Sheep Diseases and Conditions

Sheep - Medical Conditions

Lamb

BLACK DISEASE

AETIOLOGY

A generalised toxaemia of sheep, and occasionally cattle, caused by toxins of Clostridium novyi Type B which are produced in damaged liver tissue. Although any necrotic process in the liver can stimulate the bacteria to proliferate, field outbreaks of Black Disease are usually precipitated by invasion of the liver by immature liver fluke or sometimes by feeding changes which produce liver damage allowing entry of Clostridia. The causal agent C. novyi, is found mostly in soil, particularly in low-lying ground, and on pastures.

INCIDENCE

Black disease occurs on both hill and lowland farms which are infected by liver fluke. Cases usually occur at the same time of year as acute liver fluke infection, i.e. predominantly the autumn and early winter but occasionally in the early spring; adult sheep appear more susceptible although lambs commencing their first winter have also been affected. In Britain the distribution of Black Disease is not well-known and many farms where fluke is a problem are free of the disease. Once a farm becomes infected the disease is usually seen regularly in subsequent years.

CLINICAL SIGNS

The course of this disease is short and affected animals are usually found dead having shown no signs of illness. If clinically affected animals are observed they are found to lag behind the rest of the flock and they will collapse if attempts are made to drive them. Such animals can shortly be found lying in sternal recumbency and appear as if asleep but if disturbed by a noise, they become hyperaesthetic and show twitching of the eyes and ears. Gradually they become comatose and death ensues within a few hours of the illness being first apparent.

TREATMENT

Affected animals are not treated because the disease runs such a rapid course that there is usually no time for treatment to be effective. A less acute form might respond to high levels of penicillin. When the disease occurs it is advisable to treat all sheep with triclabendazole to remove any fluke infection.

Control is by annual vaccination of all breeding stock with a multivalent clostridial vaccine.

HYPOMAGNESAEMIA (Grass Staggers)

A condition resulting in sudden death in both the hill and lowland ewe and similar to hypomagnesaemia of cattle.

AETIOLOGY

At certain times of the year (particularly April-May) pasture may contain insufficient magnesium to meet the requirements of the grazing animal and so a simple deficiency state may result. However, sheep developing hypomagnesaemia often graze pasture with a magnesium content as high as or higher than that of pasture grazed by sheep which do not develop the disease.

The demands of lactation in combination with low pasture levels of magnesium may result in a reduction in the serum magnesium levels.

Grass, especially when it is growing rapidly, may contain some factor which interferes with magnesium uptake from the gut. As in cattle, the onset of the clinical disease is often associated with a sudden cold, wet spell.

INCIDENCE

Hypomagnesaemia is essentially a disease of the lambing period and occurs in ewes within the month before or after lambing, the highest incidence occurring after parturition. It is particularly common in the cast hill ewe which has been brought down to lowground and is carrying or feeding a heavy type of cross lamb.

A number of sheep may have an accompanying hypocalcaemia

CLINICAL SIGNS

The majority of cases present as sudden death. Animals which are observed in the initial stages of the disease show an alertness accompanied by nervousness and restlessness. As hyperaesthesia increases the affected animal develops an unsteady gait, staggering about with head held high and apparently blind. Recumbency follows with the animal lying on its side making involuntary running movements and there may be champing of the jaws and frothing at the mouth.

TREATMENT

In many cases treatment is unsatisfactory and has little influence on the course of the disease. Magnesium is administered by injection in the form of a 25 per cent solution of magnesium sulphate, up to 50m1 of this solution being given subcutaneously. Calcium borogluconate or a proprietary calcium/magnesium mixture given intravenously may also prove useful.

CONTROL

The incidence of the disease can be significantly reduced by the use of magnesium supplements in the form of rumen boluses or as magnesium-rich supplements which can be mixed with concentrates; alternatively calcined magnesite may be added to the food, to allow uptake of 7 gms. per head per day.

Magnesium licks are also useful but suffer from the disadvantage that many sheep either like or dislike them and so uniform uptake by the flock cannot be assumed.

Top-dressing of pasture with magnesium limestone or calcined magnesite could be attempted for long term protection. In this case it is necessary to seek advice on the most appropriate and cost-effective method, and the correct application rate for individual farms.

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.

PASTEURELLOSIS

Pasteurellosis is one of the most important causes of economic loss to the sheep industry in Britain at present. It occurs as two main syndromes; the pneumonic form is an acute pneumonia which is frequently fatal and from which Pasteurella haemolytica is the organism usually isolated and the systemic form, which is an acute, fatal disease occurring in hoggs in the autumn and from which P. trehalosi is the organism isolated. The pneumonic form is sometimes called enzootic pneumonia.

AETIOLOGY

P. haemolytica is a common inhabitant of the upper respiratory tract of sheep which are apparently healthy, but usually there is a relatively low incidence of the organism in a normal flock. The organism however, can be isolated from the lungs of sheep with acute exudative pneumonia, and is considered to be responsible for the disease.

PNEUMONIC PASTEURELLOSIS

CLINICAL SIGNS

Frequently premonitory clinical signs are absent and the first indication of trouble is when one or more animals die suddenly. Other affected animals in the flock may cough and are usually dull and anorexic. On closer examination these animals are breathless with a rectal temperature in the region of 106-l07oF/41-42oC. There may be slight frothing at the mouth and nose. Only a proportion of the flock will be affected and morbidity and mortality are seldom greater than 10%. Animals which recover may remain unthrifty. Occasionally pneumonia due to P. haemolytica may occur in a single sheep, especially rams.

EPIDEMIOLOGY

Outbreaks of pneumonic pasteurellosis are often associated with changes in the environment and occur in spring and summer, but can occur sporadically at any time of the year. Routine handling for management procedures may precipitate an outbreak. It can occur in all ages of sheep, whether managed intensively, extensively or housed.

SYSTEMIC PASTEURELLOSIS

CLINICAL SIGNS

As with pneumonic pasteurellosis the first indication of systemic pasteurellosis is the sudden death of several hoggs. Affected sheep are extremely dull, reluctant to move, breathing difficulties with a frothy discharge around the mouth. There is a marked pyrexia unless in the terminal stages when the temperature is likely to be subnormal.

EPIDEMIOLOGY

The systemic syndrome occurs in all ages of sheep at all times of the year, but is most common in hoggs during September, October and November, shortly after moving from poor (hill) pasture to good pasture (foggage, stubble regrowth) or after folding onto rape or turnips. Deaths begin to occur within a few days of being moved and the mortality may be up to 20%. Frequently it is the lambs in best condition which die. Deaths cease within a few days of the beginning of the outbreak without treatment.

SEPTICAEMIC PASTEURELLOSIS

In young lambs up to 2 months of age Pasteurella haemolytica can cause a septicaemia which results in sudden death. Both pneumonic pasteurellosis and the septicaemic form due to P.haemolytica may occur in a flock at the same time.

TREATMENT AND CONTROL

It would appear to be unnecessary and certainly uneconomic to carry out widespread treatment within an affected flock. In the indoor situation improved ventilation or reduced stocking rate should reduce the concentration of the aetiological agent and so theoretically limit the spread of the outbreak but will not be expected to have much effect on established clinical cases. The latter may be controlled by using antibiotics effective against Pasteurella such as oxytetracycline.

Vaccines, usually containing both P.haemolytica and P.multocida have been available for many years in Britain and have been widely used in many areas to prevent pneumonic pasteurellosis with no convincing scientific evidence that they were effective.

A vaccine has been developed for pneumonic pasteurellosis. This vaccine contains the main serotypes isolated from pneumonic pasteurellosis. Attempts should be made to reduce stress factors during the critical period of the year from October to December by avoiding sudden changes in diet and reducing handling and interference to the essential minimum.

Multicomponent vaccines containing P.haemolytica and P.multocida in combination with clostridial antigens are also available.

JOHNE'S DISEASE

A chronic wasting disease of sheep similar to Johne’s Disease of cattle.

The disease is caused by infection with Mycobacterium avium paratuberculosis, an organism which is ingested in food and water contaminated by infected faeces. Congenital infection also occurs. Sheep may be affected by several types of the organism, but the commonest type is probably the same as that causing disease in cattle.

Under field conditions the organism is very persistent and can survive on grass for months.

INCIDENCE

Johne*s disease is predominantly a disease of the young adult animal although it may also be observed in older sheep. The incidence of clinical disease in a flock is generally low although a considerable number of sheep may be infected.

CLINICAL SIGNS

The predominant clinical sign of Johne’s disease is weight loss. This takes place in a progressive fashion and may be accompanied by loss of wool. Diarrhoea is not a feature of the disease in sheep although the faeces may become soft, losing their pelleted nature. Appetite remains good and the animal is bright and alert until the later stages of the disease.

Onset of the clinical disease may be associated with stress factors such as lambing, inadequate nutrition and possibly parasitic infections.

CONTROL

The only effective method of controlling the disease from a flock is by vigorous culling of any thin adult animals.

PARASITIC GASTRO-ENTERITIS

Parasitic gastro-enteritis (PGE) in Britain is a disease primarily of lambs, characterised by weight loss and diarrhoea..

AETIOLOGY

The principal nematodes present in outbreaks are Ostertagia and Trichostrongylus occasionally Haemonchus, Strongyloides, Cooperia, Nematodirus spp. Bunostomum and Chabertia are involved. In most cases infection is by ingestion of the larvae.

PATHOLOGY

The main function of the gastro-intestinal tract is to digest and absorb nutrients. In addition, it plays a major role in fluid and electrolyte balance and protein metabolism. The presence of large numbers of parasites in the gastro-intestinal tract will interfere with these functions with obvious and serious consequences.

INTESTINAL PARASITES

Intestinal function is to complete digestion and to absorb nutrients; the intestine also plays a major role in fluid and electrolyte balance and protein metabolism. To do this it has an enormous surface area for absorption of nutrients.

The effect of the presence of parasites such as Trichostrongylus colubriformis and Nematodirus battus is to reduce surface area and therefore reduce ability to absorb. The brush border enzymes may also be lost and hence there is reduced ability to digest. If there is a severe exudate present this will act as a barrier and interfere with digestion and absorption.

The clinical consequences of these changes are:

1. Diarrhoea. This is the cardinal clinical sign of enteritis. It can be defined as a consequence of malabsorption of water and electrolytes.
2. Malnutrition. Due to malabsorption and leading to weight loss, poor quality wool and impaired milk production.

3. Excessive loss of protein through the intestine.

CLINICAL SIGNS

Outbreaks of clinical disease are predominantly seen in lambs during the months of July, August and September. They are of sudden onset and several animals are usually affected, the main clinical sign being a profuse, watery diarrhoea which results in soiling of the fleece around the tail and perineum with faecal material. Affected animals become dull and the wool loses its bloom. Initially weight gain is arrested but as the diarrhoea persists there is a loss of weight and eventually animals may become markedly dehydrated followed by recumbency and death.

Young sheep may develop a severe diarrhoea during the late winter months. The first clinical sign is a gradual loss of condition which may be difficult to appreciate and this is followed by the appearance, in a number of animals, of a severe diarrhoea which is of a very dark colour. After the onset of the diarrhoea, deterioration is rapid.

Adult sheep frequently carry a worm burden which does not appear to affect their general health provided the animals receive an adequate diet. When food is scarce any parasitic burden may exaggerate the effects of malnutrition. Under these circumstances affected animals show a progressive weight loss without diarrhoea.

EPIDEMIOLOGY

It is accepted that a large proportion of the trichostrongyles can overwinter on pasture as eggs or larvae, but the majority of the overwintered larvae die by June. Development and activity are negligible below an average temperature of about 10 degrees C, which usually persists in this country until April/May.

During spring and early summer larvae are available on the pasture from a number of sources.

1. Overwintered larvae

2. Hatching and development of overwintered eggs

3. Hatching and development of eggs from the spring or peri-parturient rise in nematode faecal egg output which occurs in ewes.

The ‘spring rise" in ewe faecal egg output can be the result of maturation of larvae previously inhibited in their development, increased fecundity of existing adult female worms and reinfection due to ingestion of overwintered larvae during late pregnancy and early lactation. Whilst both maturation of inhibited larvae and increased fecundity contribute substantially to the "spring rise" the major factor appears to be reinfection.

Although the breeding ewe is essentially resistant to reinfection at all times of the year, a partial relaxation of this resistance is apparent during the late stages of pregnancy and early lactation allowing considerable build-up of adult worm populations. The ewe therefore shows a non-specific loss of immunity at this stage of her reproductive cycle. The degree of immunosuppression may be exaggerated by a nutritional deficiency, not uncommon in the hill ewe, and may also depend on voluntary food intake which, in the lactating ewe, can exceed that of pregnant or unmated ewes by up to 50 per cent.

Larvae ingested by lambs in spring and summer will result in eggs being passed in the faeces in three weeks; the development of these eggs to larvae becomes more rapid toward mid-summer, resulting in a more intense accumulation of larvae on the pasture from mid-summer onwards. The precise bionomic requirements of the genera differ, and as a result Ostertagia spp. build up in the middle of summer, whereas Trichostrongylus, and some other species tend to reach a peak later in the season.

The end result is that towards the end of summer lambs may be exposed to high pasture burdens of larvae. If they are crowded on a high production sward which allows migration of larvae on to grass blades, in particular in those with a high clover content which will provide a humid microclimate for larval development and movement, then the conditions for the occurrence of acute parasitic gastro-enteritis are present.

DIAGNOSIS

This is usually based on the clinical signs appearing between July-October, and a knowledge of the grazing history, for example, a previous history of parasitism on these fields or an increase in stocking rate.

Whenever possible a post-mortem examination should be made to establish a definite diagnosis.

Where P.G.E. is suspected many farmers or practising veterinary surgeons will treat the flock with a wormer and if a good response is obtained this is used as an index of diagnosis.

Collection of faecal samples for examination for nematode eggs is a useful aid to diagnosis

TREATMENT

Many anthelmintics are now available for the treatment of parasite gastro-enteritis. Thiabendazole was the forerunner of the modem broad spectrum anthelmintics and is still used. Several other benzimidazole (BZ) drugs have since been developed which are more effective. For treatment of clinical parasitic gastro-enteritis the benzimidazoles, probenzimidazoles, levamisole, morantel, invermectin and some of the new avermectin/milbemycin compounds may be used

Most drugs in sheep are administered orally by the use of modern automatic drenching guns.

In order to reduce pasture contamination it is good practice to delay the return of animals to pasture for several hours or days following treatment. Where a sufficient degree of grazing control is practised, as in most lowland flocks, treated sheep should be moved to pasture ungrazed by sheep in that grazing season.

CONTROL

Control is generally based on strategic use of wormers, often combined with specific grazing management.

ANTHELMINTIC PROPHYLAXIS

The most important source of infection for the lamb crop is the periparturient rise in the ewe faecal egg count; prophylaxis will only be efficient if this rise is kept to a minimum.

This may be achieved by the use of a ruminal bolus containing albendazole which removes existing infections and provides 100 days protection against reinfection. The timing of administration depends on management systems but the bolus is most frequently used one month pre-lambing or at turnout after lambing. To be effective all ewes should receive a bolus and the ewes and lambs should remain on the same pasture. Otherwise the prophylactic routine for the ewe will depend on whether permanent pasture must be grazed all year round as is the case on the hill farm, or whether new leys are available each year, as is the case on many arable, lowground farms. In the former situation, where ewe nutritional status is frequently poor, treatment of the ewe during the fourth month of pregnancy would eliminate the worm burden, including inhibited larvae, result in improved general body condition and probably allow animals to lamb with a more adequate milk supply. As treated animals will become reinfected during late pregnancy and early lactation it is recommended that further treatment be carried out in order to reduce pasture contamination.

If ewes are brought indoors to lamb a treatment at the time of housing will remove existing worm burdens. Subsequent treatments would then depend on existing farm management practices.

On the lowground farm where fresh pasture is available each year and where ewe nutritional status is generally good, one treatment is usually sufficient. This can be carried out when the ewes leave the lambing field and before they move on to clean grazing. Provided the grazing has not been used for sheep for at least one complete season, treatment at this time will result in adequate control. Hoggs and tups should be dosed at the same time as the ewes.

Apart from specific drenching for Nematodirus in May and June, lambs from spring lambing flocks should be routinely dosed at weaning, and where husbandry permits, moved to grazing not occupied by sheep in that season. Where lambs in lowland flocks cannot be so moved, they should be drenched again 4-6 weeks later; hill lambs usually only require a single drench at weaning in late July/ early August.

Where fasciolosis is also a problem, anthelmintics effective against both Fasciola and gastro-intestinal nematodes may be used and a number of effective combined anthelmintic preparations are now available. Many of these combinations, however, contain drugs which are only effective against adult fluke and are therefore only of use late in the winter for a pre-lambing dose. Generally, the recommended timing and dosing schedule for the treatment and control of P.G.E. and fasciolosis are so different that combination products are not justified.

ENZOOTIC ABORTION OF EWES (EAE; Kebbing)

A condition, caused by infection with Chlamydia psittaci resulting in abortion during the last 2-3 weeks of pregnancy although a proportion of lambs, showing varying degrees of strength and vigour, may be born alive.

The organism is introduced by purchase of infected adult sheep or lambs and, when the fully susceptible flock is at risk, abortions may occur in 25-30% of ewes during the first two or three years; subsequently an incidence of around 5% is observed with gimmers and second-crop ewes mainly involved. Infection is usually by the oral route and develops in the gut. Aborting ewes may appear dull and anorexic for several days prior to abortion and may retain the placenta afterwards.

An attempt may be made to reduce the incidence of the disease by isolating aborting ewes. Ewes which abort will lamb normally in subsequent years.

An inactivated vaccine, if available, should be given to ewes before they go to the ram. Revaccination is recommended after 3 years.

If EAE is diagnosed early in an outbreak of abortion, prophylaxis of remaining ewes with long acting oxytetracycline has been shown to reduce the numbers of ewes which subsequently abort.

The disease is a zoonosis and can cause severe disease and abortion in pregnant women.

TOXOPLASMOSIS

A disease caused by the protozoan parasite Toxoplasma gondii The sexual stages of the life cycle of this coccidian parasite occur in the intestine of the final host, which is the cat, but all mammals including man may act as host for the asexual multiplication phases which can take place in various tissues and may result in a variety of pathological changes and clinical signs. In sheep, toxoplasmosis is most frequently associated with abortion or the birth of weak lambs due to pathological changes in the foetal membranes.

Infection of susceptible ewes in the first 2 months of pregnancy leads to foetal death with subsequent expulsion or mummification whereas if infection occurs later, apparently normal lambs are either aborted during the last month or carried to term and born dead or weak.

The main source of infection for sheep is considered to be the sporulated oocyst which is derived from cat faeces. Cat faeces may contain millions of resistant oocysts and contamination of feed, either at the mill or on the farm, which is subsequently used in feeding ewes prior to tupping or lambing, has been suggested to be a major source of infection. Asexual stages present in the products of abortion may also be a source of infection.

Serological tests may be employed in diagnosis but paired samples taken at an interval of 1-2 weeks are usually necessary to determine a rising antibody titre which would indicate recent infection.

Toxoplasmosis is rarely treated in sheep and control is difficult, although the prophylactic use of coccidiostats such as decoquinate in the feed may be of value.

Preventing access of cats to feedstuffs during manufacture and storage will reduce the possibility of infection from sporulated oocysts. Traditionally, the mixing of previously infected ewes, or those that have recently aborted, with replacement stock has been advocated but this may be contra-indicated since it may facilitate transmission of other causes of abortion, e.g., the agent of enzootic abortion of ewes.

A vaccine containing live tachyzoites of T. gondii is now available for use in breeding sheep; this should be administered at least 6 weeks before mating.

SALMONELLOSIS

In recent years salmonellosis in sheep has become more common. Although there is a specific organism associated with abortion, Salmonella abortus-ovis, this appears to be confined to south-west England. At least another 8 salmonellae have been responsible for disease in sheep, in particular, S. typhimurium, S. dublin and S. montevideo.

Infected ewes abort during the last 6 weeks of pregnancy. Prior to abortion affected ewes become dull, depressed and anorexic and fevered. Diarrhoea may or may not be present. Lambs born to such ewes may be dull, weak and diarrhoeic. Following abortion or lambing the ewe remains dull, retains the placenta and a vaginal discharge persists for several days.

In cases of salmonella abortion it is important to isolate affected ewes and pay great attention to general hygiene.

CAMPYLOBACTER

A condition of sporadic occurrence in sheep due to ingestion of the causal organism Campylobacter fetus or C. jejuni. The incidence in a flock can be as high as 50% but it is more commonly in the vicinity of 10%. The disease is rarely seen in the same flock two years in succession.

Abortion occurs during the last 6 weeks of gestation and generally there are no premonitory signs. After aborting, affected ewes may show a brown, mucopurulent vaginal discharge and the placenta may be retained.

Outbreaks may be controlled by isolating ewes which abort from those which are yet to lamb. In the U.S.A vaccination of the latter at this stage has been shown to significantly reduce the severity of the outbreak.

TICK-BORNE FEVER

AETIOLOGY

In the U.K. this disease is caused by the rickettsia Cytoecetes (Ehrlichia) phagocytophila which is transmitted by the tick Ixodes ricinus.

INCIDENCE

It is a disease of sheep, particularly lambs, and cattle. In a tick-infested area probably every lamb is infected within the first two weeks of life. Adult sheep and cattle moved on to tick infested pastures from a tick-free area are highly susceptible.

CLINICAL SIGNS

During the febrile phase, when body temperature may be in the region of 107oF/42oC, affected animals are dull and listless, and there is a gradual loss of weight. In many cases this phase may pass unobserved and, in lambs, may be followed by the clinical signs of louping-ill or tick pyaemia. In adult animals, both sheep and cattle, abortion may be the most obvious clinical sign. Affected rams may become temporarily infertile.

TREATMENT

It appears unnecessary to treat uncomplicated cases of tick-borne fever although long acting tetracyclines can be used both therapeutically and prophylactically.

CONTROL

Tick control measures will effectively reduce the level of challenge.

LOUPING-ILL

An acute encephalomyelitis producing paresis and cerebellar ataxia. This is predominantly a disease of sheep although, less frequently, cattle, pigs, horses and man may become infected.

AETIOLOGY

A tick borne virus.

INCIDENCE

Louping-ill occurs mainly in Scotland and Northern England although the disease has been recorded in other parts of Great Britain and Ireland. The disease is seasonal, being observed in the spring and early summer and affecting lambs and yearling sheep. Adult sheep brought in from non-louping-ill areas are also susceptible.

EPIDEMIOLOGY

The disease is spread by the tick vector, Ixodes ricinus. The virus can survive for over a year in unfed ticks and apparently can survive from the larva to the adult stage, infection being transmitted by both nymphs and adults. It is uncertain whether infection can be transmitted by adult females to their eggs.

CLINICAL SIGNS

During the viraemic phase of the disease there is a fever. This stage of the disease may pass undetected but if seen, affected animals are dull, anorexic and often stand on their own away from the main flock. After a variable period of time, the pyrexia disappears and the temperature remains normal only to rise again as a result of virus activity in the brain. At this stage, nervous signs appear. Affected animals are dull, frequently salivate, and may show intermittent head shaking with twitching of the lips, nostrils and ears. As the disease progresses, muscular tremors develop involving particularly the muscles of the neck and limbs and gradually this leads to variable degrees of muscular rigidity. As a result of these changes, the animal walks with jerky, stiff, almost bouncy movements. A progressive inco-ordination develops and the animal has great difficulty maintaining its balance and tends to stagger about, frequently falling. Affected animals often appear blind as they are unable to avoid walking into objects and frequently bump into anything put in their path. They may stand as if in a stupor with head almost touching the ground or pressing against a wall and, when disturbed, over react and appear startled. A sudden loud noise may cause them to fall and go into a fit. Gradually a paralysis develops and eventually recumbency. Recumbent animals frequently lie on one side and make cycling movements with their legs. In fatal cases death occurs 7-10 days after the onset of clinical signs.

PROGNOSIS

Once nervous signs are present the prognosis is hopeless.

TREATMENT

No form of treatment is effective.

CONTROL

1. Vaccination. A single injection in sheep stimulates a high level of immunity which gives protection for at least 2 years. Lambs born to ewes immunised in the last month of pregnancy acquire passive immunity via colostrum which protects for 2-3 months. Sheep can be vaccinated at any time of year but if lamb protection is required vaccination should be carried out in late pregnancy. The vaccine may also be used in cattle but here the initial course is two injections at an interval of 1-6 months with annual boosters.

2. Tick control

LISTERIOSIS

A disease of sheep caused by the bacterium Listeria monocytogenes. Infection can give rise to three syndromes in sheep i.e. meningo-encephalitis, seen mainly in adult sheep, septicaemia in lambs and abortion.

INCIDENCE

First described in 1931 in New Zealand as "circling disease", now worldwide and recorded in many hosts. Up until 20 years ago listeriosis only occurred sporadically in sheep but since that time the incidence of the disease, especially the meningoencephalitic form, has increased dramatically. This increase was very closely related to the introduction of the practice of silage feeding to sheep. There is a disproportionately high incidence of the disease in Scotland although the increase in the disease has been seen throughout Great Britain. There is a marked seasonality of the disease with the peak incidence in the spring.

CLINICAL SIGNS

Meningoencephalitic form: Dull, fevered, unwilling to graze. Head tilt, rotation and circling, unilateral facial paralysis with drooping ear, eyelid, nostril and lip, drooling saliva, poor/slow mastication. Occasionally there is muco-purulent nasal discharge and roaring respiration. Incoordination progresses to recumbency and death. Clinical course 3-4 days.

Septicsemic form: Young lambs found dead. Rarely seen inappetent with fever for 24 hours prior to death. Occasionally seen in adults as a sequel to retained listerial abortion.

Abortion form: Late gestation due to placental infection. Heavy brown vaginal discharge.

EPIDEMIOLOGY

Listeria monocytogenes survives in soil, food and faeces for many months and a high number of symptomless carriers may excrete the bacterium in their milk or faeces. The pathogenesis is not completely understood but different portals of entry may give rise to different syndromes. Experimentally, disease can be produced by infection through many routes, the oral route being considered very important. The meningo-encephaltic form which is the most common, can be reproduced through buccal cavity abrasion. Usually only one form of the disease is present at each outbreak. There is a very strong correlation with silage feeding, particularly the meningo-encepha]itic form. The bacterium can persist in poor silage especially if the pH >5. It can survive aerobically at the edge of the clamp or in a punctured bag and in one survey the bacterium was isolated from 22% of big bales analysed. Listeria monocytogenes will increase if the silage is spread before feeding or, if there is a high soil content in the silage. If silage is fed on the ground instead of out of troughs it will increase the amount of soil ingested. Soil intake can also be increased as a result of feeding root crops such as turnips. The seasonal peak incidence during Jan-April is due to silage feeding at this time. The abortion/lamb septicaemia forms will also obviously be seen at this time. The higher than normal incidence of the disease in Scotland and the North of England is probably a reflection of the poorer quality of silage made in these areas as a result of the unfavourable climatic conditions. Other factors such as late pregnancy, intercurrent disease and immunosuppression will probably influence susceptibility. Another factor which may influence the higher incidence of the meningo-encephalitic form in adults is the shedding of teeth and co-existing periodontal disease allowing the organism to penetrate the oral mucosa. The incubation period for the meningoencephalitic form of the disease is between 14 and 32 days. In a study of natural outbreaks the median time from introduction of silage feeding to the index case was 44 days. The incubation period for the septicaemic form is shorter, around 2-3 days following oral ingestion and the abortion form tends to occur in late gestation, 5-10 days following ingestion.

DIAGNOSIS

Diagnosis of the septicaemic form relies on the isolation of the bacterium from the visceral organs while the abortion form is diagnosed on isolation of the organism from the foetus. Diagnosis of the meningo-encephalitic form can be made on clinical signs and by the elimination of other causes of CNS disease in sheep

TREATMENT

The organism is sensitive to a wide range of antibiotics including penicillin and tetracycline. Treatment of septicaemic cases and for endometritis following abortion is rewarding, however once encephalitis has developed therapy can be disappointing. High doses of tetracycline s for the meningo-encephalitic form seems to give the best results. Prophylactic antibiotics during an outbreak of listeriosis seem of little benefit and it is more useful to detect and treat cases early.

CONTROL

Avoid soil contamination when making and storing silage and use additives to keep silage pH <5. Do not feed mouldy areas of silage, feed silage from troughs not from the ground and empty uneaten silage from troughs after 24 hours. If the septicaemic form is a problem, improve hygiene at lambing and provide clean lambing pens. Isolate abortion cases.

BORDER DISEASE

Border disease is an infectious viral disease of sheep in which the main signs are early foetal death, and muscle tremors and coat defects in lambs born alive (‘Hairy Shaker* lambs).

CLINICAL SIGNS

The virus is pathogenic for the foetus between 16 and 80 days of pregnancy and embryonal and early foetal death are important components of the disease accounting for 30% of losses due to Border Disease. Abortion associated with this foetal death may or may not occur. It may simply surface as an increased number of barren ewes (up to 5% of flock-barren is acceptable). There is usually no overt disease in the ewes. Live-born lambs are smaller have a stocky appearance, shorter legs and frequently a "domed" skull.

The birthcoat usually has a rather hairy appearance rather than wool. The abnormal fibres are thick and long. Sometimes this occurs as a complete "halo" over the whole body, but may only be found behind the head and in the shoulder region. A number of lambs show rhythmic contraction of skeletal muscles giving rise to a range of signs from tremors of the back end and tails to complete body tremors which may be so severe as to prevent the lambs being able to stand. Affected lambs tend to have poor teat seeking reflex.

Most of the neurological signs may regress with time but many lambs remain weak and grow slowly. Sudden death of affected lambs frequently occurs.

Diagnosis is based on the clinical signs, history of abortion and low fertility in the flock and the post mortem findings. Serological tests are possible revealing antibody titres to the virus in blood samples.

EPIDEMIOLOGY

Experimentally the disease can be transmitted by a variety of routes e.g. oral, conjunctival, tracheal, intramuscular or intravenous. The ram is unlikely to be involved in transmission of the disease. Frequently the disease first appears in a flock after the introduction of recently purchased ewes. In new outbreaks all ages of ewes may be affected. After the first year the incidence is highest in the gimmers. Affected ewes are normally resistant in the following years, but infected animals remain persistent excretors for up to 4 years.

PREGNANCY TOXAEMIA (Twin Lamb Disease/Ovine Ketosis.)

INCIDENCE

Pregnancy toxaemia is a serious metabolic disorder occuring in late pregnancy. Ewes that are overfat or carrying two or more lambs are particularly prone; clinical disease may affect up to 20% of a flock and recovery rates, despite therapy, are poor. Subclinical disease is more widespread and may account for poor foetal growth, reduced lamb viability, maternal fitness, mothering ability and poor colostrum quality.

AETIOLOGY

The energy requirements of foetal growth, mammary development and colostrum production place a tremendous strain on maternal energy metabolism. Eighty-five percent of foetal growth occurs in the last 60 days of gestation, increasing the daily energy requirements of the ewe by 175% per foetus. Failure of the diet to provide adequate energy or of the ewe to utilise this energy results in a negative energy balance and the development of pregnancy toxaemia. Factors that may account for this failure include reduced food availability e.g. snow cover, inadequate concentrate feeding and the use of poor quality or unpalatable concentrates. Voluntary food intake also becomes depressed toward term, especially in ewes that are overfat or carrying multiple foetuses. Unrestricted feeding of silage or turnips may limit overall dry matter intake during this period and reduce the contribution of concentrates to the energy intake. Dental disease, lameness and intercurrent disease may also contribute in individual animal. Stress from inclement weather, changes in management, transport and even pregnancy itself appears to play an independent role in the pathogenesis of pregnancy toxaemia..

CLINICAL SIGNS

Initially vague and non-specific: dull, weak, lethargic and inappetent ewes separate from flock.

Progression over 2-3 days: ewes appear blind with aimless wandering, incoordination, head tilt/pressing and chewing; fine muscle tremors around head and neck become apparent which may progress to convulsions.

Terminally there is extreme depression, recumbency and diarrhoea regurgitation.

Death occurs 2-16 days after onset of clinical signs i.e. the progression of the disease is relatively slow when compared with hypomagnesaemia and hypocalcaemia.

DIAGNOSIS

Diagnosis should be based on the history of the case with respect to expected time of lambing, nutrition and previous management. Blood samples should be taken prior to treatment where necessary.

TREATMENT

Recovery is dependent upon early detection and rational therapy. This should be based upon

1. Correcting the hypoglycaemia by administration of 100-200m1 40% Dextrose or l60ml concentrated Liquid Lectade orally.

2. Providing glucogenic intermediates such as oral glycerol or propylene glycol; good quality hay or cut grass should be provided.

3. Reducing the glucose drain by inducing abortion using dexamethasone, or performing a caesarian section.

PROGNOSIS

The prognosis for individual cases should be based on the time to lambing, the duration of clinical disease and the responses to therapy. The recovery rate with treatment is often less than 40%.

CONTROL

Ewes should be maintained on an adequate and increasing plane of nutrition.

Concentrate feeding should start at 250g/ ewe/day at 6 weeks before lambing progressing to 1 kg/ewe/day at parturition to satisfy the required daily energy intake. Good quality roughage in the form of hay or best quality silage should be freely available. Turnip and silage feeding should be restricted in late pregnancy. Ewe management should be tailored to identify animals that are overfat or underweight, and animals bearing multiple lambs. Nutritional intakes are difficult to assess at grass and so frequent handling and condition scoring should be practised to monitor ewe condition. Ewes should be in condition score 3-3.5 at tupping to allow the loss of body condition during pregnancy. Animals that are thin, condition score less than 2, at mating will have inadequate body stores to draw upon and should be separated out for supplementary feeding during early pregnancy. Animals that are overfat, condition score above 4, should be under-fed during the first third of pregnancy by restricting access to grass/concentrates but not during the mid and last thirds when they should be maintained on a rising plane of nutrition.

Ewes should be batched according to lambing dates (ram harnesses) and number of foetuses (ultrasonographic pregnancy diagnosis) and fed appropriately. In emergency situations high glucose mineral licks may be used.

HYPOCALCAEMIA (Milk Fever/ Lambing Sickness)

A disease of the ewe occurring late in pregnancy or during the first few days of lactation and essentially similar to milk fever in cattle. It may also occur later in lactation, particularly in ewes with twin lambs and when the flock is subjected to stress.

AETIOLOGY

The condition is attributable to a reduction in calcium in the body fluids and the severity of the clinical syndrome parallels the degree of hypocalcaemia.

INCIDENCE

Hypocalcaemia is seen more frequently in the older ewe and commonly occurs following stress, e.g. change of feed, change of weather, transportation etc. It has been described in ewes brought off bill or upland pasture and moved on to lowground grazing. Because of this association with stress it is common to observe a number of animals affected at any one time.

CLINICAL SIGNS

In the early stages of the disease the affected animal has a staggering gait and appears weak on its legs; frequently the animal trembles, this feature being most marked in the shoulder muscles. The animal becomes progressively more restless, may breath rapidly and eventually assumes sternal recumbency. Death may take place rapidly and certainly within 24 hours of onset.

TREATMENT

Administration of calcium by injection produces a rapid response and will confirm the diagnosis. The average ewe will require l00ml of a 25 per cent solution of calcium borogluconate administered intravenously or subcutaneously.

CONTROL

Due to the association of stress with the onset of clinical hypocalcaemia it is unwise to subject the ewe at lambing time to any sudden change of environment or diet. Adequate but not excessive amounts of calcium should be present in the diet of ewes in late pregnancy but this should not be a problem if adequate hay or silage is being fed.

HYPOMAGNESAEMIA (Grass Staggers)

A condition resulting in sudden death in both the hill and lowland ewe and similar to hypomagnesaemia of cattle.

AETIOLOGY

The demands of lactation in combination with low pasture levels of magnesium may result in a reduction in the serum magnesium levels.

INCIDENCE

A number of sheep may have an accompanying hypocalcaemia

CLINICAL SIGNS

TREATMENT

CONTROL

Magnesium licks are also useful but suffer from the disadvantage that many sheep either like or dislike them and so uniform uptake by the flock cannot be assumed.

MASTITIS

Mastitis is a sporadic disease of sheep which presents as two main clinical forms, each occurring at a different time of the year.

Acute Severe Mastitis

Many organisms have been isolated including Staphylococcus aureus, Pasteurella haemolytica, Streptococcus zooepidemicus and Actinomyces pyogenes, but over 80% of acute mastitis cases are caused by either S. aureus and/or P.haemolytica.

CLINICAL SIGNS

Most frequently seen following lambing during the first few weeks of lactation. The earliest clinical sign is often apparent hindleg lameness/stiffness as the ewe tries to protect the painful udder and/or an obviously hungry lamb. The ewe is extremely dull and fevered and the udder is grossly distended, with the affected quarter(s) hot, red and painful initially but becoming cold and dark purple over 1-2 days. The secretion is initially reduced in amount, thin, colourless and may contain floccules of pus. Eventually the secretion may become yellow or blood stained, but will still remain reduced in amount. Latterly the temperature will become sub-normal. The course of the disease can be as short as 24 hours. Flock morbidity is usually 1-2% but mortality is often 50%, with the surviving ewes often sloughing the affected quarter and taking months to heal.

EPIDEMIOLOGY

Incidence usually less than 2% in any one flock. Various theories on factors that influence susceptibility include; vigorous sucking by lambs (there is an increased incidence in ewes with twins), the presence of Orf lesions on the teats (leading to secondary infection with bacteria and reduced sucking of quarter), soiling of the udder (seen in ewes where too much wool has been removed from around udder), overzealous/unhygienic checking for colostrum at lambing

TREATMENT

Prompt use of effective parenteral antibiotics e.g. penicillin. Intra-mammary therapy will also be of some benefit. Non-steroidal anti-inflammatory drugs (NSAIDS) such as flunixin could be of use in the early acute stage of the disease. Intravenous fluids will be of benefit and could be justified in a valuable animal. General nursing of the ewe is important as is supplementary feeding of her lambs.

Chronic Mild Mastitis

Usually not identified until the ewes are being checked prior to turning out the tups, in the Autumn. On palpation of the udder, irregular lumps are detected especially at the teat base with distortion of the quarter. Caused by bacterial infection traditionally thought to occur at weaning time, although there is now some evidence that infection may occur around one month post-lambing. Streptococcal bacteria are commonly the cause of this type of mastitis. Treatment is rarely attempted with chronic mastitis and it is, as a result, a common cause of culling of ewes. The control of the diet and water restriction at weaning is thought to be of some benefit in reducing the incidence in a problem flock. If it is a major cause of culling (can be up to 10% on some farms) the use of half a dry cow tube per quarter at weaning is very effective.

CONTAGIOUS PUSTULAR DERMATITIS (Orf)

A virus disease predominantly affecting young sheep and goats and characterised by the initial development of papules and pustules followed by a proliferative lesion which becomes covered with thick crusts or scabs, primarily on the lips and muzzle.

The course of the naturally occurring disease is from 1 to 8 weeks depending on the severity of the lesions. Areas of scab formation become dry and drop off and the affected areas return to normal except in severe cases where scabs remain.

CLINICAL SIGNS

The disease is of widespread distribution throughout Britain and is seen predominantly during the spring and summer months. Although any age of sheep may become affected, off is most commonly seen in lambs up to 6 months of age, the majority of cases being observed during the months of July, August and September.

In the initial stages of the disease in the lamb, the sites most frequently affected are the external aspects of the lips, particularly the commissures, and the area around the muzzle. The first lesions observed are of a proliferative nature covered by thick, tenacious scabs which, on removal, expose a raised, red ulcerated area. The lesions may spread to involve a large part of the lip area, muzzle and nostrils. The tongue and mouth mucosae commonly have smaller lesions. Healing may take place beneath the scabs or, where secondary bacterial infection is a problem, the ulcerated area may proliferate into verrucose masses and bleed readily if subjected to trauma. If these lesions are present on the lips of lambs, the animals may have difficulty in sucking or prehension and this may result in growth restriction.

Although in the majority of cases lesions are confined to the mouth, in a proportion of cases lesions appear in a number of sites, including the vulva, coronary band, undersurface of the tail, inner surface of the thigh, axilla, periorbital area and on the coronary band. Lambs with lesions on the coronary band are usually lame. Frequently when sucking lambs are affected, lesions develop on the teats and udder of the ewe and these may be very severe due to secondary infections. A further sequel to udder lesions in the ewe is the development of mastitis.

EPIDEMIOLOGY

The disease is spread by contact with infected animals and once it appears within a susceptible flock it spreads rapidly. It tends to recur on the same farm year after year and probably results from the carrying over of infection in dried scabs or on inanimate objects. A wide range of mammals can become infected and infection can produce a very painful lesion in man.

The incubation period depends on the amount of virus introduced and ranges from less than 24 hours to 10 days.

TREATMENT

Once an outbreak is under way there is little that can be done to control the spread of the disease. It is unrealistic to expect to control the outbreak by separating affected and non-affected animals as some animals with early lesions will undoubtedly be missed. Again it is uneconomic to carry out widespread treatment as the majority of lesions will regress on their own. Where extensive secondary infection is present systemic antibiotics may be useful.

CONTROL

Two live vaccines are available for use on problem farms only. There is little point in introducing and disseminating the virus on farms where it is not already present.

The vaccine, according to the manufacturers, should be administered some 3-4 weeks before the disease is likely to appear in lambs, but in pregnant ewes - 8 weeks before lambing (not later than 6 weeks). All sheep should be vaccinated as the vaccine is applied to a scarified area on the inside of the thigh at which site a mild lesion develops which may be responsible for infecting unvaccinated animals. Although the vaccine does not give complete protection, if the disease does occur it assumes a mild form. Antibodies do not appear to pass to the lambs via colostrum

WATERY MOUTH

Watery mouth is usually found in lambs less than one week old in which there is intestinal stasis. Shaking of the lambs may reveal splashing or gurgling sounds. Salivation is marked causing drooling from the mouth and soiling underneath the chin. Affected lambs quickly become very dull, stop sucking and die rapidly if untreated.

At post mortem examination there is distension of the intestines with clear fluid. Pure growths of E.coli can be isolated from most internal organs, spleen, heart blood, indicating that a terminal septicaemia has occurred.

Antibiotics are normally given, both orally and by injection in an attempt to control infection and flunixin is also useful. Improved neonatal management ensuring early ingestion of colostrum will be extremely beneficial not only as a source of immunoglobulins, thus preventing the septicaemia, but also because of its laxative properties. Increased hygiene in the lambing areas should help to prevent this condition.

HYPOTHERMIA

Hypothermia, which causes at least 40% of all neonatal losses, is defined as occurring when a lambs temperature falls below the normal neonatal range of 38.8 to 40 C. Hypothermia is caused by either excessive heat loss or insufficient heat production, i.e. starvation.

Lambs are born with fat reserves sufficient for the first 5 hours of life and hypothermia below this age is generally due to adverse environmental conditions. Hypothermia after the first 5 hrs of life can be due to hypoglycaemia due to starvation and will occur even in relatively comfortable environmental conditions.

CLINICAL SIGNS

Clinical signs vary from a relatively normal looking lamb in the early stages developing into a weak lamb that is tucked up and reluctant to stand. Eventually the lamb will collapse and fall into a coma prior to death. Hypothermia may develop secondarily to other clinical conditions such as neonatal diarrhoea and in these cases other clinical features may predominate and obscure the diagnosis of hypothermia. It is essential to have a thermometer capable of measuring very low body temperatures to gauge the severity of the hypothermia.

TREATMENT

Treatment consists of drying and warming the lamb and supplementing the food supply. If lambs are hypoglycaemic simply warming the lambs will fail to alleviate the condition. In severe cases the intraperitoneal infusion of 20% glucose solution at a rate of l0ml per kg will rapidly reverse any hypoglycaemia.

CONTROL

Control of the condition requires good management of the pregnant ewe to ensure an adequate supply of colostrum to neonatal lambs. Twins and triplets should be supplemented as necessary. Environmental conditions should be improved to allow shelter to lambing ewes. Close shepherding at lambing time will allow early detection and treatment of the condition.

LAMB DYSENTERY

AETIOLOGY

Clostridium perfringens Type B

INCIDENCE

A disease of lambs under one week of age although occasionally animals in their second or even third week of life may be affected. Lamb dysentery can be a serious problem particularly in the border areas of Scotland and England but also in other parts of Southern Scotland, Northern England and North Wales. The condition is associated with permanent lambing paddocks and its incidence varies from year to year and farm to farm. One constant fact is that once the disease appears in any given year it tends to increase as the lambing season progresses. The mortality rate amongst infected lambs is high. It is now most commonly seen where vaccination has not been carried out or where colostrum was not taken from vaccinated ewes.

CLINICAL SIGNS

In most cases an outbreak of lamb dysentery commences with the sudden death of one or more lambs. Such lambs may have been ill for 24 hours or so when they may have been seen to be dull and not sucking.

More commonly, affected lambs are dull, lethargic, they stop sucking and show evidence of abdominal pain. These animals will stand with back arched and are unwilling to move. When they do walk they do so with a straddling gait. They frequently lie down and appear restless when this manoeuvre is accomplished. Within 24 hours of the onset of clinical signs a diarrhoea develops. The diarrhoea is profuse, usually brown in colour, may contain some blood and its passage is frequently accompanied by painful straining. Such animals become rapidly dehydrated, eventually lapse into a coma and death may occur within 24 hours of the onset of the diarrhoea. In 2-3 week old lambs, where the diarrhoea is often less severe, these animals may survive for 2-3 days.

EPIDEMIOLOGY

Infection occurs by ingestion of C.perfringens present on the ewe*s teats, udder, fleece and in the soil.

TREATMENT

Once the disease is apparent in individual lambs treatment will have little effect, it is essential however, once the diagnosis has been made, to use lamb dysentery antiserum is all newly born lambs. Control of the disease is best achieved by vaccinating the ewes with multivalent clostridial vaccines in subsequent years.

COPPER DEFICIENCY (Swayback)

Although copper deficiency can result in clinical disease in mature sheep in certain parts of the world, in Britain it is essentially a condition of the newborn or sucking lamb.

AETIOLOGY

In Britain copper deficiency is probably always a conditioned deficiency as it occurs in areas where the copper content of the herbage is accepted as adequate. Elevation of molybdenum and sulphur levels are believed to impair absorption of copper. Other factors may be present in "swayback* areas which result in reduced copper utilisation by the grazing animal.

INCIDENCE

Copper deficiency in sheep occurs throughout the world in both temperate and tropical areas. In the United Kingdom it is most commonly observed in areas where the soil type is of peat, limestone or clay. The incidence of the disease in Britain is variable from year to year and is generally high if there is mild weather during the winter months.

The relative susceptibility appears to vary with the species and age of the animal concerned. In sheep, defective keratinisation of the wool is the first manifestation of copper deficiency in some environments but in other cases ataxia may appear without specific impairment of wool quality. The latter is the situation which exists in Britain and is seen in lambs whose dams have received inadequate copper in mid-pregnancy.

CLINICAL SIGNS

Swayback is a disease of unweaned lambs characterised by hindlimb inco-ordination.

Two types of swayback occur in Britain; a common form in which the animal is affected at birth and a less common, delayed form, in which clinical signs do not appear until the animal is several weeks old.

The predominant clinical sign is swaying of the hindquarters as the affected animal walks and this results in a stiff staggering gait. Such animals are bright, alert, able to suck and when lying down frequently appear normal.

A proportion of lambs are so ataxic at birth that they soon die whilst others appear normal and the condition develops gradually until walking is impossible. In mild cases ataxia may only become apparent when the lamb is excited or driven.

In multiple births it is common for all lambs to be affected but not necessarily to the same degree.

TREATMENT

Because the lesions are irreversible treatment is of no value and severely affected lambs should be destroyed. Lambs suffering from a mild form of the disease may be fattened satisfactorily.

CONTROL

The pregnant ewe should receive a copper supplement during the last three months of gestation and it is important to remember the sheep’s low tolerance of copper. Blood copper levels should be measured to assess status prior to prophylaxis with copper due to toxicity risks in sheep. Therefore, the supply of copper is best controlled and the shortage remedied in as specific a manner as possible, either by the use of copper in an injectable form or the use of copper oxide needles. The injections are given on one occasion between the 10th and 16th week of pregnancy.

Mineral licks containing 0.25 to 0.5 per cent copper sulphate are available but these do not guarantee that the correct amount is ingested.

Top-dressing of pasture is unlikely to be of value as in many areas there is no definite evidence that copper is lacking in the soil.

ILL-THRIFT IN HILL LAMBS

A condition of ill-thrift due to copper deficiency has been described in young Scottish Blackface lambs suckling ewes on improved bill pasture. The condition in the lambs is characterised by poor weight gains and poor fleeces which are stringy, sparse and grey in colour. Hypocupraemic lambs have also been found to be more susceptible to bone fractures than normal controls although histological examination revealed that the bones of both groups were osteoporotic. It was considered that the copper deficiency was induced by the high levels of molybdenum and sulphur in the reseeded pasture. The ewes, although also hypocupraemic, were clinically normal, with normal fertility, conception rates and body condition.

COPPER PREPARATIONS

In sheep a number of injectable copper salts and ruminal boluses are available for the treatment and control of conditions related to copper deficiency. Care should be taken in the use of these products since some have higher toxicity risks than others.

BORDER DISEASE

Border disease is an infectious viral disease of sheep in which the main signs are early foetal death, and muscle tremors and coat defects in lambs born alive (‘Hairy Shaker* lambs).

CLINICAL SIGNS

Most of the neurological signs may regress with time but many lambs remain weak and grow slowly. Sudden death of affected lambs frequently occurs.

EPIDEMIOLOGY

BACTERIAL POLYARTHRITIS (JOINT-ILL)

A suppurative arthritis which occurs in lambs during the first month of life.

AETIOLOGY

Various organisms have been isolated from cases of joint ill.

These organisms include Corynebacterium ovis (not in UK), Escherichia coil, several Streptococci and Staphylococci and Pasteurella haemolytica. The organisms gain entry through the lamb*s navel or by various wounds such as those resulting from castration or docking or through tick bites. After an initial bacteraemia the organisms become established in the joints.

CLINICAL SIGNS

During the septicaemic phase of the disease the affected animal is dull, fevered and unwilling to suck. This is followed by sudden lameness or stiffness as a result of involvement of one or more joints. Affected joints become hot, swollen and painful and the infection may spread to the associated tendon sheaths. The shoulder, elbow and stifle joints are most frequently affected. Many of these animals die within a few days of the onset of the condition but a large proportion will survive and, in these animals, affected joints become distended with pus which may discharge through the skin. Damage to the joint is such that many animals remain permanently crippled with resulting inability to gain weight satisfactorily.

In certain cases the joints in the spine become involved and this, as with spinal abscess, may give rise to posterior paralysis.

EPIDEMIOLOGY

The disease results from unhygienic conditions for example often where the entire lambing takes place within the same building or where temporary outdoor lambing pens remain on the same area for the whole of the lambing season. In these circumstances, once infection builds up more lambs will become affected as the season progresses. Where older lambs are affected the disease may result from the use of dirty instruments or the confinement of lambs in dirty pens following castration and docking.

TREATMENT

This meets with a variable amount of success and in general the earlier the treatment can be carried out the better the chances of recovery. Long-standing cases are best destroyed. If treatment is carried out high levels of antibiotic must be maintained for several days: the drugs of choice are penicillin or penicillin/streptomycin or possibly the potentiated sulphonamides especially if E.coli is suspected.

CONTROL

The disease can be prevented by adopting hygiene measures. The lambing paddock should be moved to clean ground at least once during the lambing season and, as an added precaution, the navel of newborn lambs should be disinfected with tincture of iodine which will also allow the umbilical cord to dry earlier. At castration and docking, clean instruments should be used and lambs should be turned out on to clean grass immediately after the operation. As in the control of all neonatal lamb disease, adequate colostrum intake is extremely important.

ENTROPION

Entropion is a relatively common problem in neonatal lambs especially in white faced breeds of sheep. The lower eyelid inverts and causes irritation of the cornea with secondary ulceration in severe cases. Early signs are easily detected as there is profuse tear production in affected eyes which will overflow to cause staining of the lambs face. There is a hereditary component to the development of the condition.

There are a variety of treatments available. Mild cases respond to repeated manual eversion of the eyelid. In more severe cases the eyelid needs to be stitched down to prevent inversion.

One of the most simple and effective methods is the injection of a subconjunctival bleb of a thick solution to keep the offending eye-lashes away from the cornea. The most suitable solution is a long acting antibiotic as this will treat any secondary infection in the eye. As the bleb of solution disperses the mild fibrosis caused at the injection site appears to evert the eyelid.

Control can be achieved by rejection of rams which produce affected lambs.

NEONATAL DIARRHOEA

Most of the microbiological agents associated with neonatal diarrhoea of calves have been isolated from diarrhoeic lamb faeces; enterotoxigenic E.coli (ETEC), rotavirus, and cryptosporidium. Salmonella spp. are occasionally responsible for outbreaks of disease among lambs, frequently in association with abortion and mortality in the ewe flock. It should be remembered that losses due to non-infectious causes, such as exposure and starvation, are probably of greater importance than disease caused by infectious agents. However, the intensive management of the ewe flock at lambing and the continued use of lambing pens can quickly lead to a build-up of infectious agents and a high challenge to the later born lambs.

Apart from the syndrome caused by ETEC and Salmonella spp. it is impossible to differentiate the syndromes produced by other agents clinically.

ESCHERICHIA COLI

Affected lambs are very young, they have a profuse watery diarrhoea and dehydration occurs quickly. The mortality rate among affected lambs can be very high.

Septicaemia due to E.coli occurs in lambs but the prevalence is unknown. Affected lambs will usually be less than five days old. Dullness, anorexia, and fever in the early stages and an illness of very short duration are the likely clinical signs. Affected lambs usually have very poor colostrum intake at birth. E.coll septicaemia may be associated with ‘watery mouth*.

ROTAVIRUS

In lambs, rotavirus has been isolated from 25% of diarrhoeic lambs in one survey carried out in Scotland, and antibodies to rotavirus are widespread in the sheep population.

CRYPTOSPORIDIUM

The prevalence of cryptosporidial infection in lambs is not known, but severe outbreaks of diarrhoea due to Cryptosporidium have been described with mortality rates ranging from 10% to 33%. This condition is most likely to affect lambs during their second and third weeks of life. Clinically they are dull, diarrhoeic and non fevered, with a greatly reduced appetite. When death occurs it is likely to happen after diarrhoea of two to three days duration. Some lambs will be diarrhoeic for up to seven days before recovering. Frequently there may be a fairly prolonged convalescent period in which the lambs fail to thrive.

SALMONELLA

Salmonellosis occurs only sporadically in sheep. S.typhimurium, and S.dublin are the serotypes most commonly associated with disease in young lambs, although exotic serotypes, such as S. montevideo, are frequently responsible for heavy losses in some geographically localised areas. Clinically, lambs are dull, depressed and anorexic, with diarrhoea which may or may not contain blood. Affected lambs are often fevered, and death is usually caused by an accompanying septicaemia.

TREATMENT

The use of antibiotics and chemotherapeutic agents, such as the sulphonamides and potentiated sulphonamides, is generally accepted in the treatment of diarrhoea in lambs as it is in calves. There is no specific treatment available for cryptosporidiosis or rotavirus infections. Affected lambs should be encouraged to suckle or given oral electrolyte therapy to maintain their fluid intake. Nursing is probably the major factor in the survival of affected lambs.

CONTROL

Control measures are aimed at reducing the challenge to which lambs are exposed and increasing their non-specific and specific immunity. Any lambs which become diarrhoeic should be isolated with their mothers, and, if housed, the pen in which they were kept should be thoroughly cleansed and disinfected with an approved product. If lambing occurs outside, new lambing pens, especially those built with straw bales, should be erected at least twice during a four week lambing period. More permanent pens should have the bedding removed and replaced every three to four days. Moving the ewes to a fresh, uncontaminated field half way through the lambing period should be carried out.

Where lambing occurs indoors, the young lambs should be turned outside as soon as possible after the ewe-lamb bond has been established. Frequent cleaning and renewal of bedding in individual lambing pens should be undertaken.

Lambs should receive adequate colostrum as soon as possible after birth; this will increase the non-specific immunity of the lamb. The ewes should therefore be on an adequate plane of nutrition to ensure that they have a sufficient volume of colostrum to supply the needs of the lambs, especially in the case of twins or triplets.

To increase the specific immunity in the colostrum, an E.coli vaccine containing F5 (K99) antigen is now available for immunising ewes, but it should be remembered that this will only be efficacious against diarrhoea caused by Enterotoxicgenic E.coli, which may not be very prevalent in the lamb population. Vaccines are available for some serotypes of Salmonellae.

PULPY KIDNEY DISEASE

AETIOLOGY

C.perfringens Type D, proliferates in the intestinal contents, given favourable conditions, producing toxins which are highly lethal.

INCIDENCE

This is an acute fatal disease of widespread distribution and is seen in sheep of all ages but it is most frequently observed in lambs, particularly singles, between the ages of three and 12 weeks although it also occurs intermittently in weaned lambs and adult sheep. The disease is nearly always associated with the thriving animal and affects those sheep which are in the best and most forward condition. The period of greatest danger is always the few days after the sheep are introduced to an improved diet, such as lush grazing or increased levels of concentrate.

CLINICAL SIGNS

These are rarely observed as affected animals characteristically die suddenly.

Occasionally an animal may show evidence of abdominal pain and possibly convulsions, lapsing terminally into a coma.. These animals have a rapid weak pulse, respiratory distress and frequently lie in sternal recumbency making paddling movements with their legs.

DIAGNOSIS

This is based on the post-mortem findings together with the presence of glucose in the urine. Toxin can be detected in the gut contents even when lesions are not apparent.

TREATMENT

Treatment of clinically affected animals is pointless.

CONTROL

1 During an outbreak of disease. Once initial deaths have occurred within a group of sheep it is unlikely that any more will occur. The most common procedure, however, is to move the remaining animals on to bare pasture or restrict their diet and gradually reintroduce them to the diet on which the deaths occurred. In the fully susceptible flock a vaccination programme should be initiated.

2. Vaccination. Today most farms in Britain vaccinate against enterotoxaemia but it is important to ensure that a proper regime is being employed. A vaccination programme can be commenced at any point in the year. Multivalent clostridial vaccines are available and, as these are economical to use and each component is as efficient when mixed with related antigens as it is on its own, its efficiency is high. Because of the marginal price difference between the multi-component and single component clostridial vaccines the latter are largely obsolete. There are several multivalent clostridial vaccines available which contain antigens against C.perfringens (B,C,& D), C.septicum, C.chauveoi,. C.oedematiens (B & D) and C. tetani

(a) Initial protection of all classes of sheep. The initial course consists of administering two doses of vaccine subcutaneously at an interval of not less than 6 weeks. Subsequently breeding stock should receive two doses annually, one to ewes and gimmers as close to lambing as possible to ensure that the maximum level of protection can be transferred to their lambs by way of colostrum and a second about two weeks before flushing which will ensure adequate protection against the increased plane of nutrition and also against Black Disease which is a problem on certain farms in wet years.

(b) Protection of lambs. Provided the lambs receive adequate amounts of antibody from the colostrum of a vaccinated dam they will be protected for the first 12 to 16 weeks of life. Pulpy Kidney antiserum also available. As a result the farmer who is able to put his lambs off the farm by 3 months of age will not require to protect them further. However, all lambs kept on the farm over this age, whether as replacement breeding stock or as late fatteners, must be vaccinated. In order that these lambs are able to produce adequate protective titres of their own by 12 weeks of age they ought to receive a first dose of vaccine at 5-6 weeks of age followed by the second dose at 11-12 weeks.

It must always be borne in mind that under this vaccination system lambs born at the start of the lambing season may receive more passive immunity from the dam than those born towards the end of the season, hence the necessity of commencing lamb vaccination at a relatively early stage

PASTEURELLOSIS

AETIOLOGY

PNEUMONIC PASTEURELLOSIS

CLINICAL SIGNS

EPIDEMIOLOGY

SYSTEMIC PASTEURELLOSIS

CLINICAL SIGNS

EPIDEMIOLOGY

SEPTICAEMIC PASTEURELLOSIS

TREATMENT AND CONTROL

Multicomponent vaccines containing P.haemolytica and P.multocida in combination with clostridial antigens are also available

ERYSIPELOTHRIX ARTHRITIS (Stiff Lamb Disease)

Although this disease can occur in both acute and chronic forms, the latter is the more common and results in a chronic arthritis of lambs usually 3-4 months of age.

AETIOLOGY

Erysipelothrix rhusiopathiae is the causative organism.

CLINICAL SIGNS

During the acute phase of the disease affected lambs may be dull, unwilling to suck and show a degree of stiffness. This syndrome is infrequently observed however and is followed by the more common chronic form of the disease. In the chronic disease there is lameness in one or more legs with no obvious swelling of the joints. On closer examination of the joints there is heat and pain but no detectable swelling although the leg below affected joints may be swollen in early cases. Initially only a handful of lambs are affected but gradually more become affected until perhaps 25 per cent of the lamb flock are showing signs of stiffness. Deaths from this condition are rare but the lameness can persist for a long time resulting in marked unthriftiness.

EPIDEMIOLOGY

This form of arthritis usually follows docking and castration when the organism which is present in the soil of particular farms or even particular fields, gains entry through the wounds. It is also seen after dipping and has been called "post-dipping lameness".

DIAGNOSIS

Based on clinical signs confirmed by the presence of antibody to E.rhusiopathiae, and isolation of the organism from the joints of untreated chronically affected lambs at slaughter.

TREATMENT

The organism is sensitive to penicillin and success rates are encouraging provided treatment is carried out at an early stage. Once the lameness is well-established the majority of affected animals remain permanently unthrifty despite treatment.

CONTROL

The adoption of hygienic conditions at docking and castration will go a long way to eliminating the disease. Lambs should always be turned out to grass immediately the operation is completed and kept there till the wounds have healed. They should not be allowed to stand in a pen where infection may be present.

TETANUS

AETIOLOGY

Caused by a bacterium called Clostridium tetani.

INCIDENCE

All ages of sheep can be affected, but tetanus is primarily a disease of lambs and occurs 10 to 21 days after castration and docking, particularly where the rubber ring method is used. Ewes may be affected shortly after lambing. Several animals are usually affected, and the disease tends to occur on the same farm from year to year.

CLINICAL SIGNS

The clinical signs of tetanus in sheep are variable and may be mild or severe. In mild cases the affected animal appears stiff and walks with a stilted gait for a number of days after which time complete recovery may ensue without the necessity of treatment. Many shepherds may be unaware of the existence of the condition and may think the stiffness is a result of pain associated with castration.

In more severe cases the stiffness is more obvious and widespread; it is accompanied by extension of the head and neck and the musculature is firm to touch. The legs are usually extended and the tail is cocked. On pinching the skin the affected animal is hyperaesthetic. It is unable to lower its head, has difficulty in eating, and attempts to open the animal*s jaw are unsuccessful. Eventually the animal falls over in lateral recumbency and lies with legs outstretched and head thrown back.

DIAGNOSIS

This is mainly based on clinical signs

TREATMENT

Penicillin by injection. Severe cases will not recover and should be euthanased

CONTROL

Practice good hygiene at castration, lambing etc, the use of tetanus antitoxin may be useful and vaccination with multivalent Clostridial vaccines which often include a tetanus component.

NUTRITIONAL MYOPATHY - SELENIUM/VITAMIN E DEFICIENCY (White Muscle Disease)

Before 1957, selenium was mainly recognised for its toxic effects in those parts of the world where the selenium content of the soil is high. Sheep are more susceptible than cattle to the toxic effects. The selenium concentration of feedstuffs should not exceed 5 ppm dry matter.

SELENIUM DEFICIENCY

In the late 1950*s it was recognised that selenium was also a metabolically essential element and that selenium, Vitamin E and sulphur containing amino acids, act together to protect tissues from oxidative damage.

CLINICAL SIGNS

Lambs can be affected at any time between birth and six months of age. Lambs (or calves) born to dams severely deficient in selenium/Vitamin E may be born dead or die within a few days of birth. Death in this form of the disease is due to sudden heart failure. If seen alive there is a sudden onset dullness with respiratory distress and a raised heart rate. A frothy bloodstained nasal discharge may accompany the respiratory distress. The temperature is usually normal and the calf is mentally normal with no indication of blindness. Death occurs within 6-12 hours of the onset of signs. Classically, this syndrome has occurred when the dams are fed a diet of turnips and straw during pregnancy.

In slightly older lambs (and calves), affected animals walk with a stiff, straddling gait. If the animal is lying down when approached it has difficulty in rising, and if able to rise (some animals may remain in sternal recumbency), it may tremble. Because of the muscle weakness a peculiar posture is adopted when standing; the legs are spread out and the head is held low; the shoulder blades are prominent with the chest sagging between them. Affected animals remain bright and will suckle if held to the teats or if hand fed. The temperature is normal but occasionally may be slightly raised. If there is involvement of the intercostal muscles and diaphragm some cases may have breathing difficulty. There may be an increased heart rate.

Hoggs, fed mainly on turnips for a long period may also become affected, with recumbency or a reluctance to move, or they may collapse when driven. This may be precipitated by severe weather.

A syndrome of ‘ill-thrifts’ has been described in Australia and New Zealand. Affected animals have poor growth rates and respond to selenium therapy but not to Vitamin E treatment. Also in New Zealand a syndrome of infertility in ewes has also been ascribed to selenium deficiency, which responds to selenium supplementation but not Vitamin E therapy.

A syndrome called Paralytic Myoglobinuria has been described, mainly in young adult cattle, which have been fed on moist stored grain over the winter. Within a week of turning out in the spring, affected animals show stiffness, recumbency, blood in urine, and breathing difficulty. Severely affected animals die within a few days. This is considered to be mainly a Vitamin E deficiency.

Dietary requirements. The suggested level of intake is 0.05 mg Se/kg dry matter, but many flocks and herds are ingesting food which contains much lower levels.

TREATMENT

This is best achieved by a single s/c or i/m injection of selenium at 0.2 mg Se/kg. Combined vitamin E and selenium injections are available and animals given this preparation should not be slaughtered for human consumption for 8 weeks and milk from treated animals should not be used for human consumption. With treatment cases usually recover in 3-5 days.

LOUPING-ILL

An acute encephalomyelitis producing paresis and cerebellar ataxia. This is predominantly a disease of sheep although, less frequently, cattle, pigs, horses and man may become infected.

AETIOLOGY

A tick borne virus.

INCIDENCE

EPIDEMIOLOGY

CLINICAL SIGNS

PROGNOSIS

Once nervous signs are present the prognosis is hopeless.

TREATMENT

No form of treatment is effective.

CONTROL

1. Vaccination. A single injection in sheep stimulates a high level of immunity which gives protection for at least 2 years. Lambs born to ewes immunised in the last month of pregnancy acquire passive immunity via colostrum which protects for 2-3 months. Sheep can be vaccinated at any time of year but if lamb protection is required vaccination should be carried out in late pregnancy. The vaccine may also be used in cattle but here the initial course is two injections at an interval of 1-6 months with annual boosters.

2. Tick control

COCCIDIOSIS

In grazing sheep coccidiosis appears to be an increasing problem and occurs typically as diarrhoea in young lambs under intensive conditions.

AETIOLOGY

Of the eleven Eimeria spp which may infect sheep only two are highly pathogenic and lead to disease. Infection is by ingestion of sporulated oocysts during grazing. This is followed by various multiplication stages within intestinal cells and after 15 days oocysts are passed in the faeces to contaminate the environment and continue the cycle.

CLINICAL SIGNS

Heavy infections usually occur in lambs of 4-8 weeks of age and may lead to loss of weight, severe diarrhoea with straining and blood stained faeces. Untreated infections can result in dehydration and death.

EPIDEMIOLOGY

Lambs may be infected by overwintered oocysts or from oocysts produced by low levels of infection in ewes. Intensive husbandry with unhygienic conditions and the feeding of concentrates in stationary troughs, lead to heavy pasture contamination which often results in disease.

DIAGNOSIS

This is based on the history, the age of animals affected and the clinical signs. High faecal oocyst counts may be detected but because many Eimeria species are non-pathogenic, normal lambs may have equally high faecal oocyst counts. Also some lambs may die of acute disease before oocysts are shed in the faeces making diagnosis based on faecal oocyst counts difficult. Culture and identification of sporulated oocysts of the pathogenic species is a specialist task. If possible a severely affected animal should be post mortemed. Clinical response to therapy may be helpful in confirmation of diagnosis. There is some evidence that concurrent Nematodirus battus infection increases the severity of coccidiosis and the possibility of dual infections should be considered in outbreaks of diarrhoea in young lambs.

TREATMENT AND CONTROL

Treatment of acutely affected animals may be best instituted by the use of anticoccidials such as sulphadimidine and sulphanethoxypyridazine, or by the oral drenching of individuals with sulphonamides; amprolium and ethopabate would also be effective but are not licensed for sheep.

The other drug currently available for the treatment of animals which are still eating, and for the prophylaxis of coccidiosis in lambs, is decoquinate which is administered in feed. Decoquinate is also recommended for administration in ewe feed to aid in the control of disease in their offspring.

Control is difficult because of the persistence of oocysts on pasture but rotation of lambing paddocks and movement of concentrate feeding troughs twice weekly may be of value. Incorporation of anti-coccidial drugs with concentrate feed may help reduce the level of infection in intensive lowland sheep flocks.

NEMATODIROSIS

Nematodirosis is an acute and often fatal enteritis which occurs commonly in Britain, as well as in some other Northern European countries. It has clearly defined age and seasonal incidences, occurring in lambs between early May and late June, although some later outbreaks have recently been reported.

AETIOLOGY

The small intestinal nematode, Nematodirus battus, whose life cycle is similar to that of the other trichostrongyes, except in one important respect, which is that the egg does not hatch until the larvae is present.

CLINICAL SIGNS

Outbreaks of disease occur in lowland flocks from late May until mid-July, the time of onset varying with the locality and the year, and are confined to that season*s lamb crop. The onset of an outbreak is sudden and dramatic with a number of lambs being affected simultaneously. Affected animals have a severe diarrhoea which soils the hindquarters and tail and is followed by the passing of variable amounts of mucus. Lambs appear to have abdominal pain, are reluctant to move and, when they do so, walk with a stilted gait and tucked-up abdomen. The majority show a marked thirst and are constantly looking for water; in many, the eyes become sunken and develop a mucopurulent discharge.

Affected lambs appear prone to secondary bacterial and coccidial infections.

In fatal cases the condition lasts for some 2-3 days and death ensues as a result of severe dehydration. Animals which survive can take months to recover and often remain stunted for the rest of their lives.

EPIDEMIOLOGY

The epidemiology of the disease is based on three factors:

1. The egg has a high resistance to freezing and desiccation, and can survive on pasture for up to two years.

2. Hatching, with release of the larvae, requires special stimuli in the form of a period of chill followed by a mean day/night temperature of more than l0 degrees C.

3. Adult sheep are resistant although they may carry very small burdens of N. battus.

Because of the great survival capacity of the eggs, infection can be continued from lamb-crop to lamb-crop, without the necessity for any intervening multiplication passage in the host animal. Accumulation of infection on pasture therefore, may take place over a period of years, and not in a single season as in Parastic Gastroenteritis (P.G.E.). Disease never occurs on first year grass, is rare on second year grass, but by the third year of lamb grazing the contamination may be at pathogenic level. Although primarily a disease of lowland flocks nematodirosis has been recorded from flocks on re-seeded hill grazing.

As a result of the critical hatching requirements there is an almost simultaneous appearance or flush of large numbers of larvae on the pasture. Though the flush happens every year, disease does not always follow even on heavily contaminated grazing; if it is too early the lambs will not be grazing sufficiently to take in large numbers of larvae, and if it is late they will be able to resist the larval challenge as age resistance appears at ten to twelve weeks of age, and is high by six months.

DIAGNOSIS

This is based on the clinical signs of weight loss, diarrhoea and anorexia, the seasonality of outbreaks, which are limited to the period late May to mid-July, a grazing history of pasture being used in previous years for lambs, and if a post-mortem is available.

It is important to remember that clinical signs often result from damage by larvae and faecal egg counts are not necessarily high at this stage of the disease.

TREATMENT

Several drugs are highly effective, including levamisole, morantel, the avermectins/ milbemycins or one of the modem benzimidazoles.

The response to these drugs is usually rapid, and where diarrhoea persists coccidiosis should be considered as a complicating factor; response to appropriate sulphonamide therapy in these cases is good.

CONTROL

Due to the specific hatching requirements of the larvae nematodirosis can only occur on fields grazed by young sheep or cattle (calves are also susceptible to N. battus infection) in the previous year. Successful control can be obtained by avoiding grazing successive lamb crops on the same pasture. Where alternative grazing is not available, anthelmintic prophylaxis should be applied.

The drugs mentioned above may all be used in prophylaxis, the timing of treatments being based on the knowledge that the peak months for the flush of larvae on the pasture are May and June. Ideally, 2-3 doses should be given at approximately three-weekly intervals over this period though many farmers are prepared to wait for the appearance of clinical signs before administering drugs.

The Ministry of Agriculture in U.K. has developed a forecasting system based on soil temperatures in early spring. When severe disease is predicted farmers are alerted through the Farming Press or Advisory Groups.

PULPY KIDNEY DISEASE

AETIOLOGY

C.perfringens Type D, proliferates in the intestinal contents, given favourable conditions, producing toxins which are highly lethal.

INCIDENCE

CLINICAL SIGNS

These are rarely observed as affected animals characteristically die suddenly.

DIAGNOSIS

This is based on the post-mortem findings together with the presence of glucose in the urine. Toxin can be detected in the gut contents even when lesions are not apparent.

TREATMENT

Treatment of clinically affected animals is pointless.

CONTROL

(a) Initial protection of all classes of sheep. The initial course consists of administering two doses of vaccine subcutaneously at an interval of not less than 6 weeks. Subsequently breeding stock should receive two doses annually, one to ewes and gimmers as close to lambing as possible to ensure that the maximum level of protection can be transferred to their lambs by way of colostrum and a second about two weeks before flushing which will ensure adequate protection against the increased plane of nutrition and also against Black Disease which is a problem on certain farms in wet years.

(b) Protection of lambs. Provided the lambs receive adequate amounts of antibody from the colostrum of a vaccinated dam they will be protected for the first 12 to 16 weeks of life. Pulpy Kidney antiserum also available. As a result the farmer who is able to put his lambs off the farm by 3 months of age will not require to protect them further. However, all lambs kept on the farm over this age, whether as replacement breeding stock or as late fatteners, must be vaccinated. In order that these lambs are able to produce adequate protective titres of their own by 12 weeks of age they ought to receive a first dose of vaccine at 5-6 weeks of age followed by the second dose at 11-12 weeks.

PASTEURELLOSIS

AETIOLOGY

PNEUMONIC PASTEURELLOSIS

CLINICAL SIGNS

EPIDEMIOLOGY

SYSTEMIC PASTEURELLOSIS

CLINICAL SIGNS

EPIDEMIOLOGY

SEPTICAEMIC PASTEURELLOSIS

TREATMENT AND CONTROL

Multicomponent vaccines containing P.haemolytica and P.multocida in combination with clostridial antigens are also available

ERYSIPELOTHRIX ARTHRITIS (Stiff Lamb Disease)

Although this disease can occur in both acute and chronic forms, the latter is the more common and results in a chronic arthritis of lambs usually 3-4 months of age.

AETIOLOGY

Erysipelothrix rhusiopathiae is the causative organism.

CLINICAL SIGNS

EPIDEMIOLOGY

DIAGNOSIS

Based on clinical signs confirmed by the presence of antibody to E.rhusiopathiae, and isolation of the organism from the joints of untreated chronically affected lambs at slaughter.

TREATMENT

CONTROL

CONTAGIOUS PUSTULAR DERMATITIS (Orf)

CLINICAL SIGNS

EPIDEMIOLOGY

The incubation period depends on the amount of virus introduced and ranges from less than 24 hours to 10 days.

TREATMENT

CONTROL

Two live vaccines are available for use on problem farms only. There is little point in introducing and disseminating the virus on farms where it is not already present.

CEREBROCORTICAL NECROSIS (CCN)

A degenerative disease of the central nervous system of cattle and sheep characterised clinically by varying degrees of ataxia and, in the case of sheep, usually terminating in death.

At the present time the cause of cerebrocortical necrosis has not been established although it is thought that deficiency of thiamine is involved.

CLINICAL SIGNS

The disease is seen in lambs from 6 weeks of age to old ewes but the vast majority of cases are seen in lambs between 8 to 16 weeks old. Initially affected animals wander aimlessly and develop an ataxia which increases in degree to produce staggering and swaying. Animals at this stage have difficulty in standing and require to prop themselves up with feet spread apart. The bead is characteristically drawn back in a series of convulsive extensor spasms. Eventually the affected animal falls over to lie with legs extended and if disturbed in this position lapses into galloping movements which end in spasms. Once recumbent the outcome is usually fatal.

EPIDEMIOLOGY

The disease does not appear to be associated with any particular environmental or nutritional pattern. Although the majority of affected animals receive supplementary feeding this is varied in type and no specific diet can be blamed.

TREATMENT

Treatment of sheep suffering from CCN has been disappointing. Although many bovine cases show a marked, although not necessarily complete, response to thiamine therapy affected sheep show varied responses to treatment.

LOUPING-ILL

An acute encephalomyelitis producing paresis and cerebellar ataxia. This is predominantly a disease of sheep although, less frequently, cattle, pigs, horses and man may become infected.

AETIOLOGY

A tick borne virus.

INCIDENCE

EPIDEMIOLOGY

CLINICAL SIGNS

PROGNOSIS

Once nervous signs are present the prognosis is hopeless.

TREATMENT

No form of treatment is effective.

CONTROL

1. Vaccination. A single injection in sheep stimulates a high level of immunity which gives protection for at least 2 years. Lambs born to ewes immunised in the last month of pregnancy acquire passive immunity via colostrum which protects for 2-3 months. Sheep can be vaccinated at any time of year but if lamb protection is required vaccination should be carried out in late pregnancy. The vaccine may also be used in cattle but here the initial course is two injections at an interval of 1-6 months with annual boosters.

2. Tick control

NEMATODIROSIS

AETIOLOGY

CLINICAL SIGNS

Affected lambs appear prone to secondary bacterial and coccidial infections.

EPIDEMIOLOGY

The epidemiology of the disease is based on three factors:

1. The egg has a high resistance to freezing and desiccation, and can survive on pasture for up to two years.

2. Hatching, with release of the larvae, requires special stimuli in the form of a period of chill followed by a mean day/night temperature of more than l0 degrees C.

3. Adult sheep are resistant although they may carry very small burdens of N. battus.

DIAGNOSIS

It is important to remember that clinical signs often result from damage by larvae and faecal egg counts are not necessarily high at this stage of the disease.

TREATMENT

Several drugs are highly effective, including levamisole, morantel, the avermectins/ milbemycins or one of the modem benzimidazoles.

CONTROL

PARASITIC GASTRO-ENTERITIS

Parasitic gastro-enteritis (PGE) in Britain is a disease primarily of lambs, characterised by weight loss and diarrhoea..

AETIOLOGY

PATHOLOGY

INTESTINAL PARASITES

The clinical consequences of these changes are:

1. Diarrhoea. This is the cardinal clinical sign of enteritis. It can be defined as a consequence of malabsorption of water and electrolytes.

2. Malnutrition. Due to malabsorption and leading to weight loss, poor quality wool and impaired milk production.

3. Excessive loss of protein through the intestine.

CLINICAL SIGNS

EPIDEMIOLOGY

During spring and early summer larvae are available on the pasture from a number of sources.

1. Overwintered larvae

2. Hatching and development of overwintered eggs

3. Hatching and development of eggs from the spring or peri-parturient rise in nematode faecal egg output which occurs in ewes.

DIAGNOSIS

Whenever possible a post-mortem examination should be made to establish a definite diagnosis.

Where P.G.E. is suspected many farmers or practising veterinary surgeons will treat the flock with a wormer and if a good response is obtained this is used as an index of diagnosis.

Collection of faecal samples for examination for nematode eggs is a useful aid to diagnosis

TREATMENT

Most drugs in sheep are administered orally by the use of modern automatic drenching guns.

CONTROL

Control is generally based on strategic use of wormers, often combined with specific grazing management.

ANTHELMINTIC PROPHYLAXIS

The most important source of infection for the lamb crop is the periparturient rise in the ewe faecal egg count; prophylaxis will only be efficient if this rise is kept to a minimum.

If ewes are brought indoors to lamb a treatment at the time of housing will remove existing worm burdens. Subsequent treatments would then depend on existing farm management practices.

COBALT DEFICIENCY (Pine)

A disease of ruminants characterised by poor appetite and weight loss.

AETIOLOGY

This condition is caused by a primary deficiency of cobalt in the diet.

INCIDENCE

Cobalt deficiency occurs in particular areas of many countries extending from tropical to temperate regions. The growing animal is more severely affected than the adult and sheep appear to be slightly more susceptible to the effects of cobalt deficiency than cattle.

PATHOLOGY

Dietary cobalt is utilised by the rumen micro-organisms in the production of vitamin B 12 and the whole function of cobalt can be accounted for in terms of this vitamin. Only a small proportion of dietary cobalt is converted into true vitamin B12 capable of utilisation by ruminants, the rest being incorporated into B 12 like compounds with no known physiological activity.

The basic defect in cobalt deficient ruminants is an inability to metabolise propionic acid which results in loss of appetite and eventual death from starvation.

The blood cobalt or vitamin B 12 levels of the affected animal are a poor guide as to the status of the animal but low liver cobalt and vitamin B12 levels can frequently be detected.

Less directly cobalt deficiency may be suspected on estimating the cobalt content of pasture or diet. If the cobalt is less than 0.1 ppm dry matter cobalt deficiency is likely.

CLINICAL SIGNS

In sheep the clinical signs are relatively non-specific and are most commonly observed in lambs. The most conspicuous feature is a loss of appetite. Lambs on a cobalt deficient diet cease to grow and eventually show a frank loss of weight. Such animals become progressively dull and listless and in advanced cases pallor of visible mucous membranes may be observed.

Cobalt deficiency affects all the lambs in the flock and hence there is a uniform pattern throughout the flock.

DIAGNOSIS

Blood vitamin Bl2 estimations can be performed but a more sensitive indicator of cobalt deficiency in sheep is the concentration of formiminoglutamic acid (FIGLU) in urine. It is usually necessary to sample several animals for representative data. In the absence of these estimations response to therapy is the only method of confirmation.

TREATMENT

Affected animals can be given cobalt and/or vitamin B12.

The administration of cobalt bullets is less costly than repeated vitamin B12 injections and entails less handling. A reasonable regime for the treatment would be a single injection of vitamin B12 and simultaneous administration of a cobalt bullet. A single drench of a cobalt salt solution is unsatisfactory.

CONTROL

Because of the continuous need for cobalt in the diet, attempts must be made to provide this element on a permanent basis.

Cobalt can be applied to pasture as a dressing every 3 or 4 years or so depending on the climatic and environmental factors which allow its persistence. The amount required is in the region of 16 to 20 oz. cobalt sulphate per acre applied before grass growth.

Cobalt bullets provide a continuous supply of supplementary cobalt and persist in the rumen for months or even years. Occasionally bullets may be regurgitated but this is seldom a problem.

COPPER DEFICIENCY (Swayback)

Although copper deficiency can result in clinical disease in mature sheep in certain parts of the world, in Britain it is essentially a condition of the newborn or sucking lamb.

AETIOLOGY

INCIDENCE

CLINICAL SIGNS

Swayback is a disease of unweaned lambs characterised by hindlimb inco-ordination.

In multiple births it is common for all lambs to be affected but not necessarily to the same degree.

TREATMENT

Because the lesions are irreversible treatment is of no value and severely affected lambs should be destroyed. Lambs suffering from a mild form of the disease may be fattened satisfactorily.

CONTROL

Mineral licks containing 0.25 to 0.5 per cent copper sulphate are available but these do not guarantee that the correct amount is ingested.

Top-dressing of pasture is unlikely to be of value as in many areas there is no definite evidence that copper is lacking in the soil.

ILL-THRIFT IN HILL LAMBS

COPPER PREPARATIONS

COCCIDIOSIS

In grazing sheep coccidiosis appears to be an increasing problem and occurs typically as diarrhoea in young lambs under intensive conditions.

AETIOLOGY

CLINICAL SIGNS

EPIDEMIOLOGY

DIAGNOSIS

TREATMENT AND CONTROL

NEMATODIROSIS

AETIOLOGY

CLINICAL SIGNS

Affected lambs appear prone to secondary bacterial and coccidial infections.

EPIDEMIOLOGY

The epidemiology of the disease is based on three factors:

1. The egg has a high resistance to freezing and desiccation, and can survive on pasture for up to two years.

2. Hatching, with release of the larvae, requires special stimuli in the form of a period of chill followed by a mean day/night temperature of more than l0 degrees C.

3. Adult sheep are resistant although they may carry very small burdens of N. battus.

DIAGNOSIS

It is important to remember that clinical signs often result from damage by larvae and faecal egg counts are not necessarily high at this stage of the disease.

TREATMENT

Several drugs are highly effective, including levamisole, morantel, the avermectins/ milbemycins or one of the modem benzimidazoles.

CONTROL

UROLITHIASIS

Urolithiasis in sheep is associated with excess urinary mineral excretion and inadequate urinary volume.

INCIDENCE

Clinical disease occurs in males only, affecting housed rams and wethers, or intensively fed lambs on creep feed and high concentrate intake.

CLINICAL SIGNS

In sheep clinical signs result from urethral obstruction which is more common in castrates or wethers due to the relatively small urethral diameter. Affected animals show discomfort including straining, kicking at the abdomen, twitching of the tail and general restlessness. Drops of blood stained urine are produced and a precipitate of crystals can generally be found on the preputial hairs. After rupture of the distal urethra or bladder discomfort fades, depression continues and there is leakage of urine into the peripenile tissues or abdominal cavity (‘water belly").

TREATMENT

Treatment is generally through surgical exteriorisation of the urethra although in some cases smooth muscle relaxants have been successful.

CONTROL

The disease can frequently be prevented by feeding sodium chloride at 4 per cent of the concentrate mix or ammonium chloride at 10 g per day. A plentiful supply of clean water should be available at all times

ATYPICAL PNEUMONIA

This is a chronic non-supportive pneumonia seen predominantly in young sheep reared in intensive or semi-intensive systems. It is of widespread incidence throughout Great Britain.

AETIOLOGY

The cause of this form of sheep pneumonia is likely to be Mycoplasma ovipneumoniae and secondary bacterial infection particularly with Pasteurella haemolytica, but Clamydia have also been associated with this condition.

CLINICAL SIGNS

This is predominantly a pneumonia of housed sheep, particularly lambs and hoggs producing mild clinical signs which might readily be missed. The main clinical sign is coughing which is usually sporadic but will spread through the lamb flock. Individual animals may be fevered with a variable degree of breathlessness but they remain bright and their appetite is apparently unimpaired.

EPIDEMIOLOGY

This is a disease of intensification, particularly housing, and might be expected wherever sheep are kept in a confined environment. Under these circumstances rapid multiplication and spread of a microbiological agent such as a virus or mycoplasma can be expected to take place resulting in widespread clinical disease. In sheep, since a housed population tends to remain constant over a given period of time, most outbreaks will be self-limiting after all of the animals become immune from natural exposure. The situation may become more complicated if secondary infection e.g. with Pasteurella becomes established.

TREATMENT

Therapy with broad-spectrum antibiotics such as oxytetracycline may reduce the clinical signs but rarely eliminates the problem.

PASTEURELLOSIS

AETIOLOGY

PNEUMONIC PASTEURELLOSIS

CLINICAL SIGNS

EPIDEMIOLOGY

SYSTEMIC PASTEURELLOSIS

CLINICAL SIGNS

EPIDEMIOLOGY

SEPTICAEMIC PASTEURELLOSIS

TREATMENT AND CONTROL

Multicomponent vaccines containing P.haemolytica and P.multocida in combination with clostridial antigens are also available.

OVINE PARASITIC BRONCHITIS AND PNEUMONIA

A parasitic condition of young sheep characterised by coughing and weight loss.

AETIOLOGY

The lungworm Dictyocaulus filaria which is found in the trachea and bronchi.

LIFE-CYCLE

This is similar to that of the bovine lungworm Dictyocaulus viviparus and first stage larvae are passed in the faeces. Under suitable conditions of temperature and moisture, usually during summer, these larvae develop into infective larvae. When ingested the larvae pass to the lungs, patency being established some 4 weeks after infection.

CLINICAL SIGNS

The most noticeable clinical signs are coughing and an increased respiratory rate.

There may be some reduction in appetite with weight loss and frequently there is a discharge from the eyes and nose. In most cases the condition is non-pyrexic but in severe cases, where there is the complication of secondary infection, affected animals run a temperature and may have difficulty breathing.

EPIDEMIOLOGY

The disease is probably carried on from year to year by larvae overwintering on pasture and carrier sheep.

Outbreaks may occur at any time between June and November but are most commonly observed between August and October.

The disease occurs primarily in lambs during their first grazing season but it may also be seen in older sheep.

TREATMENT

Levamisole, an avermectin/milbemycin or a benzimidazole such as fenbendazole, oxfendazole or albendazole will control outbreaks of disease.

PULMONARY ADENOMATOSIS (Jaagsiekte)

Pulmonary adenomatosis is a chronic progressive disease of the lungs, which results in breathing difficulty and finally death. The lesion is essentially a tumour which is contagious and transmissible.

AETIOLOGY

Pulmonary adenomatosis can be transmitted by nasal discharge. The incubation period is usually 1-3 years but in experimentally infected lambs the incubation period may be only six to eight months. The tumour is caused by an oncovirus of the Retroviridae family. Virus particles found in the lung fluid can be used to transmit the disease.

CLINICAL SIGNS

Pulmonary adenomatosis is practically always seen in adult sheep of 3-4 years, although it has occasionally been observed in hoggs. The disease is a slowly developing condition. In the early stages there is occasional coughing accompanied by shallow, rapid respiration especially noticeable if affected animals have been driven. As the disease progresses the respiratory rate increases until breathing difficulty is present. At this stage fluid may be heard in the chest. Gradually the affected animal becomes emaciated and in most cases when the head is held low or the animal is held up by its hind legs a profuse, watery discharge pours from the nostrils. Clinically affected sheep die within 3 months after onset of the disease.

EPIDEMIOLOGY

The disease is spread by the respiratory route after the introduction of clinically normal but infected animals into a susceptible flock. Where sheep are kept for part of the year in close contact e.g. if housed, the disease may be expected to progress more rapidly through the flock as the spread is assisted by animals being within aerosol inhalation distance of each other for a considerable time. On the hill, as one would expect, the spread of the disease will not be so rapid. Thus pulmonary adenomatosis is a disease which one would expect to increase with intensification of sheep production methods.

No treatment is available, control is best achieved by culling affected animals as soon as they are detected.

MAEDI

This is a chronic, progressive, invariably fatal pneumonia of sheep which occurs in many parts of the world. Its presence in Britain was confirmed in 1979.

AETIOLOGY

The disease is caused by the visna virus which belongs to the sub-family lentiviruses. The disease has a prolonged incubation period, often of 3-4 years and animals become persistently infected.

The lungs are the primary site of infection although the virus spreads to many other organs.

CLINICAL SIGNS

In many flocks the infection is subclinical and is only detected by serological examination of the sheep. In some flocks however it can result in serious loss due primarily to chronic pneumonia although mastitis and arthritis may also occur. The neurological form, visna, is rarer.

As a result of the prolonged incubation period the disease is rarely seen in sheep less than two years of age.

Loss of condition and lethargy are frequently the first clinical signs noted in this insidious disease. The respiratory rate is raised and shallow, and may be as high as 80- 120/minute at rest. As the disease progresses the animal becomes very breathless even at rest. Occasionally affected animals may cough. A slight nasal discharge may be present.

In uncomplicated cases, the temperature is normal. There is a progressive loss of weight and affected animals succumb within 3 to 6 months of clinical signs becoming evident. Occasionally an acute pneumonia exacerbates the condition and hastens inevitable death. There may also be clinical signs related to arthritis or mastitis.

EPIDEMIOLOGY

The lungs and udder are the main source of virus. Transmission occurs through the colostrum or by the respiratory tract following direct contact between sheep. Infection may become more prevalent in sheep indoors because of respiratory spread between sheep. In infected flocks the prevalence increases with age from 20% in yearlings to 80% in animals older than 7 years but the vast majority of infections are asymtomatic.

DIAGNOSIS

Confirmation of suspected clinical cases can be undertaken by blood sampling. Post-mortem examination is also useful, particularly in advanced cases.

CONTROL

Control is either by slaughtering affected cases, or by the establishment of maedi free flocks by rearing lambs in isolation. Because transmission of the virus from dam to offspring occurs via the colostrum and/or milk, removing lambs immediately after birth and rearing in isolation will enable the establishment of a disease-free flock. This is obviously a laborious and expensive procedure and an alternative method, which may reduce the prevalence of infection in a flock, is to only keep replacements from young ewes which are reared separately from the main flock.

VISNA

Visna is a rare neurological disease in sheep.

AETIOLOGY

The neurological disease visna is caused by the visna virus which is the same lentivirus which causes maedi, the common pulmonary manifestation of the infection.

CLINICAL SIGNS

The disease is rarely observed in animals under 2 years of age. The onset is insidious, the affected sheep beginning to have progressive paralysis of the hind legs resulting in posterior ataxia. There is no fever. Eventually paralysis develops and the outcome is invariably fatal.

DIAGNOSIS

This depends on serological identification of the viral infection and the histopathological changes in the central nervous system.

FOOT ROT

AETIOLOGY

Foot rot is caused by an association between (Dichelobacter) Bacteroides nodosus and Fusobacterium necrophorum. The association is synergistic with each organism contributing to the pathogenic process while assisting the other to grow in the infected tissues. Some injury to the skin or horn and lowering of its resistance is necessary to provide a portal of entry, the intact healthy skin being resistant to infection. Maceration caused by continued wetness and injury or overgrown horn are the main factors in rendering sheep susceptible

INCIDENCE

This is primarily a disease of adult sheep but growing lambs can also be affected.

PATHOLOGY

Following invasion by the causal agents, the interdigital skin becomes inflamed and moist. This is followed by a breach in the skin-horn junction and damage to the underlying tissue. The separation of the horn is most marked initially at the bulbs of the heel but subsequently spreads to involve the sole and the walls of the hoof.

CLINICAL SIGNS

The earliest sign is a swelling and moistening of the skin of the interdigital cleft particularly in the region of the heel. This is soon followed by a break in the skin-horn junction and then a separation of the adjacent soft horn. At this stage the lesions are usually mild and there is little or no pus, but the sheep shows lameness and the feet feel warmer than usual. During the next 5 to 10 days the infection spreads, causing separation of the horn across the whole sole, and the sheep becomes very lame. The infection may then extend under the walls so that nearly all the hoof is separated from the soft tissues. Both digits on the one foot are almost invariably involved.

After infection has spread under the sole there may be a new growth of horn over the sole but this usually again becomes involved in the destructive process extending from the skin in the interdigital space, where the infection tends to persist for long periods. On feet which have been affected for several weeks or months the hoof becomes long and misshapen. Some cases develop deep abscesses.

In advanced cases there is extreme lameness, and if only one foot is affected it is usually carried. Two or more feet are frequently affected in the one animal, and in this case the animal lies down most of the time, moves with great difficulty, and becomes thin with inability to graze properly. When the two forefeet are affected the animal adopts a characteristic attitude of kneeling while grazing.

TREATMENT

The feet of the entire flock should be examined and all affected sheep separated. The feet of affected animals should be pared taking care to remove all horn which shows the slightest separation. Adequate and careful paring is essential and care should be taken to prevent bleeding particularly when granulation tissue is being exposed. Following paring each foot should be dipped in an antiseptic solution, or 10% formalin, or sprayed with an oxytetracycline spray. Zinc sulphate (10%) or zinc lauryl sulphate (improved penetration) are probably the best foot bath preparations. Animals must stand in this for 30 mins for eradication.

The unaffected portion of the flock should be passed through a footbath of 5% formalin or 10% zinc sulphate and moved after 1 hour*s rest on a concrete floor to grass which has been free of sheep for at least 14 days. The affected group will require further treatment and should be moved to another fresh pasture or, if not available, back to the original grazing; they should be passed through the above footbath on two or three occasions at no sooner than weekly intervals accompanied by gradual paring of regressing granulation tissue, until the feet are healed. Any animals which resist treatment should be culled. In severe cases treatment with penicillin may be necessary.

CONTROL

This can be achieved by segregating affected animals as described above and not putting them back to the main flock until all lesions have healed. Because of the high labour costs involved in farming it is generally not possible to pass sheep through foot baths regularly but the footbath containing 5% formalin or 10% zinc sulphate should be used whenever sheep have to be gathered and the flock should be watched closely for lameness, particularly during wet weather, when prophylactic measures can be carried out without delay. Newly purchased sheep should be examined for foot rot and routinely put through a footbath.

Vaccination is possible using inactivated strains of Dichelobacter (Bacteroides) nodosus. Two vaccines are currently available. Vaccination in conjunction with other control measures gives good results.

BLOWFLY MYIASIS (Strike)

A condition occurring in Britain between June and September affecting both hill and lowground sheep. The clipped adult and young lambs are generally not affected but as fleece length increases, the incidence of the disease increases, particularly when the weather is warm and wet.

Sheep are struck by flies which attack soiled areas of the fleece, particularly the body, breech, tail, and poll. The larvae which develop from the eggs deposited by the flies irritate and migrate into the skin releasing enzymes which cause further damage.

Affected sheep are restless and unwilling to graze, moving around with their heads held low. Attempts are made to bite or kick the affected area. The struck area has an offensive odour and the wool is moist and usually brown in colour. In the early case maggots (<10-14 mm long) may be seen in the wool and on the skin but as the affected area increases in size the wool falls out leaving an area of moist dermatitis.

The disease is common and the course can be rapid where successive strikes occur. The condition is most debilitating and may be complicated by a septicaemia which can be fatal.

The condition can be controlled by dipping or spraying all sheep in early or midsummer with an organo-phosphorous or pyrethroid compound.

Blowfly strike may also be prevented by the ‘pour-on* application of the insect growth regulator cyromazine. This is applied along the back and around the tail and crutch and will provide protection for 8-10 weeks. It has no therapeutic activity and cases already showing strike lesions should be treated with organo-phosphate or pyrethroid compounds.

DERMATOPHILOSIS/ MYCOTIC DERMATITIS (Lumpy Wool)

A condition which is ubiquitous in British sheep and caused by infection with the bacterium Dermatophilus congolensis. It occurs most commonly under warm, moist climatic conditions. All ages of sheep can be affected.

Lambs show lesions predominantly on the ears and face but in adult sheep lesions are more frequently observed on the wooled areas of the neck, back and sides. In rams the skin of the scrotum may be involved.

The disease is essentially an exudative dermatitis and in the early stages there is reddening and moistening of the skin with exudation of fluid. This is followed by drying of the exudate and the formation of light yellow coloured crusts which can be seen at the base of the wool when the fleece is parted. Successive attacks result in the formation of bands of crusts at varying levels in the wool. Affected animals are not usually itchy.

Dermatophilus infections result in the hair follicles becoming enlarged and the leather grain becomes spoiled on the outer surface.

Penicillin is the drug of choice in the treatment of dermatophilosis while control is based on the use of mycotic dips containing zinc or aluminium salts.

MANGE (Sheep Scab)

The most important mange of sheep in U.K. is caused by Psoroptes ovis and is commonly referred to as Sheep Scab.

Outbreaks of Sheep Scab occur during the winter months, generally from October to February, when the mange mite is active: during the summer months the mite remains quiescent in certain sites, particularly in the axilla, groin, around the eyes and inside the ears. This is the reason why outbreaks may cease in spring only to reappear the following winter.

Psoroptic mange affects the wooled areas of the sheep, in particular the shoulders and the sides of the body trunk.

The earliest signs of this form of mange are restlessness and scratching or rubbing of affected areas on posts, fences and gates. Initially the wool becomes lighter in colour, or rather the disarrangement reveals light areas, before it begins to fall out. The underlying skin is damaged by the piercing mouth parts of the mites leading to exudation of serum and crust formation. Because of the intense itch and subsequent gnawing and scratching of affected areas, secondary infection is common with extension of lesions. Skin scrapings, best taken from the edge of affected areas, reveal the presence of mites although it is important to remember that if sheep have been recently dipped or treated mites may be extremely difficult to find. Diagnosis is based on clinical signs and recognition of the mite. Treatment and control is by the use of dips containing organophosphorus compounds such as diazinon or propetamphos, or the pyrethroid flumethrin. If dipping is not practicable then dectomax or 2 injections of ivermectin 7 days apart are effective in eliminating mites.

The other mange mite which can affect sheep in Britain is Chorioptes ovis. The lesions of chorioptic mange, or foot scab, are mainly seen above the coronary band and below the accessory digits, in the interdigital space and may also occur in the orbital regions, brisket and frequently the scrotum. Again there is hair loss accompanied by crust formation and itch. Chorioptic mange responds well to treatment with most acaricides.

PHOTOSENSITISATION (Facial eczema; Yellowes; Head Grit)

Photosensitisation is caused by the exposure to sunlight of sheep which have a photodynamic substance present in their tissues. Photodynamic substances absorb energy from light, and the cells in the exposed tissues are severely damaged as a result. As with cattle, there are two major types of photosensitisation; primary, in which the photodynamic substance is absorbed intact from the alimentary tract; secondary, in which the photosensitisation is secondary to a disease of the liver.

Some plants, such as St. John*s Wort (Hypericum perforatum), buckwheat (Polygonum fagopyrum) and wild carrot (Cynopterus spp), contain photodynamic substances, which cause primary photosensatisation. Some chemical compounds are also photoactive. Secondary photosensitisation follows the pathological effects of the mycotoxin produced by the fungus Pithomyces chartarum or ragwort poisoning. An inherited congenital photosensitivity as a result of an inherited defect has been described in Corriedale and Southdown lambs.

PREVALENCE

This is unknown but can be quite high in lambs in certain flocks, often upland or bill flocks. It is seen mainly in late May, June and early July.

CLINICAL SIGNS

As with cattle, it is the non-pigmented thin-skinned areas of the body which are affected. Thus, lesions are mainly seen on the head and ears. Normally, a thick and/or pigmented fleece will protect the body but lesions can occur along the dorsal midline parting of wool on the back.

Affected animals are quite distressed and inappetent. Initially, there is severe swelling and oedema of the white parts of the head and ears, the latter being very pendulous due to their increase in weight. The eyelids, face and lips also become swollen. There appears to be severe irritation and affected lambs frequently rub themselves on objects in an attempt to alleviate the irritation with further self-inflicted trauma. Serous exudation through the skin occurs and this dries to form yellow crusts or scabs. This acute inflammation is followed by death and sloughing of the affected skin, often leaving the ears dried, twisted and withered. Regeneration of the skin may take several weeks.

Affected lambs usually regain their appetite and recover to a certain extent but do not gain weight as quickly as non-affected lambs.

In Norway photosensitisation in lambs has been attributed to Bog asphodel which is quite common on many Scottish hills: photosensitisation also occurs in sheep on rape. In New Zealand facial eczema is a serious problem in sheep grazing rye grass pastures contaminated by the fungus Pithomyces chartarum.

SHEEP TICKS

The main species of significance in sheep and cattle is Ixodes ricinus.

ECOLOGY & LIFE HISTORY

A constant high relative humidity such as is provided by rank matted vegetation is necessary for the survival of Ixodes. As this type of vegetation dies yearly it creates a dead matted structure which protects ticks from winter frost and summer desiccation by conserving high relative humidity values. Such a bioclimate is only found in the rough hill and moorland grazing of the Borders, West Scotland, Wales, Ireland and S.W. England but recently there have also been reports of heavy tick populations in East Anglia.. Particularly suitable are areas of heather, tall grasses and fern.

The life cycle lasts 3 years and Ixodes is a 3-host tick. 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 eggs will feed for about 6 days in the following year; then they drop to the ground and moult to the nymph stage. In the third year this stage feeds, again for about 6 days, drops off and becomes adult. All stages occur in the host simultaneously.

There is a distinct seasonal activity of the tick; this corresponds with the period when ‘questing* ticks can be found on vegetation tips and infection of sheep and cattle occurs.

Two peak periods of activity occur, namely:

1. March - June - ‘spring feeders*

2. August - November - ‘autumn feeders*

Ticks will only feed once per year and therefore there appear to be two distinct populations of ticks, one active in spring and the other in autumn. In the Borders only spring feeders occur but in other tick areas, e.g. West Scotland, S.W. England, Wales and Ireland, autumn feeders also occur.

Although the life-cycle takes 3 years to complete, the larvae and nymphs only feed for approximately 6 days and the adult for 14 days, i.e. a total of 26 days. Ixodes is thus a temporary parasite.

CONTROL

There are three possible approaches to the control of tick populations.

1. Pasture improvement. Ixodes survives particularly well in the bioclimate provided by rank matted vegetation such as abounds in bill or moorland grazing; burning of such areas destroys this protection. Re-seeding will obviously also reduce the area suitable for ticks. Unfortunately such improvement schemes are often limited by financial and topographical difficulties.

2. Resting pasture from sheep and cattle. This has little application because of the wide range of tick hosts.

3. The commonest method is by the application of acaricides to sheep or cattle at the time the ticks are feeding. These are often applied by dipping the animals in a tank or running them through a spray race. Dipping of cattle and sheep for tick control is common in the tropics but only sheep are dipped in Britain.

There are a range of effective acaricidal dips which include organo-phosphorus compounds such as diazinon and propetamphos, the amidine amitraz and the pyrethroid flumethrin. Pryethroid spot-on or pour-on preparations such as cypermethrjn and deltamethrin can also be used.

In contrast to summer dipping for the control of blowflies, the merits of spring tick dipping are often questioned. The protagonists claim that in addition to good reduction of tick numbers, keds and lice are also eliminated. The antagonists point out that control is not absolute, the cost is yet another reduction in already narrow profit margins and that mis-mothering of young lambs frequently occurs after dipping: the use of spot on pyrethroids, however, probably reduces the coat and the danger of mis-mothering.

Perhaps the fairest evaluation is that while tick control measures reduce the tick populations on sheep, some ticks remain to transmit disease and outbreaks do occur in farms where such control measures are practised; these outbreaks are however of reduced severity.

INFECTIOUS KERATOCONJUNCTIVITIS

Infectious keratoconjunctivitis is a disease of sheep characterised by conjunctivitis and keratitis (corneal inflammation). It is highly contagious and usually spreads rapidly through the flock.

AETIOLOGY

Mycoplasma conjunctivae is the most common cause of this condition. Other agents such as Chlamydia and Branhamella ovis have been associated with the condition.

CLINICAL SIGNS

The disease starts as a simple conjunctivitis with the entire conjunctiva becoming inflamed, resulting in photophobia and excessive tear production. Spontaneous recovery may start from two to four days after the onset of clinical signs before opacity has spread far from the margins of the cornea. Usually opacity is only partial although in about 5% of cases the whole cornea becomes completely opaque and later vascularised and there is a purulent discharge from the eyes. Ulceration of the cornea occurs in some of these cases.

The severity of the disease varies greatly from one individual to another but both eyes are usually affected to more or less the same degree. Initially one eye is affected but the other eye becomes affected within a few days. In the majority of sheep the lesions are mild and there is no serious interference with vision, recovery commencing in about 3-4 days and being complete about a week later. Lesions may persist for as long as 6 weeks in severe cases which may be partly blind for several weeks but sheep*s eyes have a remarkable power of recovery and eyes showing a completely vascularised, ulcerated cornea usually heal leaving little or no blemish. Cases of permanent loss of sight are extremely rare

EPIDEMIOLOGY

The disease is spread indirectly by flies, long grass or dust which have been contaminated by the lachrymal secretions of infected sheep or directly by means of exhaled droplets or immediate contact. Thus the disease is more common in dry warm weather when large numbers of flies and dusty conditions predominate. However, it also occurs in winter when sheep are housed in close contact.

After clinical recovery most eyes continue to harbour organisms for a variable period. Some eyes become permanently free of infection as soon as 6-10 days after being infected but in about 50% of cases organisms are still present in one or both eyes 100 days after contracting the infection and in 3% of cases organisms have persisted for 250 days. The latter animals can provide a source of infection the following year. More than 50% of recovered animals remain resistant for periods in excess of a year.

TREATMENT

The majority of cases recover within 2 weeks without treatment but treatment certainly appears to reduce the number which develop an ulcerative keratitis. Sub-conjunctival injections of penicillin/streptomycin or the tetracyclines are particularly effective in controlling the disease producing a marked response within 48 hours. Cloxacillin ointment can also be used topically in mild cases.

COPPER POISONING

Of all the farm species, sheep are the most susceptible to copper poisoning and the condition can occur in both the acute and chronic form. The acute form, which is uncommon, results from the accidental ingestion of copper compounds, such as copper sulphate from a foot bath whilst the chronic form of the disease results from the feeding of copper in a concentrate mixture over a period of time.

Acute copper poisoning is due to the irritant action of copper on the alimentary tract. Thus the clinical signs are dullness, abdominal pain, salivation and diarrhoea containing mucus. The faeces are commonly dark green in colour.

The chronic form of copper poisoning is relatively common particularly in indoor sheep fed concentrates ad lib. Following concentrate feeding the time of appearance of the clinical disease will depend on the amount of copper present in the feed and the time period over which the feed is given. Sheep can retain large amounts of copper in the liver but eventually a point is reached when a large proportion of this stored copper is released into the bloodstream, causing a massive breakdown of the blood cells. Although this form of copper poisoning is referred to as chronic copper poisoning the clinical disease itself is presented as an acute syndrome.

At post-mortem the entire carcase is noticeably jaundiced. Copper estimation carried out on liver usually reveals a copper level in excess of 1,000 p.p.m. on a dry matter basis.

Affected animals and their companions should be put on to a low copper concentrate immediately. There is no effective treatment.

There are breed differences in susceptibility to copper toxicity; Suffolks, Texels and their crosses are much more susceptible than Blackfaces.

CEREBROCORTICAL NECROSIS (CCN)

A degenerative disease of the central nervous system of cattle and sheep characterised clinically by varying degrees of ataxia and, in the case of sheep, usually terminating in death.

At the present time the cause of cerebrocortical necrosis has not been established although it is thought that deficiency of thiamine is involved.

CLINICAL SIGNS

EPIDEMIOLOGY

TREATMENT

NUTRITIONAL MYOPATHY - SELENIUM/VITAMIN E DEFICIENCY

(White Muscle Disease)

SELENIUM DEFICIENCY

CLINICAL SIGNS

Hoggs, fed mainly on turnips for a long period may also become affected, with recumbency or a reluctance to move, or they may collapse when driven. This may be precipitated by severe weather.

Dietary requirements. The suggested level of intake is 0.05 mg Se/kg dry matter, but many flocks and herds are ingesting food which contains much lower levels.

TREATMENT

COPPER DEFICIENCY (Swayback)

Although copper deficiency can result in clinical disease in mature sheep in certain parts of the world, in Britain it is essentially a condition of the newborn or sucking lamb.

AETIOLOGY

INCIDENCE

CLINICAL SIGNS

Swayback is a disease of unweaned lambs characterised by hindlimb inco-ordination.

In multiple births it is common for all lambs to be affected but not necessarily to the same degree.

TREATMENT

Because the lesions are irreversible treatment is of no value and severely affected lambs should be destroyed. Lambs suffering from a mild form of the disease may be fattened satisfactorily.

CONTROL

Mineral licks containing 0.25 to 0.5 per cent copper sulphate are available but these do not guarantee that the correct amount is ingested.

Top-dressing of pasture is unlikely to be of value as in many areas there is no definite evidence that copper is lacking in the soil.

ILL-THRIFT IN HILL LAMBS

COPPER PREPARATIONS

COBALT DEFICIENCY (Pine)

A disease of ruminants characterised by poor appetite and weight loss.

AETIOLOGY

This condition is caused by a primary deficiency of cobalt in the diet.

INCIDENCE

PATHOLOGY

The basic defect in cobalt deficient ruminants is an inability to metabolise propionic acid which results in loss of appetite and eventual death from starvation.

The blood cobalt or vitamin B 12 levels of the affected animal are a poor guide as to the status of the animal but low liver cobalt and vitamin B12 levels can frequently be detected.

Less directly cobalt deficiency may be suspected on estimating the cobalt content of pasture or diet. If the cobalt is less than 0.1 ppm dry matter cobalt deficiency is likely.

CLINICAL SIGNS

Cobalt deficiency affects all the lambs in the flock and hence there is a uniform pattern throughout the flock.

DIAGNOSIS

TREATMENT

Affected animals can be given cobalt and/or vitamin B12.

CONTROL

Because of the continuous need for cobalt in the diet, attempts must be made to provide this element on a permanent basis.

Cobalt bullets provide a continuous supply of supplementary cobalt and persist in the rumen for months or even years. Occasionally bullets may be regurgitated but this is seldom a problem.

UROLITHIASIS

Urolithiasis in sheep is associated with excess urinary mineral excretion and inadequate urinary volume.

INCIDENCE

Clinical disease occurs in males only, affecting housed rams and wethers, or intensively fed lambs on creep feed and high concentrate intake.

CLINICAL SIGNS

TREATMENT

Treatment is generally through surgical exteriorisation of the urethra although in some cases smooth muscle relaxants have been successful.

CONTROL

COENUROSIS (Sturdy: Gid)

Usually this is a condition seen in the older lamb and adult sheep due to Coenurus cerebralis, the cystic stage of the dog tapeworm Taenia multiceps. Following ingestion of grass contaminated with eggs, embryos burrow their way through the intestinal wall and reach the brain via the bloodstream. Once in the brain a cyst develops taking several months to grow to a size which will result in the appearance of clinical signs.

The pattern of clinical disease which develops depends on the location of the cyst which exerts pressure on adjacent brain tissue. Most commonly cysts exert pressure on the cerebral hemi-spheres and this can result in inco-ordination, with the head held to one side and a tendency to circle in that direction; there may be blindness in the opposite eye. A jerky or very ataxic gait may be observed when the cerebellum is involved and where the cyst occupies a superficial position there may be some softening of the bones of the skull. Affected animals may survive for several weeks following the onset of clinical signs.

Sometimes acute coenurosis occurs in lambs when large numbers of embryos migrate simultaneously through brain tissue producing an acute encephalitis. Clinical signs of affected lambs include ataxia varying degrees of blindness, muscle tremors, nystagmus and hyperexcitability; occasionally lambs are found dead without prior signs. In many instances the metacestodes in the brain die or succumb to the host defence mechanisms and the lambs recover; in a few there is progression to the chronic stage.

Diagnosis of the acute disease is difficult and careful examination of the brain at postmortem is the only reliable method at present.

Although surgical treatment of coenurosis is frequently successful, the best method of control is prevention and all dogs on the farm should receive regular treatment for tapeworms. Anthelmintics, such as praziquantel, nitroscanate and some benzimidazoles are effective against the adult tapeworms.

SHEEP TICKS

The main species of significance in sheep and cattle is Ixodes ricinus.

ECOLOGY & LIFE HISTORY

There is a distinct seasonal activity of the tick; this corresponds with the period when ‘questing* ticks can be found on vegetation tips and infection of sheep and cattle occurs.

Two peak periods of activity occur, namely:

1. March - June - ‘spring feeders*

2. August - November - ‘autumn feeders*

Although the life-cycle takes 3 years to complete, the larvae and nymphs only feed for approximately 6 days and the adult for 14 days, i.e. a total of 26 days. Ixodes is thus a temporary parasite.

CONTROL

There are three possible approaches to the control of tick populations.

2. Resting pasture from sheep and cattle. This has little application because of the wide range of tick hosts.

BLOWFLY MYIASIS (Strike)

The disease is common and the course can be rapid where successive strikes occur. The condition is most debilitating and may be complicated by a septicaemia which can be fatal.

The condition can be controlled by dipping or spraying all sheep in early or midsummer with an organo-phosphorous or pyrethroid compound.

OVINE PARASITIC BRONCHITIS AND PNEUMONIA

A parasitic condition of young sheep characterised by coughing and weight loss.

AETIOLOGY

The lungworm Dictyocaulus filaria which is found in the trachea and bronchi.

LIFE-CYCLE

CLINICAL SIGNS

The most noticeable clinical signs are coughing and an increased respiratory rate.

EPIDEMIOLOGY

The disease is probably carried on from year to year by larvae overwintering on pasture and carrier sheep.

Outbreaks may occur at any time between June and November but are most commonly observed between August and October.

The disease occurs primarily in lambs during their first grazing season but it may also be seen in older sheep.

TREATMENT

Levamisole, an avermectin/milbemycin or a benzimidazole such as fenbendazole, oxfendazole or albendazole will control outbreaks of disease.

COCCIDIOSIS

In grazing sheep coccidiosis appears to be an increasing problem and occurs typically as diarrhoea in young lambs under intensive conditions.

AETIOLOGY

CLINICAL SIGNS

EPIDEMIOLOGY

DIAGNOSIS

TREATMENT AND CONTROL

NEMATODIROSIS

AETIOLOGY

CLINICAL SIGNS

Affected lambs appear prone to secondary bacterial and coccidial infections.

EPIDEMIOLOGY

The epidemiology of the disease is based on three factors:

1. The egg has a high resistance to freezing and desiccation, and can survive on pasture for up to two years.

2. Hatching, with release of the larvae, requires special stimuli in the form of a period of chill followed by a mean day/night temperature of more than l0 degrees C.

3. Adult sheep are resistant although they may carry very small burdens of N. battus.

DIAGNOSIS

It is important to remember that clinical signs often result from damage by larvae and faecal egg counts are not necessarily high at this stage of the disease.

TREATMENT

Several drugs are highly effective, including levamisole, morantel, the avermectins/ milbemycins or one of the modem benzimidazoles.

CONTROL

MANGE (Sheep Scab)

The most important mange of sheep in U.K. is caused by Psoroptes ovis and is commonly referred to as Sheep Scab.

Psoroptic mange affects the wooled areas of the sheep, in particular the shoulders and the sides of the body trunk.

FASCIOLOSIS

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 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 minimal period for completion of one entire life cycle of F.hepalica is therefore 17-18 weeks.

ECOLOGY AND LIFE HISTORY OF L.truncatula

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

2. Moisture

3. Temperature

THE DISEASE IN SHEEP

Acute Fasciolosis

CLINICAL SIGNS

DIAGNOSIS

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

F. hepatica eggs are present in the faeces.

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

Eggs are usually found In the faeces.

DIAGNOSIS

This is again based on clinical signs, faeces examination and post-mortem findings.

TREATMENT

PROPHYLAXIS OF FASCIOLOSIS

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.

USE OF ANTHELMINTICS

Based on these criteria the following control programme for sheep is recommended for years with normal or below average rainfall.

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.

PARASITIC GASTRO-ENTERITIS

Parasitic gastro-enteritis (PGE) in Britain is a disease primarily of lambs, characterised by weight loss and diarrhoea..

AETIOLOGY

PATHOLOGY

INTESTINAL PARASITES

The clinical consequences of these changes are:

1. Diarrhoea. This is the cardinal clinical sign of enteritis. It can be defined as a consequence of malabsorption of water and electrolytes.
2. Malnutrition. Due to malabsorption and leading to weight loss, poor quality wool and impaired milk production.

3. Excessive loss of protein through the intestine.

CLINICAL SIGNS

EPIDEMIOLOGY

During spring and early summer larvae are available on the pasture from a number of sources.

1. Overwintered larvae

2. Hatching and development of overwintered eggs

3. Hatching and development of eggs from the spring or peri-parturient rise in nematode faecal egg output which occurs in ewes.

DIAGNOSIS

Whenever possible a post-mortem examination should be made to establish a definite diagnosis.

Where P.G.E. is suspected many farmers or practising veterinary surgeons will treat the flock with a wormer and if a good response is obtained this is used as an index of diagnosis.

Collection of faecal samples for examination for nematode eggs is a useful aid to diagnosis

TREATMENT

Most drugs in sheep are administered orally by the use of modern automatic drenching guns.

CONTROL

Control is generally based on strategic use of wormers, often combined with specific grazing management.

ANTHELMINTIC PROPHYLAXIS

The most important source of infection for the lamb crop is the periparturient rise in the ewe faecal egg count; prophylaxis will only be efficient if this rise is kept to a minimum.

If ewes are brought indoors to lamb a treatment at the time of housing will remove existing worm burdens. Subsequent treatments would then depend on existing farm management practices.

SCRAPIE

Scrapie is a slowly progressive, degenerative disease of the central nervous system of sheep and goats. All breeds of sheep appear susceptible and the peak incidence of clinical disease occurs in sheep of 3 to 4 years of age. It is one of a group of similar disease found in over 20 species of mammals.

AETIOLOGY

The aetiology of scrapie is still not clearly defined but experimental evidence suggests that the cause is a transmissible, filterable and self-replicating agent.

Susceptibility to infection is under genetic control and this allows the opportunity for control using PrP genotyping. There is clear evidence for a single Scrapie Incubation Period (SIP) gene which is dominant for susceptibility.

CLINICAL SIGNS

Clinical disease develops progressively over months or years and several clinical syndromes have been described. Different strains of scrapie agent causing characteristic clinical and pathological features have been described in goats. The two well recognised strains are termed "drowsy" and "scratching" because of the characteristic clinical signs that each induces.

In sheep the "scratching" form is the most common and the affected animal scrapes, rubs and nibbles or bites at its skin due to the presence of a marked itching. The animal, in the early stages of the disease, rubs itself against fixed objects e.g. fence posts, stall divisions, bites and nibbles at its skin and rubs itself frequently with its horns, thus removing large quantities of wool. A "nibbling reflex" can be demonstrated when an affected animal is rubbed gently over the back, rump or flanks, this manipulation resulting in characteristic nibbling movements of the lips and licking movements of the tongue. This "nibbling reflex" is also apparent when the animal rubs itself on objects and can also be seen in animals suffering from intensely itchy conditions such as sheep scab but in the latter case skin lesions will be evident.

A second form of the disease in sheep results in changes in excitability when affected animals may become hyperexcitable and tremble markedly when approached or driven. Such animals exhibit fine tremors over the head and neck which produce a nodding action. A small proportion of these sheep become sleepy and stupid.

A third and less common form of the disease results in varying degrees of posterior inco-ordination which, in the early stages, is difficult to appreciate being seen best when an affected animal is being driven or made to turn sharply. Later pronounced swaying of the hindquarters becomes apparent with eventual progression to recumbency.

The majority of scrapie sheep lose weight and at death are almost at the stage of emaciation but a small number actually put on weight. Affected sheep all die within 1 to 6 months of the onset of the clinical disease.

EPIDEMIOLOGY

The disease spreads either by vertical transmission to the progeny of affected ewes or by lateral transmission by direct contact between animals or contact with premises which have previously been occupied by infected sheep. Thus the incidence can be expected to increase with intensification. The incubation period of scrapie ranges from 18 months to 3 years before clinical signs become apparent but sheep of less than 12 months of age have developed the naturally acquired disease.

TREATMENT

No form of treatment is possible.

CONTROL

Scrapie become notifiable in the U.K. in 1992. At the present time control is limited to the removal and slaughter of clinically affected animals from the flock. To eliminate infection associated with vertical transmission all the progeny of affected cases should be culled. It may be advisable also to remove close relatives of affected male sheep as they may be more susceptible to infection with the scrapie agent but as yet this has not been established.

CLOSTRIDIAL INFECTION OF WOUNDS IN SHEEP

(including Post-parturient Gas Gangrene, Blackquarter and Malignant Oedema)

AETIOLOGY

Several clostridial organisms have been recovered from wound infections in sheep but they all give rise to a basically similar lesion.

INCIDENCE

Clostridial wound infections occur in all ages of sheep. These infections are usually of sporadic occurrence and generally affect individual animals although under certain circumstances outbreaks may occur. Cases are most likely to appear at lambing time, following castration and docking, and at shearing time.

PATHOLOGY

Clostridial infections frequently develop in deep puncture wounds which provide the conditions necessary for the proliferation of the bacteria. The trauma may be due to surgical or accidental wounds, may follow an injection with a contaminated needle or may result from laceration of the vulva at lambing.

The local lesion, irrespective of its location, is usually dark red in colour and is infiltrated by blood-stained fluid and gas.

CLINICAL SIGNS

These usually appear within two days of trauma. Affected animals become dull and depressed and develop a fever. They usually show a variable degree of stiffness and/or lameness. The local lesion consists initially of a soft, hot swelling but later the overlying skin becomes tense and dark in colour.

In cases associated with parturition there is severe swelling and darkening of the tissues within and around the vaginal passage and this is accompanied by a reddish-brown fluid discharge.

Another less common manifestation of the disease is seen in rams which have been fighting. In this case oedematous lesions develop initially on the head and neck.

In all forms of the disease death occurs within 24-48 hours of onset of clinical signs.

TREATMENT

By the time most cases are observed treatment is of little value. Antiserum and antibiotics such as penicillin may be of value in early cases.

CONTROL

1.Hygiene: Hands and surgical instruments should always be clean when carrying out operations on sheep. Lambing, castration etc. should always be carried out in clean surroundings. Where a ewe receives assistance at parturition, antibiotic, preferably penicillin, should be administered.

2. Vaccination: use of a multivalent clostridial vaccine.