carrier and susceptible animals, particularly in yarded cattle and in cool damp conditions in late summer and autumn. Rodents may form a reservoir of infection.
Clinical signs such as abortion storms and fever or mastitis occur when a new serotype is introduced to a herd (by the purchase of a carrier cow, for instance) or when susceptible animals (e.g. in calf heifers) are introduced to an infected environment (e.g. a carrier herd or pasture infested with infected rodents).
Serum antibody levels are used to determine the extent of leptospiral infection. In one survey in Scotland 54% of 3,000 cows were found to have serum antibody to L.hardjo.
DIAGNOSIS
Leptospirosis may be suspected as a result of the clinical signs or post-mortem findings but as the clinical signs (other than the mastitis which is fairly characteristic) are non-specific, laboratory findings are required to confirm a diagnosis of leptospirosis.
TREATMENT
A number of antibiotics can be used to treat leptospiral infections. The elimination of the organism from the kidneys can be achieved using 3-5 daily injections of streptomycin 10 mg/kg or 25 mg/kg in a single injection. Tetracyclines and ampicillin may also be satisfactory. Penicillin will prevent death from septicaemia but will not eliminate leptospira.
CONTROL
Carrier animals should be eliminated by treatment or blood testing and removal. The problem of the reservoir of infection in wild life means that, with many serotypes, the source of infection cannot be removed although rat infestations in buildings can be controlled.
Vaccination of herds where leptospirosis has been identified with vaccines containing inactivated cultures of L.hardjo is now widely practiced in Britain. Vaccination does not eliminate renal or uterine carriage and should take place before first exposure to infection.
In open herds, the treatment of incoming animals for possible leptospirosis may be considered worthwhile to prevent the introduction of new serotypes.
Hygiene, the provision of clean water supplies and the fencing-off of stagnant surface water may also reduce the transmission of the disease.
LOUSE INFESTATION
This usually presents as a chronic, generally mild dermatitis.
AETIOLOGY
The sucking lice of cattle belong to the genera Haematopinus, Linognathus and Solenopotes; the only biting species is Damalimia bovis.
PREVALENCE
Louse infestation is extremely common.
SIGNIFICANCE
Louse infestation can cause direct losses through hide damage and indirect losses through loss of production.
CLINICAL SIGNS
Skin irritation is evident, with rubbing and licking of the affected areas. Any part of the body may be affected. Most cases are mild and not associated with loss of hair, but in severe cases some hair is lost in an irregular pattern and there may be superficial abrasions and skin scaling. Bareness of the necks of cattle tied in stalls. In wintertime is sometimes associated with the presence of lice. Very heavy infestations of sucking lice can occasionally cause an anaemia.
PATHOGENESIS
Local irritation caused by the feeding of both sucking and biting lice is often followed by mechanical abrasion due to licking and rubbing. With heavy infestations of sucking lice, blood loss anaemia occasionally develops.
EPIDEMIOLOGY
Infection is mainly by direct contact of animal to animal since all stages of the life cycle occur on the host and heavy louse burdens are generally seen in groups of cattle during the winter when the hair coat is long.
DIAGNOSIS
By careful examination and recognition of the insects or their eggs (‘nits*) stuck on the hairs. Cattle lice are small and dark and move so little that they may appear inanimate and are only recognised by very close inspection.
TREATMENT AND CONTROL
Various pyrethroid and organophosphorus insecticides and amitraz are effective against lice. Both ivermectin and doramectin are highly effective against the sucking lice of cattle.
Although it is difficult to eliminate lice completely treatment of groups of cattle at housing in the autumn will help to reduce louse populations during winter.