The most common bacterial diseases affecting small ruminants in sub-Saharan Africa are pneumonia, brucellosis, footrot, dermatophilosis, caseous lymphadenitis, anthrax and clostridial infections such as blackquarter, tetanus, malignant oedema and enterotoxaemias.

Colibacillosis and salmonellosis are also encountered particularly under the intensive production systems.

PNEUMONIA

Pneumonia refers to the inflammation of the pulmonary parenchyma usually accompanied by the inflammation of bronchioles and often pleurisy and, it is characterised by respiratory embarrassment or sometimes toxaemia. Upper respiratory infections are accompanied with respiratory abnormalities and very often they descend to pneumonia.

Aetiology

The aetiologic classification of bacterial pneumonia is complicated by the fact that many types of bacteria may be isolated from the same pneumonic lesions. However, Pasteurella spp are the most common bacteria isolated from cases of clinical pneumonia in goats and sheep. P. haemolytica biotype A is the commonest isolate from pneumonic pasteurellosis although P. haemolytica biotype T and P. multocida may also be encountered. Other bacteria isolated from pneumonic lungs of goats and sheep in sub-Saharan Africa include Corynebacterium pyogenes, Streptococcus spp, Staphylococcus aureus, Proteus mirabilis, Pseudomonas aeruginosa and Escherichia coli. Bacteria and mycoplasmas are commonly involved together in the pathogenesis of pneumonia in goats and sheep.

Epidemiology

Pneumonia is widespread among goats and sheep in sub-Saharan Africa and it is considered to be one of the most important causes of losses in the small ruminant industry. Pneumonia has been reported to be responsible for heavy losses in goats in Nigeria, Ghana, Mali, Sudan, Kenya, Somalia, Tanzania, Republic of South Africa and many other sub-Saharan countries. Morbidity has been estimated to be 33 % in West Africa and 24 % in East Africa while mortality up to 4 % is commonly encountered. These figures are gross underestimates because they are based on few studies in areas accessible to researchers and on abattoir records while the prevalence and importance of the disease in the traditional sector where many goats and sheep are kept have not yet been well studied.

Some of the bacteria commonly isolated from pneumonic lungs such as Pasteurella spp, Staphylococcus spp, Streptococcus spp and Corynebacterium spp are normal flora of the respiratory tract. Predisposing factors such as poor ventilation in animal houses, inclement weather, exhaustion during transport, severe parasitism are important in the epidemiology of pneumonia. Kids and lambs are more susceptible than adults. Some workers in West Africa have found that the incidence of pneumonia is higher in intensively managed than in semi-intensively or extensively managed goats while the harmattan winds have also been found to be associated higher incidences of pneumonia in small ruminants. In Somalia, malnutrition during the dry season is considered to be the major predisposing factor to caprine and ovine pneumonia while in Tanzania, long distance trekking of goats from rural areas to markets near or in urban centres and overcrowded housing conditions are considered responsible for many cases of pneumonia in small ruminants encountered in slaughter houses and abattoirs. The poor housing systems characteristic of traditional small ruminant management systems in most sub-Saharan countries subject animals to various stresses such as cold, wind, rain and dust which predispose them to pneumonia.

Pathogenesis

The main route of transmission of pneumonia and other respiratory infections is by inhalation of infective aerosols. The pathogenesis of the disease depend on the presence of virulence factors in the bacterium, host immunity and presence or absence and severity of the predisposing factors. P. haemolytica possess adhesive fimbriae, secrete proteolytic enzymes and a cytotoxin, all of which enhance its establishment on the respiratory system. The fimbriae facilitates attachment on the mucosa, proteolytic enzymes break down the mucosal barrier and impair the mucocilliary function of the respiratory tract thus facilitating colonisation and, the cytotoxin cause lysis of respiratory tract cells. The presence of other pathogens in the respiratory tract such as para-influenza-3 virus and adenoviruses disrupt the phagocytic mechanisms and lower the host immunity thus favouring proliferation of pasteurellae.

Clinical features

Acute, subacute and chronic pasteurellosis may occur. Acute pneumonic pasteurellosis is characterised by laboured breathing, coughing, nasal discharges, lacrimation, anorexia, depression and sometimes pyrexia if there is a systemic involvement. Exercised animals exhibit tachypnoea and dyspnoea. Some of the acutely affected animals may die without showing any clinical signs. The subacute and chronic diseases are mainly characterised by unthriftiness.

Pathological features

The gross pathological features of pneumonic pasteurellosis include oedema, haemorrhage, congestion, emphysema and red or grey hepatisation of the lung tissue. The lesions are found predominantly on the cardioventral aspects of the lung although other areas may also be affected. Tracheal froth, adhesive pleuritis and enlargement of bronchial and mediastinal lymph nodes are common features. A serofibrinous or fibrinopurulent exudate may be expressed from the bronchioles of the cut lung surface. Other features include presence of gelatinous exudate over the pericardium and straw-coloured exudate in the pleural cavity and in the interlobular spaces resulting in distension of the interlobular septa. Pulmonary abscess and adhesive fibrinous pleuritis and pericarditis are features of the subacute and chronic syndromes. Abscesses may be encountered in regional lymph nodes.

At histopathology, acute pneumonic pasteurellosis is characterised by dilation of the alveolar capillaries which are engorged with blood and mucus. The lumina of the bronchi, bronchioles and alveoli contain a serofibrinous exudate which is mixed with neutrophils, macrophages and desquamated epithelial cells. There may be diffuse alveolar necrosis, oedema of the interlobular septae and necrosis of the bronchial mucosa. Gram-negative bacteria are abundant around the necrotic foci. Thrombosis of the blood and lymphatic vessels is also evident. Abscessation, organisation and fibroplasia of the affected tissue are evident in the subacute and chronic syndromes.

Diagnosis

A tentative diagnosis of pneumonia can be achieved by consideration of the epidemiological, clinical and pathological findings. In Pasteurella spp infections, Gram- or methylene blue- stained smears from the lungs reveal Gram-negative Small coccobacilli which may show bipolar staining. The bacteria can be isolated from the lung lesions, pleural exudates and mediastinal lymph nodes by culturing on sheep or ox blood or MacConkey agar. The cultures are incubated aerobically at 37 °C for 24-48 hours. In MacConkey agar P. haemolytica produces pin-point red colonies surrounded by a narrow β-haemolytic zone. P. multocida colonies are larger, non-haemolytic and, may be mucoid and produce a characteristic sweetish odour. P. multocida does not grow on MacConkey agar. In septicaemic cases a large number of organisms can be isolated from the liver, spleen, kidneys, heart blood, pharyngeal and oesophageal mucosa. Intraperitoneal mice inoculation with suspensions of the organisms from affected tissues elicits a clinical disease with large numbers of the bacteria in tissues.

Acute pneumonic pasteurellosis should be differentiated from contagious caprine pleuropneumonia (CCPP) and other mycoplasmal pleuro-pneumonias, aspiration pneumonia and septicaemic colibacillosis. CCPP does not affect sheep and can be confirmed by isolation and identification of the causative Mycoplasma spp. Aspiration pneumonia is commonly associated with gangrenous lesions which are not common features of acute pneumonic pasteurellosis. Chronic pneumonic pasteurellosis can be differentiated from abscesses caused by C. pseudotuberculosis and Actinomyces pyogenes by isolation and identification of the causative bacteria while verminous pneumonia can be confirmed by demonstration of eggs or larvae in the bronchi, bronchioles and alveoli. Ovine progressive pneumonia can be differentiated from chronic pneumonic pasteurellosis by histopathological examination. Pneumonia caused by other bacteria can be confirmed by bacteriological tests.

Treatment and Control

P. hemolytica is sensitive to oxytetracycline at 20 mg/kg given parenterally. The treatment should be repeated after 4-6 days because relapses may occur. Penicillins are also used although some strains of P. haemolytica are not responsive to Penicillins. Ampicillin, sulphadimidine and trimethoprim-sulphonamide combinations have also been found to be effective.

There is no effective vaccine against bacterial pneumonia because of the diversity of aetiologic bacteria and serotypes but in some countries, vaccination of lambs and kids with vaccines prepared from local strains of P. haemolytica have been used. Control of pneumonia in a herd can be achieved by isolation and treatment of the affected animals. Avoidance or minimisation of predisposing factors such as overcrowding, long distance trekking and inclement weather can greatly reduce the incidence of pneumonia in a herd or farm.

This is a disease caused by infection with bacteria of the genus Brucella and it is characterised by abortion in late pregnancy and subsequent high rate of infertility. The disease is zoonotic and occupational causing undulant or Malta fever in man.

Aetiology

Brucellosis in goats and sheep is normally caused by a Gram-negative coccobacillary rod, Brucella melitensis although Brucella abortus may also cause clinical brucellosis. Brucella ovis is a cause of epididymitis of rams but it has also been associated with abortions and infertility. B. melitensis infection causes a fulminating disease in man (undulant or Malta fever) which is characterised by intermittent fever, malaise, fatigue, night sweats, muscle and joint pains whereas, B. abortus causes a mild disease. Osteomyelitis is a common complication in human brucellosis.

Epidemiology

Brucellosis has been reported to be an important cause of reproductive losses in small ruminants in some sub-Saharan countries. For example, the seropositivity of goats for B. melitensis infection in the northern, eastern and western parts of Nigeria has been estimated to be 4.3-12.5 % while 9.4-14.5 % of sheep in the same area have also been found to B. melitensis- seropositive. A 36.8% and 69.6% reactor rate of goats and sheep to B.ovis in Northern Nigeria has also been reported. In Central Ethiopia, about 1.5% of goats and 1.5% of sheep have been reported to be brucellosis-seropositive while in Tanzania, the prevalence of brucellosis in goats and sheep has been estimated to be 4.3 % and 2.2 % respectively. B. melintesis infection in goats has also been reported to occur in Somalia, Kenya, Zambia, Malawi, Namibia and South Africa. Although correct estimates of the losses associated with brucellosis in most sub-Saharan countries are lacking, the disease may be responsible for many cases of reproductive wastage and infertility in small ruminants. The consumption of raw milk in rural areas may be a potential public health hazard since it is possible for the milk to be infected with Brucella spp. Human brucellosis caused by B. melitensis has been reported in Kenya.

The source of infection is the infected doe or ewe and Brucella spp tend to be abundant in the placenta, placental fluid, uterine exudate and aborted foetuses. The bacteria may persist in the uterus for about 5 months after abortion. Inhalation is the most important route of infection in goats and sheep but infection may also be acquired through ingestion of infected material and by penetration of the bacteria through the conjuctival mucosa. In utero transmission may occur. The infective discharges can contaminate the environment very rapidly causing grazing animals to ingest massive numbers of the organisms. B. melitensis is known to be the most pathogenic of the Brucella spp and is more contagious than B. abortus. Overcrowding of animals in houses, communal grazing areas and water sources and, poor hygiene favour the rapid spread of the disease. The unrestricted movement of animals and personnel can facilitate the transmission of brucellosis between herds. Man can be infected through handling of contaminated materials, consumption of infected meat or milk or accidental inoculation with the live attenuated Rev B. melitensis vaccine.

Pathogenesis

After infection, Brucella spp multiply in macrophages and neutrophils of the regional lymph nodes causing lymphadenitis. This is followed by bacteraemia and subsequent localisation of the bacteria in various organs. The gravid uterus is the primary target organ but the organisms also lodge in the mammary tissue and supramammary lymph nodes. Brucella spp produce an exotoxin which is enables it to establish and cause lesions. The consequences of the infection are determined by the virulence of the bacteria, resistance and reproductive status of the host. The presence of erythritol, steroid hormones and other substances in the uterus, placenta and foetal fluids favours the proliferation of B. melitensis. Spontaneous recovery usually occurs in animals which were infected when not pregnant.

Clinical features

Abortion storm in late pregnancy is the principal manifestation of brucellosis. An abortion storm involving about 60 % of the pregnant does in the farm or herd is common. Other features include reduced milk yield and birth of weak kids or lambs which become asymptomatic carriers.

An acute septicaemic form of brucellosis may occur and is characterised by fever, depression, weight loss and sometimes diarrhoea. The presence of bacteria in the mammary tissue may cause mastitis. Epididymitis, orchitis, synovitis, hygromas, osteoarthritis, lameness and infertility are usually observed in male animals. B. abortus infection has been associated with neonatal deaths in lambs in Nigeria.

B. ovis infection in rams causes inflammation of the scrotum which is manifested by oedema, enlarged and hard palpable epididymis and, obliteration of the groove between the testis and epididymis. In the advanced stages of the disease the testis become atrophic. The infection in ewes is characterised by abortion, stillbirths or birth of weak lambs.

Pathological features

The pathological features of B. melitensis infection are mainly localised to the genital organs. Greyish-white necrotic areas are observed in the placenta and there is a brownish red exudate between the allantochorion and the endometrium. Acute endometritis is a common feature. Abscesses may also be present in the spleen and other parenchymatous organs. Histopathologically, there are necrotic foci around the placentomes and granulomatous foci may be encountered in the costochondral junction.

Thickening and fibrosis of the tunicae, granulomata or caseation necrosis of the testis and infiltration of the semen with inflammatory cells are the main features associated with B. ovis infection in rams. The semen is characterised by reduced total sperm count, morphologically abnormal sperm cells which also have poor motility. In the affected ewes, there is purulent exudate in the uterus, necrosis of the uterine surface, thickening of the placenta and raised yellowish-white or whitish areas in the intercotyledonary area. The aborted foetus is oedematous.

Diagnosis

The clinical history, endemicity of the disease in the area and clinical signs may be suggestive of the disease. The disease can be confirmed by demonstration of the bacteria in smears made from the vaginal discharges, placenta, colostrum and the abomasum of the aborted foetus using the modified Ziehl-Neelsen stain (MZN) or Koster method. In MZN-stained smears the bacteria appear as red intracellular coccobacilli. Brucellae can be isolated from the abomasal contents and lungs of the foetus; mammary glands; supramammary, retropharyngeal, parotid and mandibular lymph nodes and, seminal vesicles by culturing on 5-10 % blood or selective serum agar. After incubation for about 15 days at 37 °C pinpoint, smooth, glistening, bluish and translucent colonies appear. The colonies become opaque as they age. Farrels' medium and Albimi Brucella medium are selective enriched media for isolation of Brucella spp.

The serological methods used in the diagnosis of brucellosis include serum agglutination test, Rose Bengal plate test, ELISA, agar gel immunodiffusion and complement fixation test. The complement fixation test is considered to be the most specific and most sensitive method for the diagnosis of brucellosis in small ruminants. The milk ring test, Coomb's test and whey complement fixation test are used to detect the infection in milk. Cross-reaction occur between B. melitensis and B. abortus but not with B. ovis.

Brucellosis should be differentiated from other causes of abortion such as toxoplasmosis, Rift Valley fever, chlamydiosis, campylobacteriosis, listeriosis, salmonellosis and Coxiella burnetii infections. Hepatic necrosis is a characteristic feature of RVF and is distinguishable histologically. The other causes of abortion can be confirmed by demonstration of the causal organisms through bacteriological or other microbiological tests.

Treatment and Control

Treatment of the affected animals in usually not undertaken and such should be culled in order to reduce the sources of infection. Regular testing of animals, restriction of movement of animals and personnel between herds and purchase of animals with known health and reproductive records can prevent introduction and reduce the spread of the disease. Pasteurisation of milk is recommended in order to reduce incidence of the disease in man. All the infected materials should be incinerated and the contaminated premises disinfected. A test and slaughter policy can only be effective if it is preceded by a well organised educational programme to the livestock owners and assurance for compensation.

Vaccination with a live attenuated B. melitensis Rev 1 strain vaccine confers strong immunity but it causes abortion if used in pregnant does and ewes. It is recommended that kid and lambs should be vaccinated at 3-8 months while adults should be vaccinated 2 months before breeding. A formalin-killed adjuvant vaccine 53 H 38 has been in use in pregnant animals elsewhere.

FOOTROT

Footrot is a contagious infection of the feet characterised by inflammation of the skin-horn junction, under-running of the horn, ulceration and necrosis of the sensitive laminae of the foot and severe lameness. The disease is associated with production losses and sometimes mortality due to starvation.

Aetiology

Footrot in goats and sheep is caused by a large Gram-negative rod-shaped bacterium, Bacteroides nodosus which is commonly associated with Treponema penortha. Fusobacterium necrophorum and other aerobic or anaerobic bacteria may be isolated together with B. nodosus from the footrot lesions. Three serotypes A, B and C of B. nodosus exist. Serotypes A and B cross-react while serotype C is antigenically distinct.

Epidemiology

Footrot has been reported to be an important cause of morbidity in many countries. For example, the prevalence of footrot in goats in Kenya has been estimated to be 0.3 % while in northern Nigeria the prevalence of footrot in small ruminants has been estimated to be 4.9 %. In Tanzania, a 5.4-21.0 % prevalence of footrot has been reported in goats and sheep causing about 1.8-3.2 % mortality.

Footrot is a contagious infection and discharges or exudates from the affected feet contaminate the pasture or bedding. Infection occurs through contact with infected material and the organism gain entry into the body by penetration through broken skin. Prolonged wetting of the skin, scratches and bruises or surgical wounds facilitate the penetration of the bacteria and are therefore important predisposing factors. In Kenya, housing of goats in stony floors has been found to predispose goats to footrot. Penetration of nematode larvae such as Bunostomum spp and Strongyloides spp and, trombiculid mites through the skin can also facilitate the entry of the causative bacteria.

Wet and warm weather conditions favour the proliferation of the bacteria and soften the animal's skin thus making it easily breakable and penetrable. Dry and hot conditions are unfavourable for proliferation of B. nodosus and transmission of footrot and hence, the incidence of footrot tend to rise during the rainy season and drop during the dry season. In Tanzania, it has been noted that footrot is an important disease in areas of high rainfall and relative humidity and in intensively managed herds. The intermingling and congregation of animals in communal grazing areas, poor floor types and poor disposal of urine and faeces favour the spread of the disease. Carrier animals may harbour the organism for 2-3 years.

Pathogenesis

B. nodosus produces a growth factor and extracellular proteolytic enzymes which facilitates its penetration, establishment and growth in the host tissues. The proliferation of the bacteria causes severe tissue destruction leading to interdigital dermatitis and suppuration.

Clinical features

Initially, there is a moist, swollen, hyperaemic and macerated interdigital skin and later on, a foul smelling discharge from the lesion is observed. Fever may or may not occur. Severe lameness occurs and the affected animals become recumbent. Affected animals may be seen to graze on their knees to relieve pain in affected fore feet. There is also reduced feed intake, weight gain and milk yield. Animals may die because of starvation.

Pathological features

There are no characteristic pathological features associated with footrot although grossly there is always interdigital necrosis. There is almost always some under running of the horn of the wall and usually the sole of the affected claws. A characteristic black, foul smelling material is present due to the bacterial necrosis of the horn. Spread of the infection to joints may result in pyo-arthritis and accumulation of pus in the joint cavity. At histopathology, neutrophils are abundant in pus.

Diagnosis

Clinical signs are highly suggestive of the disease. The disease can be confirmed by demonstration of B. nodosus in pus smears and scrapings taken from the edge of the lesions. The smears can be stained by Gram's method or by dilute carol fuchsin. The bacteria stain faintly by Gram's method but in carol fuchsin, they appear as large Gram-negative rods with terminal enlargement at one or both ends. The bacteria can be isolated from pus by culturing on a B. nodosus specific medium containing Eugon agar base with 0.2 % yeast extract, 10 % defribrinated horse blood agar and 1 μg lincomycin. Colonies of pathogenic strains of B. nodosus appear as beaded or papillate while the less pathogenic strains produce mucoid colonies Mouse or rabbit inoculation and fluorescent antibody tests are also used in the confirmation of the disease.

Footrot should be differentiated from other causes of lameness such as traumatic injury, necrobacillosis, dermatophilosis (strawberry footrot), bluetongue, parasitic dermatitis, arthritis, foot and mouth disease and vesicular stomatitis. The clinical signs of footrot and necrobacillosis (foot abscess) are very similar but in necrobacillosis the principal bacterial isolate is F. necrophorum. The characteristic signs of necrobacillosis also include swelling of the tissues of the pastern, and the development of one or more sinceses at the coronet. The infection often spreads to involve the inter-digital space. Mixed infections with other bacteria is, however, not uncommon. Strawberry footrot is a proliferating dermatitis caused by Dermatophilus congolensis and it is characterised by itching and, lesions extending from the coronet to the hock or knee joints. Apart from coronitis which may be accompanied by separation of the hoof, the presence of fever, salivation, severe erosions on the muzzle and buccal cavity can be used to distinguish bluetongue from footrot. Lameness is not a feature of parasitic dermatitis but a foul smelling discharge and separation of the hoof may be confused with footrot. In addition, the demonstration of larvae of Strongyloides spp, Bunostomum spp and trombiculid mites may be suggestive of parasitic dermatitis.

Treatment and Control

A single heavy dose of penicillin-streptomycin (containing 70,000 IU penicillin and 70 mg/kg streptomycin) given intramuscularly can effective in the treatment of the disease. A follow-up treatment may be required if the response after the initial injection is not satisfactory. Chloramphenicol, tetracycline, erythromycin, tylosin, clindamycin, nitrofurazole parenteral and topical preparations can also be used in the treatment of the disease. Regular hoof trimming is recommended and has been found to facilitate recovery of the treated animals. Furthermore, hoof trimming can help to reduce the carrier state.

Control is based on the prevention of the spread of the bacteria, maintaining good hygienic conditions in the herds and minimisation of predisposing factors. Foot-baths containing 5 % copper sulphate, 10 % zinc sulphate and 5 - 10 % formalin are used in intensive production systems.

Although vaccines containing B. nodosus in an oil adjuvant or pili of B. nodosus cells and Pseudomonas aeruginosa in incomplete Freund's adjuvants are used in intensive production units, vaccination of small ruminants against footrot in the traditional small ruminant systems in sub-Saharan countries is not common because of the low mortality and seasonal incidence of the disease.

DERMATOPHILOSIS (STREPTOTHRICOSIS)

This is an acute, subacute or chronic and sometimes fatal exudative dermatitis of animals and less frequently man which is characterised by exudation, matting of the hair/wool and formation of crusts and thick scabs. The disease is caused by a dimorphic Gram positive bacterium, Dermatophilus congolensis.

Epidemiology

Dermatophilosis causes losses in terms of skin damage, reduced meat and milk production, culling or death of the affected animals and, costs of control and treatment. The disease is common among small ruminants in Nigeria, Ghana, Cameroon, Mali, Somalia, Kenya, Tanzania, Uganda, Malawi, Zimbabwe, Angola, Zaire and Madagascar. Fatal caprine dermatophilosis has been reported in Tanzania.

The source of infection is the sick or carrier animal and the disease spreads by contact. Prolonged wetting and mechanical damage to the skin either by bruises, scratches or surgical wounds are the predisposing factors. Arthropod vectors such as ticks (Amblyomma spp), flies (Stomoxys spp, Glossina spp and Musca spp), lice (Linognathus spp) and sheep ked (Mellophaga ovinus) may be involved in the transmission of dermatophilosis. Amblyomma spp ticks seem to play the most important role in the transmission of the disease in the field. The incidence of the disease increases with increase in rainfall, humidity and insect activity and hence the prevalence of the disease tends to higher during the rainy season compared to the dry season. Grazing of animals in spiky vegetation types predisposes them to damage of the skin and thus facilitating the penetration of the organisms.

Pathogenesis

After penetration through the skin D. congolensis causes an exudative epidermitis. Secondary bacterial infection cause extensive suppuration of the lesions or toxaemia. The lesions begin with the production of a greasy exudate and crusts on the skin which later on turn into yellowish scabs. Tension of the skin caused by adherent scabs at flexion points results in fissures. The yellowish scabs then become hard, horny and confluent resulting into alopecia. Localised lesions are common but a generalised condition has also been observed.

Clinical features

Goats are more susceptible to dermatophilosis than sheep. Clinical signs include papular and scab formation on the muzzle, face, nose, ears, scrotum and feet. The under surface of the scabs is covered with a yellow, creamy or haemorrhagic and hair-matting exudate. Concurrent infection with the contagious ecthyma virus and stress factors such as malnutrition, pregnancy and lactation exacerbate the disease. The case fatality in untreated goats is high although spontaneous recovery may Occur.

In sheep, the lesions start on the dorsal parts of the body and spread laterally and ventrally. Lesions may also occur on the ears, neck, face, muzzle and outer sides of legs. D. congolensis may cause strawberry footrot which is a proliferative dermatitis characterised by development of small, raised and dome-shaped crusts on legs especially on the anterior aspect of the pastern. Coalescence of the lesions results in the formation of wart-like masses which may extend from the coronet to the hock or knee regions.

Pathological features

At necropsy, the disease is characterised by ulceration of the skin, extensive dermatitis and secondary bacterial pneumonia. Histopathologically, there is oedema, congestion and infiltration of the epidermis with neutrophils, vacuolation of skin cells and mononuclear cell infiltration. Occasionally, the bacteria may spread to the liver, kidneys and lymph nodes and cause hepatitis, nephritis and hyperplasia of lymph nodes.

Diagnosis

Epidemiological and clinical features are highly suggestive of the disease. The disease is confirmed by demonstration of Gram-positive mycelial organisms in impression smears made from the under surface of the scabs. The smears can be stained with 10 % Giemsa for 30 minutes or 1 % methylene blue for 30 seconds. The bacteria can be isolated by culturing suspensions of scab material which has been ground with sterile sand on blood agar containing 1,000 IU aerosporin per ml of medium. The cultures are incubated in a candle jar at 37 °C for 48-72 hours, after which whitish-yellow raised colonies with an irregular surface and clear zone of haemolysis are observed. The colonies are hard to lift from the medium. Serological methods of diagnosis include fluorescent antibody test, ELISA and counterimmunoelectrophoresis.

The differential diagnosis of dermatophilosis include mange, contagious ecthyma, fungal dermatitis, fleece rot and photosensitisation. The haemorrhagic or yellowish under surface which is evident when scabs are removed and the absence of itching differentiates dermatophilosis from mange. In addition, the mange mites can be demonstrated in skin scrapings. Contagious ecthyma can be differentiated by the presence of large, thick, greyish- black and tenacious scabs which may also distort the lips and muzzle. The causal virus can be demonstrated by virological and serological tests. Fleece rot, which is caused by Pseudomonas aeruginosa is characterised by formation of a mat of exudate on the wool which may also be stained green, red, yellow, brown, or blue following proliferation of chromogenic bacteria on the lesions. The restriction of scabs on unpigmented and hairless parts of skin and, a history of grazing on photosensitising plants will be highly suggestive of photosensitisation.

Treatment and Control

Heavy doses of penicillin-streptomycin (containing 70,000 IU/kg penicillin and 70 mg/kg streptomycin) are effective if administered in early stages of the disease. Heavy doses of long acting tetracyclines (20 mg/kg) may be used and a 2.5% chloramphenicol ointment may be applied topically. Cyclophosphamide (25 mg/kg) given orally has been found to be effective in the treatment of the disease in sheep.

Control of ticks and biting insects by dipping or spraying with insecticides may limit transmission of the disease. Zinc sulphate (0.5 %), copper sulphate or magnesium flurosilicate (0.2 %) solutions have been found to be effective in reducing the spread and incidence of the disease. Wherever possible injury of the animal's skin should be avoided.

CASEOUS LYMPHADENITIS

This is a chronic insidious disease affecting small ruminants and it is characterised by caseous abscesses in peripheral lymph nodes although the organism can spread and cause abscessation in other organs. The disease is caused by a Gram-positive facultative anaerobic and pleomorphic bacterium, Corynebacterium pseudotuberculosis. The economic importance of caseous lymphadenitis is related to the condemnation of the affected carcasses.

Epidemiology

Caseous lymphadenitis occurs among goat and sheep populations world-wide. The disease is documented to be an important cause of organ and carcass condemnation in goats and sheep in South Africa, Tanzania, Kenya, Ethiopia, Mali and Nigeria. The prevalence of caseous lymphadenitis in Kenya has been estimated to be 7% in goats and 2% in sheep, while a 50% morbidity of caseous lymphadenitis in goats has been reported in Nigeria.

Caseous lymphadenitis affects animals of all ages although it is commonly encountered in adult animals because of cumulative chances of getting infected rather than a true age- related susceptibility. Infection is mainly acquired by contact and, wounds or skin abrasions are the major portal of entry. Occasionally, the disease can be acquired by ingestion. Inhalation of infective material can lead to lung abscesses or pneumonia.

Wet skin can be easily macerated and thus enhance penetration of bacteria. The bacteria can survive in soils which are rich in organic matter or in formites at low temperature for along time. Pastures, animals shed and dips contaminated with pus discharges from ruptured or incised abscesses may be a source of infection. Biting insects or ticks can damage the skin and facilitate transmission. In addition, un-hygienic surgical procedures such as vaccination, ear marking, wool shearing and castration can spread the disease. The use of contaminated hypodermic needles was reported to be responsible for an outbreak of the disease in a goat herd in Nigeria.

Pathogenesis

After penetration through the skin C. pseudotuberculosis is carried via the lymphatic and blood vessels either as free or within macrophages to the regional lymph nodes or other parts of the body. The pathogenicity of C. pseudotuberculosis is related to its ability to produce a haemolysin and a toxic wall factor. It has been found that the haemolysin has a phospholipase activity and it acts on the sphingomyelin of the erythrocytes and endothelial cell membranes causing haemolysis and increased vascular permeability. This facilitates further invasion of the bacteria in the tissues. The toxic wall factor protects the bacterium from phagocytosis by lysosomes thus enabling it to survive within phagolysosomes. This is considered responsible for the chronicity of the lesions associated with C. pseudotuberculosis. The final outcome of the infection is determined by the initial number of bacteria entering the body of the host, the multiplication rate of the organisms and efficiency of the host defence mechanisms.

Clinical features

The incubation period can extend from 3 weeks to 4-5 months. Caseous lymphadenitis is a mild disease characterised mainly by abscessation of the prescapular, parotid, submandibular and precrural lymph nodes. Occasionally, abscessation may occur in the lungs, kidneys, spleen, heart, tongue, spinal cord, brain and joints. The general health of the animals is usually not affected although the presence of numerous active abscesses leads to progressive weight loss, weakness, collapse, coughing or respiratory distress. Other non-specific but rare signs may occur when the location of the abscesses interfere with the normal function of a particular organ or system. It has also been observed that toxaemia may occur in kids and lambs leading to arthritis and sometimes death.

Pathological features

The major gross pathological feature is the suppuration of the affected lymph nodes. The incised lymph nodes contain a thick greenish-white or yellowish-white insipissated or semi­ fluid pus surrounded by a fibrous capsule. Insipissation may not occur in goats. On histopathology, there is a necrotic central area surrounded by neutrophils, giant cells, macrophages, plasma and epithelial cells. Gram-negative organisms can be demonstrated in smears made from the edge of the lesion. Infection of the lungs is associated with interstitial fibrosis.

Diagnosis

A provisional diagnosis of the disease can be based on clinical and pathological features. Confirmation of the disease is achieved by the demonstration of C. pseudotuberculosis in smears made from pus. In Gram-stained smears, the bacteria appear as pleomorphic Gram- positive rods. Pus cultured on sheep or ox blood agar for 24-48 hours at 37 °C produce small white and dry colonies surrounded by a narrow zone of haemolysis. The colonies become dry, crumbly and creamy in colour with time.

Other bacteria such as S. aureus, C. pyogenes and Actinomyces pyogenes which cause similar abscesses in or close to lymph nodes can be differentiated by isolation and characterisation of the bacteria. Other causes of chronic wasting such as chronic parasitism and malnutrition should also be considered in the differential diagnosis.

Treatment and Control

Treatment of affected animals is considered to be not economically justifiable because of the non-fatal and non-progressive nature of the disease. However, treatment may be needed for valuable stock such as breeding animals. C. pseudotuberculosis responds to penicillin although the perfusion of the drug through the capsule of the abscess is poor. Parenteral antibiotics may be used in severe cases. Surgical drainage of the affected lymph nodes is recommended.

The disease can be controlled by elimination of the source of the infection through culling of the affected animals. Surgical procedures such as castration, shearing or mass vaccination should be carried out under aseptic or hygienic conditions and, infected premises should be disinfected. Vaccination of 2-3 month old kids and lambs is practised in some countries.

ANTHRAX

This is a peracute, acute or subacute and often fatal disease of animals and man and, in small ruminants it is characterised by septicaemia, splenomegaly and gelatinous infiltration of subcutaneous and subserosal tissues. The disease is caused by a large Gram-positive, spore-forming bacterium, Bacillus anthracis.

Epidemiology

Anthrax has been reported to affect goats and sheep across the sub-Saharan region and was associated with heavy mortalities in the 1960-70s. Outbreaks of the disease have been reported in Sierra Leone, Ghana, Chad, Ivory Coast, Nigeria, Chad, Uganda, Tanzania, Kenya, Botswana, Namibia and Republic of South Africa. Strict vaccination programmes have reduced the incidence of the disease in most countries in recent years. Nevertheless, sporadic cases are still being reported.

Spores are formed when the vegetative bacteria are exposed to atmospheric oxygen, suitable temperature (20-40°C) and relative humidity (> 60%). Spores may remain viable in the soil or water holes for many years. They may be dispersed by wind, predators, fertilisers or effluent from factories processing contaminated animal products. Animals are infected by ingestion of food, water or soil contaminated with spores. Infection may also occur by inhalation or through broken skin. Abrasion of the oral mucosa facilitates the penetration of bacteria. Mechanical transmission by biting insects has been reported. Movements of nomadic flocks of sheep and goats can introduce the disease to non-endemic areas. Outbreaks of the disease may occur following vaccination with inadequately attenuated vaccines. Wild animals can act as carriers of the disease and this makes it difficult to eliminate the disease in areas bordering national parks or game reserves because it not possible to control the movement of wild animals or institute effective vaccination programmes.

Pathogenesis

The pathogenicity of B. anthracis is related to the presence of the antigenic capsule and the ability of the organism to produce a leucocidal protein toxin which is antiphagocytic, increase vascular permeability, delays blood clotting and produces capillary thrombosis. Increased capillary permeability causes leakage of body fluids into tissues and body cavities causing oedema and haemonchoncentration. Oedema of the lungs interferes with pulmonary perfusion leading to hypoxia, respiratory distress and inadequate supply of oxygen to the central nervous system. Leakage of body fluid into body tissues also results in decreased serum calcium and increased serum potassium leading to hyperirritability and convulsions which are observed in some animals. Presence of the toxin in the circulation causes severe anoxia, hypoglycaemia, alkalosis and shock which terminate into death.

Clinical features

The incubation period is 1-3 weeks. Peracute and acute forms of the disease occur in sheep and goats. The peracute disease is characterised by sudden death without premonitory signs, although there may be fever, dyspnoea, muscle tremors, congestion of the mucosae and terminal convulsions in few animals. The course of the acute disease takes about 2 hours and it is initially characterised by severe depression and listlessness. Fever (42 °C), anorexia, laboured breathing, congested and haemorrhagic mucosae, increased heart rate, rumenal stasis and reduced milk production are common features. There may blood discharges from the mouth, nostrils, anus and vulva. Diarrhoea or dysentery and oedema of the tongue, sternum, flanks and perineum have been observed. Pregnant animals abort and blood-stained or reddish-yellow milk is produced. Animals then collapse and die after terminal convulsions.

Pathological features

Post mortem examination of carcasses suspected to have died from anthrax is not recommended because of the risk of exposure of the vegetative organisms to air which triggers the formation of endospores and, hence contamination of the environment. There is also an additional occupational risk. The common gross post mortem features of anthrax in goats or sheep include complete absence of rigor mortis and rapid putrefaction and bloating of the cadaver. Non-clotting dark tarry blood oozes from the mouth, ears, nostrils, anus and vulva. The spleen is grossly enlarged with softening and sometimes liquefaction. Severe enteritis, ecchymotic haemorrhages throughout the body tissues and blood-stained fluid in body cavities are frequently observed.

Histopathologically there is widespread necrosis and haemorrhage in tissues and, capillary thrombosis. Large numbers of vegetative B. anthracis can be demonstrated in peripheral blood during the terminal stages of the disease.

Diagnosis

Clinical signs are highly suggestive. The disease can be confirmed by demonstration of large square-ended rods in thin blood smears prepared from the ear and tail veins or from the oedema fluid. Smears stained with 1 % polychrome methylene blue (McFadyean reaction) for two minutes reveal square-ended blue rods in chains surrounded by a pink capsule while those stained with 10 % Giemsa for 30 minutes show a red-mauve capsule. Spores can also be demonstrated by the Schaeffer and Fulton malachite green technique.

B. anthracis can be cultured from portions of the spleen and ear or blood by inoculating on sheep or ox blood agar. After aerobic incubation at 37 °C for 24-48 hours flat, dry greyish colonies with a granular 'ground glass' appearance are observed. At low magnification the edges of colonies show curved and curled projections giving rise to a 'medusa head' appearance. Intramuscularly inoculation of guinea pigs with 1 ml broth culture or oedema fluid leads to death in 24-48 hours with marked inflammatory reaction at the site of inoculation and extensive gelatinous oedema in subcutaneous tissues. Blood smears prepared from guinea pigs show typical capsulated organisms. Inoculation of mice also produces a fatal disease. The selective medium for B. anthracis is polymyxin-lysozyme- EDTA thallous (PLET) medium. The Ascoli test is also commonly used in the diagnosis of anthrax.

The differential diagnosis of anthrax include lightening stroke, acute bloat, peracute lead poisoning, peracute blackquarter and other clostridial infections. Lightening stroke is associated with singeing of the hair and, in addition there will be a history of an electrical storm. Peracute blackquarter is mainly restricted to young animals and the crepitating swelling of the affected muscles is not observed in anthrax. Demonstration of B. anthracis in tissues of suspected affected animals will help to rule out acute bloat whereas, in acute lead poisoning nervous symptoms dominate.

Treatment and Control

Treatment of peracute cases is usually untimely because of sudden death. An anthrax antiserum may result in recovery if used in early stages of the disease. Oxytetracycline at a dose rate of 5 mg/kg body weight parenterally can be effective if used in early stages of the disease. Large doses of penicillin-streptomycin combinations at 12-hour interval given concurrently with the antiserum for 5 days have also been found to be effective.

Control of anthrax in endemic areas is achieved by annual vaccination with live attenuated vaccines or avirulent spore vaccines. Inadequately attenuated organisms may revert to virulent forms and cause a clinical disease. If an outbreak occurs, affected animals should be isolated and strict quarantine measures should be imposed and followed by vaccination of the unaffected animals. The infected premises should be disinfected using strong disinfectants such as 5 % sodium hydroxide or formalin. Clothes can be disinfected by soaking in 10 % formaldehyde and, where facilities are available hides and skin should be disinfected with gamma irradiation to avoid human infection. Carcasses should be buried in 2-metre deep pits and covered with quicklime to prevent spore formation.

BLACKQUARTER (BLACKLEG)

Blackquarter is an acute infectious disease of ruminants which is characterised by inflammation of muscles, severe toxaemia and high mortality. The disease is caused by Clostridium chauvoei which is a Gram-positive, spore-forming and rod-shaped bacterium.

Epidemiology

Blackquarter is associated with significant mortalities in goats in some sub-Saharan countries. The disease has been encountered in small ruminants in Nigeria, Mali, Chad, Cameroon, Uganda, Kenya, Tanzania, Zambia, Malawi, Botswana and Madagascar. In some countries, blackquarter occurs in the same zones as anthrax. Vaccination programmes have greatly reduced the incidence of the disease in East Africa although sporadic outbreaks are not uncommon.

C. chauvoei may be present in the liver, spleen and alimentary tract of apparently healthy animals and the clinical disease occurs when conditions in tissues become favourable for spore formation. Spores are resistant to heat and common disinfectants and can persist in soils which are rich in humus or in water holes for many years. The source of infection contaminate the soil, pasture and water reservoirs. Dead animals may be sources of spores to the environment. Animals are infected by ingestion of contaminated food or water. Spores may also enter the body through broken skin. Un-hygienic mass vaccination or surgical procedures such as wool shearing or tail docking may spread the spores and result in outbreaks of the disease. Infection may occur through laceration wounds which occur in the genital tract during parturition. Sheep appear to be more susceptible than goats.

Pathogenesis

Ingested C. chauvoei spores pass through the intestinal wall and are carried through the lymphatic channels and blood circulation to muscles and other tissues where the lie dormant. When the muscles are bruised or necrotised the latent spores germinate and elaborate alpha, beta, gamma and delta toxins. The alpha toxin is a necrotising and lethal histotoxin which causes necrotising myositis and absorption of the toxin by muscles lead to toxaemia and death. The beta toxin destroys the nuclei of muscle cells. Exotoxins and other metabolites produced by the multiplying bacteria may cause lesions in the myocardium. Bacteraemia has also been found to develop terminally.

Clinical features

Affected animals exhibit stiff gait and hot painful swelling of the affected muscles. The muscles become oedematous and spongy. There may be crepitation but this not as marked as in cattle. Muscles of the shoulder, loin and buttocks are the most commonly involved. Serous or blood-stained fluid may ooze from the affected areas. Fever, lameness, severe depression are common features. The skin over the affected area becomes dark or black and, in later stages the swellings become cold and painless. Extensive local lesions can occur at the portal of entry.

Pathological features

The carcass rapidly putrefies and bloats. Sometimes, blood stained fluid may ooze from the nostrils and nose. There is excess fluid in body cavities which contain air bubbles, fibrin or blood. A blood-tinged or yellowish subcutaneous oedema fluid which may contain gas is a common feature. The incised affected muscles are dark-red or black with a characteristic rancid odour. Regional lymph nodes may be oedematous and haemorrhagic. Lesions tend to be deeper in sheep than in goats. The liver may decompose and produce gas.

Diagnosis

Clinical and pathological features can aid a tentative diagnosis of blackquarter. The disease is confirmed by the demonstration of large Gram-positive single rods or chains with oval, sub-terminal or central spores in smears made from the affected tissues or exudates. Smears should be made as soon after death as possible from aseptically removed pieces of the affected tissues such as muscles, subcutaneous tissue, liver, kidney and intestinal mucosa in order to avoid invasion with enteric facultative anaerobes such as C. perfringens and Cl. septicum. C. chauvoei is a strict anaerobe and difficult to culture. However, the bacteria can be cultured from affected muscles, liver or kidneys using Cl. chauvoei sheep blood agar medium incubated anaerobically at 37 °C for 24-48 hours. Colonies are small (1-2 mm), grey and rough. They are surrounded with a clear zone of haemolysis. Colonies of most clostridia resemble and can be differentiated by Gram stain or fluorescent antibody test. The latter test uses a fluorochrome-labelled C. chauvoei antiserum.

The differential diagnosis of blackquarter includes anthrax, lightning strike, snake bites, malignant oedema and other clostridial infections. Anthrax can be differentiated by its characteristic splenic lesion and the demonstration of the large square-ended bacilli in Giemsa-stained or polychrome methylene blue-stained smears (McFadyean reaction) from the ear or tail veins. It is recommended to rule out anthrax by the McFadyean reaction before carrying out a post mortem examination of the suspected cases. A history of an electrical storm and singeing of the hair will help to differentiate blackquarter from lightning strike. Malignant oedema and other clostridial infections may be differentiated by the fluorescent antibody test.

Treatment and Control

In early cases of the disease large doses of penicillin (10,000 IU/kg body weight) given intravenously may result in recovery. Infiltration of the affected tissues with penicillin may also be effective in early stages of the disease. Long acting preparations of Penicillins are usually recommended. Annual vaccination using polyvalent clostridial vaccines is the main method of control of the disease in endemic areas. Vaccines derived from local strains of the bacterium are recommended. Combined blackquarter and anthrax or multi-component clostridial vaccines are commonly used in the field. Vaccination of pregnant ewes or does 2- 4 weeks before parturition is useful in order to stimulate the production of antibodies that can passively protect the neonates. Quarantine measures can prevent spread of the disease in the event of an outbreak. Carcasses should be burned and buried in deep pits as for anthrax.

MALIGNANT OEDEMA (GAS GANGRENE)

This is an acute, febrile and fatal soil-borne wound infection of animals characterised by acute gangrenous inflammation at the site of infection, oedema and toxaemia. The disease is caused by clostridial organisms and Clostridium septicum, C. chauvoei, C. perfringens, C. sordellii and C. norvyi have all been isolated from the malignant oedema lesions. However, C. septicum is the most frequent isolate.

Epidemiology

Malignant disease is a sporadic disease which occurs world-wide. C. septicum occurs as normal flora in the intestinal tract of animals and faeces from such animals are a source of environmental contamination. The spores of C. septicum can persist in the soil and water reservoirs for a long time. All breeds and age groups of domestic animals are affected and infection occurs by contamination of wounds with spores of the bacteria. Deep puncture wound and severe trauma to tissues create anaerobic conditions which are favourable for the proliferation of the organisms. Contamination of wounds which may occur during castration, docking, wool shearing, vaccinations, intramuscular injections and dipping can result in outbreaks. The organism may also gain entry through the umbilical vessels of the new-born animals or lacerations in the genital tract which may occur during parturition.

Pathogenesis:

Injury to the skin and mucous membranes facilitates penetration of the organisms into the body. Trauma of tissues is associated haemorrhage and effusions which create anaerobic conditions that are favourable for the proliferation of the bacteria. The bacteria multiply and produce an alpha toxin which is haemolytic, necrotising and lethal. The toxin causes necrosis, gangrenous inflammation and oedema at the site of infection. Absorption of the toxin into blood circulation is associated with toxaemia and shock. Other toxins which help to amplify the pathogenic effects of the alpha toxin such as beta, gamma and delta are also produced.

Clinical features

Clinical signs may be observed as early as 12-48 hours or 4-5 days after infection. Initially there is a soft swelling, marked erythema and pain of the affected area. The swelling expands rapidly, becomes tense and the skin over it becomes dark. Emphysema and marked frothy exudation from the wound may occur, but it is not observed in C. norvyi infections. Fever (41-42°C), weakness, depression, muscle stiffness and tremors and lameness occur. Death occurs within 24-48 hours after the onset of the clinical disease. In infection acquired through the genital tract clinical signs appear within 12-24 hours and they include swelling of the vulva, perineal region and pelvic tissues. A reddish-brown discharge from the vulva is also observed.

Pathological features

At necropsy, there is gangrene of the skin and oedema of the subcutaneous and intermuscular connective tissue around the site of infection. A serous or blood-stained gelatinous oedema fluid which contain gas accumulates at the lesion but in C. norvyi infection, the oedema fluid is clear or gelatinous but contains no gas. When muscles are involved they become congested, pale red or brownish. Haemorrhages are observed in the subserosal tissues and the body cavities contains a serosanguinous fluid. A foul putrid odour is common in C. perfringens and C. sordellii infection. The uterus becomes atonic, reddish in colour and emphysematous.

Diagnosis

The clinical and necropsy features are quite characteristic but the disease has to be confirmed by isolation of the causative bacteria in smears made from the affected tissues. Blocks of affected tissues for laboratory diagnosis should be collected and chilled as soon as possible after death because post mortem invasion of tissues with enteric clostridia may complicate the diagnosis. Malignant oedema should be differentiated from blackquarter, anthrax, snake bite and other histotoxic clostridial infections. The characteristic muscle involvement which is evident in blackquarter is not a frequent feature in malignant oedema. Exudation of dark tarry blood from natural orifice is highly suggestive of anthrax and, the latter can be confirmed by demonstration of capsulated organisms by the McFadyean reaction. Other clostridial organisms can be differentiated by immunofluorescence.

Treatment and Control

Injection of penicillin or cephalosporidine on the periphery of the lesion is commonly practised in suppress replication and production of toxins by the bacteria. Other broad spectrum antibiotics can also be used. Antibiotic therapy should be accompanied with surgical drainage and irrigation of the infected wound with hydrogen peroxide. The infection can be controlled by maintaining asepsis when performing surgical procedures on animals. Prevention of animals from other causes of wounds may reduce transmission and incidence of the disease. Infected premises should be properly disinfected. In endemic areas annual vaccination of animals with specific or polyvalent formalised bacterins is recommended. In high risk areas, animals may be protected from accidental contamination by vaccination prior to anticipated surgical operations.

TETANUS

This is a highly fatal infectious disease of all domestic animals and man caused by a neurotoxin produced by Clostridium tetani and it is characterised clinically by hyperaesthesia, tetany and convulsions. C. tetani is a rod-shaped, spore forming Gram-positive bacterium in young cultures but becomes Gram-negative in old cultures.

Epidemiology

Tetanus is a sporadic disease which occurs world-wide. C. tetani is normal intestinal flora of mammals which are sources of environmental contamination. The bacterium form resistant spores which can persist in the faeces of herbivores or soil for many years. Spores enter the body through deep puncture wound and they normally lie dormant in tissues until condition become favourable for the proliferation and production of the toxin. Outbreaks of the disease may occur following mass contamination of animals during vaccination, castration, docking, shearing or other surgical procedures. Grazing on rough and spiky pastures may traumatise the buccal mucosa and facilitate entry of the bacteria. The wound may heal and close leaving the dormant spores in tissues, and they may proliferate later on when conditions become favourable. Although the disease is primarily caused by toxins produced by organisms already in tissues, pre-formed toxins in feeds or toxins produced in the gut by ingested organisms may also cause a clinical disease.

Pathogenesis

Trauma and necrosis of tissues create anaerobic conditions which favours the proliferation of dormant C. tetani spores and production of a potent neurotoxin (tetanospasmin). The toxin travels from site of production to the central nervous system through the blood system or through the peripheral nerves. The presence of the tetanospasmin at the inhibitory synapses or motor neurones blocks the release the gamma aminobutyric acid thus blocking the inhibitory neural impulses. As a result, there is constant potentiation of the sensory stimuli which leads to constant spasticity of muscles and hyperaesthesia. Tetanic spasms of the respiratory muscles cause asphyxia, cardiac arrest and death.

Clinical features

The incubation period is 1-3 weeks but may be longer depending on the pathogenicity of the strain, amount of toxin produced and amount of toxin entering the neural pathways or blood stream. The earliest signs include muscle stiffness, tremors and prolapse of the third eyelid. This is followed by trismus, unsteady gait and inability to move which is caused by stiffness of the limbs and abnormal flexion of joints. Tetany of the masseter muscles causes drooling of saliva from the mouth and regurgitation of food through the nostrils. There is also anxiety, dilatation of the nostrils, retraction of the eyelids and hyperaesthesia. Increased muscular activity may result in increased body temperature (up to 42°C). Spasms of the alimentary and urinary tract muscles cause constipation and retention of urine. Abnormal muscular contractions may cause opisthotonus, curvature of the spine and bending of the tail. Startled animals fall down with their fore and hind limbs stretched. The disease is highly fatal and death occurs 3-4 days after the onset of the clinical signs. However, spontaneous recovery may occur in animals which show a mild disease. A transient period of temporary improvement may occur before severe terminal spasms of the respiratory muscles.

Pathological features

No specific pathological lesions are associated with the disease except for the wound or traumatised tissue at the site of entry and toxin production. C. tetani may be cultured from such lesions.

Diagnosis

The muscular spasms and prolapse of the third eyelid are characteristic features of tetanus and a history of recent surgical procedures or trauma of tissues can be very supportive in the diagnosis of the disease. The disease can be confirmed by demonstration of the organisms in Gram-stained smears from the wounds in which they appear as Gram-positive single rods or chains with bulging round or spherical spores at the end giving a typical 'drumstick' appearance. On blood agar, small, slightly raised, feathery, semi-translucent or grey colonies which are surrounded with zone of haemolysis appear after 48 hours of incubation. Smears from young cultures reveal Gram-positive rods whereas, those from old cultures show Gram-negative organisms.

The differential diagnosis of tetanus include strychnine poisoning, plant poisoning, heartwater, enterotoxaemia of lambs and cerebral meningitis. The muscular spasms in strychnine poisoning are not as marked as in tetanus and, a history of exposure to strychnine or demonstration of C. tetani or the toxin tissues of the suspected animals will help to differentiate the two conditions. In heartwater, the nervous signs are less severe and fever is a frequent feature. Enterotoxaemia can be differentiated by isolation of the causative bacteria while cerebral meningitis is accompanied with depression.

Treatment and Control

A tetanus antitoxin is used to treat affected animals and is effective if given in early stages of the disease. Large doses of penicillin given parenterally or injected locally at the site of infection has been found to reduce further proliferation of the bacteria and toxin production. Local injection of antitoxin near the wound before debridement and irrigation with hydrogen peroxide is recommended to prevent spread of the toxin from the wound. Muscle relaxants such as acepromazine (0.05 mg/kg) should be given intramuscularly twice per day until the signs subside. Affected animals should be kept in a quiet environment and provided with enough space and soft bedding to avoid injury which may occur following muscle spasms. Intravenous or stomach tube feeding may be necessary.

Prevention of wound contamination with the C. tetani is the major principle of control of the disease. Surgical or other procedures which may be associated with trauma to the tissues should be carried out under strict hygienic conditions. A tetanus antitoxin should be given before mass surgical operations are carried out to prevent outbreaks should contamination of the wounds occur. In endemic areas, animals should vaccinated to prevent outbreaks. A toxoid produced from an alum precipitated, formalin-treated toxin is available commercially and it provides protection for one year beginning from 2 weeks post vaccination. A booster vaccination given after 12 months provides life long immunity. Vaccination of ewes 8 weeks and then 2-3 weeks before parturition stimulates antibody production for passive protection of neonatal animals.

INFECTIOUS NECROTIC HEPATITIS

This is an acute septicaemic disease of animals especially sheep which is characterised by sudden death, hyperaesthesia, severe depression and sternal recumbency. It is caused pathogenic strains of Clostridium norvyi type B but the occurrence of a clinical disease is associated with necrosis of the liver tissue which makes the environment favourable for the proliferation of the bacterium and production of a lethal alpha toxin.

Epidemiology

C. norvi B is present in the intestinal tract of clinical normal animals which act as carriers. Faeces from carrier animals and cadavers of dead sheep are the source of infection. Faecal contamination by carrion animals is also a source of infection. Water and soils may be contaminated by spores carried away from other areas by floods. Wild animals and birds have also been reported to be involved in the spread of spores. Infection occurs mainly through ingestion of spores and all ages of sheep are affected although the incidence of the disease has been found to be higher in healthy mature sheep of 2-4 years old. Neonatal animals may be infected through the umbilicus and infection through the genital tract can also occur. The occurrence of the disease is related to the distribution of liver flukes {Fasciola spp). A seasonal incidence of occurrence of the disease which is related to the seasonal incidence of Fasciola spp and their snail hosts has been demonstrated. In communal grazing system, overstocking and the congregation of animals in watering points during the dry season can result in outbreaks of fasciolosis and infectious necrotic hepatitis. Irrigation creates favourable habitats for snail hosts of liver flukes and may be associated with high incidences of both fasciolosis and infectious necrotic hepatitis. Damage to the liver tissue caused by Dicrocoelium dendriticum and hepatoxic chemicals can precipitate the occurrence of the disease.

The disease is said to occur world-wide although specific reports from sub-Saharan countries are lacking. However, the disease has been reported to affect sheep in Mali. It is quite possible that some cases of infectious necrotic hepatitis are misdiagnosed for fasciolosis.

Pathogenesis

After infection, the spores cross the intestinal barrier and are transported through the lymphatics and blood circulation to the liver and the spleen where they remain dormant. Damage of the liver tissue caused by migrating liver flukes create anaerobic conditions which activate latent spores. The bacteria multiply and elaborate alpha and beta toxins which are necrotising, lethal and haemolytic. The toxins cause necrosis of the hepatic tissue and the presence of toxins in blood circulation result in diffuse toxaemia.

Clinical features

Sudden death without evidence of premonitory signs may occur. Animals which survive sudden death become depressed, show disinclination to move and lag behind or separate from the rest of the flock. The neck and head may be extended and the back may be arched. There is fever (40-42°C) which fall to subnormal temperature prior to death. Rapid and shallow respiration, ruminal stasis and hyperaesthesia which is manifested by spasmodic twitching of the ears are common features The animals then falls on sternal recumbency and dies without struggling.

Pathological features

Usually the animal is in good condition but rapid putrefaction occurs. Blood-stained froth at the mouth and nostrils may be observed. There is an extensive haemorrhagic subcutaneous oedema in the sternum, ventral abdomen and inguinal regions. Congestion and cyanosis of the subcutaneous tissue results in blackening of the skin and hence, the name black disease. Thickening and oedema of the abomasal wall and congestion of the duodenal mucosa may be evident. The liver becomes engorged and dark-brown with characteristic 1-4 cm yellowish necrotic areas which are surrounded by a bright red zone of congestion are seen

especially under the capsule of the diaphragmatic lobes. These areas may be deeply seated and only evident after careful incision of the liver. Haemorrhagic tracts caused by migrating immature liver flukes are evident but adult flukes may be absent. The serous cavities contain a blood-stained or serous fluid which may lead to ascites, hydrothorax and hydropericardium. Subendocardial and subepicardial haemorrhages are evident and congestion of the parietal surface of the rumen, reticulum and omasum may occur. Large numbers of C. norvi B may be demonstrated in impression smears made from the liver sections.

The presence of a central zone of necrosis surrounded by a leucocytic zone containing mainly polymorphonuclear cells and occasionally lymphocytes in histological sections taken from the suspected liver is considered to be pathognomonic. A large number of vegetative or sporulating C. norvyi are present within the leucocytic zone.

Diagnosis

Epidemiological, clinical and pathological features may be suggestive. The disease is confirmed by demonstration of C norvi type B in impression smears made from the edges of the necrotic lesion. The bacteria may be cultured from pieces of the necrotic liver which have been aseptically removed from the carcass. Pieces of the liver tissue can be preserved in formalin for histological examination. The demonstration of organisms in typical lesions and demonstration of toxins in peritoneal fluid or in the liver is considered to be a positive diagnosis. The fluorescent antibody test is a rapid and simple method of diagnosis of infectious necrotic hepatitis. The clinical pathology of black disease is characterised by elevation of the liver enzymes especially gamma glutamyl dehydrogenase and, eosinophilia.

Infectious necrotic hepatitis has to be differentiated from fasciolosis. In the latter, the course of the disease is longer and the affected animals exhibit depression and anorexia. In fasciolosis, the liver is enlarged, friable and mottled and, immature flukes may be seen through the capsule together with subcapsular haemorrhages which they cause by perforation, but the necrotic foci characteristic of infectious necrotic hepatitis are absent. Other disease characterised by sudden death such as anthrax, blackquarter, malignant oedema, pulpy kidney and other clostridial enterotoxaemias can be differentiated from infectious necrotic hepatitis by identification of the causative bacteria in smears from the affected tissues using the fluorescent antibody test.

Treatment and Control

Sudden death often precludes timely and effective treatment although antibiotic therapy may be helpful in early stages of the disease. In endemic areas, vaccination of animals with an alum precipitated toxoid is commonly practised and may confer life long immunity. The use of multi-component vaccines with other clostridial species is recommended. Vaccination may reduce mortality during outbreaks. Control of fasciolosis and snail hosts can greatly reduce the incidence of the disease. Infected carcasses should be properly destroyed to avoid contamination of the environment with C. norvyi type B spores and infected premises should be disinfected.

ENTEROTOXAEMIA caused by CLOSTRIDIUM PERFRINGENS Types B and C.

Clostridium perfringens type B causes lamb dysentery and enterotoxaemia in goats. Few reports of the conditions are available in the sub-Saharan region although lamb dysentery is reported to be considerable losses in intensive sheep production units in South Africa. C. perfringens type C also causes acute enteritis in lambs.

Epidemiology

C. perfringens is found in the intestinal tracts of clinically normal or sick animals and pastures or soils are contaminated with faeces from such animals. Resistant spores are formed and can persist in the soil for months. Overcrowding and prolonged confinement have been found to be favourable for the spread and increased severity of the disease. Infection is acquired by ingestion of contaminated food or water. Lambs may also acquire the infection from contaminated udders or teats during suckling.

Pathogenesis

Following ingestion, the organism colonise and proliferate on the intestinal mucosa. C. perfringens type B producing alpha, beta and epsilon toxins whereas, C. perfringens type C produce alpha and beta toxins only. The beta toxin causes a severe haemorrhagic and ulceration of the intestinal mucosa. In adult animals the toxins produced are inactivated by trypsin but the neonate animals do not produce enough quantities of trypsin to destroy the beta toxin. Hence the disease is restricted to lambs under 1-2 weeks old. Necrosis and desquamation of the mucosa occurs resulting into ulcers. The irritation of the intestinal mucosa caused by presence of the organisms and toxins increases peristaltic movements and disturb the absorptive mechanisms on the mucosa resulting in loss of water and electrolytes from tissues into the gut. This is followed by dehydration, and acidosis. In addition, toxaemia which is caused by presence of toxins in the circulation cause shock which progress into death.

Clinical signs

Peracute, acute, subacute and chronic syndromes may occur. The peracute disease is characterised by sudden death without any premonitory signs. The acute syndrome is characterised by depression, failure to suckle, severe abdominal pain, bleating and lagging behind the flock or recumbency. A brownish or bloody diarrhoea is also present. The lambs then become comatose and die within 24 hours from the onset of the disease. The subacute syndrome is manifested by dullness, sluggish movements and abdominal pains. Tenesmus and a mucoid yellowish or blood-stained diarrhoea are observed. Death follows after prostration and coma. The chronic disease is mainly characterised by unthriftiness and a mucoid or blood-stained diarrhoea may be observed.

Pathological features

The acute and subacute cases are characterised by haemorrhagic enteritis, congestion and ulceration of the mucosa which becomes dark red. The intestinal contents are blood-stained and the peritoneal cavity contains excess serous or serosanguinous fluid. Adhesions of intestinal loops and presence of frank blood in the intestinal lumen have been reported. Perforation of the ulcerated intestine may occur resulting in peritoneal effusion, fibrinous peritonitis and adhesions. Subepicardial and subendocardial haemorrhages and, hepatic and renal degeneration may be evident. In chronic cases, there may be splenomegaly and clotted milk may be found in the abomasum. Large numbers of C. perfringens can be demonstrated in smears made from the affected portions of the intestine.

In adult sheep, C. perfringens type C causes a condition known as struck which is often characterised by sudden death although the affected animals may exhibit abdominal pain and convulsions. Ulcerative and haemorrhagic enteritis, fibrinous peritonitis, petechiae in serosal tissues and transudation in the peritoneal, pleural and pericardial are observed at post mortem. If the examination is delayed, rapid putrefaction of the carcass occurs and the disease may resemble malignant oedema.

Diagnosis

A provisional diagnosis can be made on the basis of clinical and pathological features but the syndromes caused by C. perfringens can be confirmed by demonstration of the bacteria in Gram-stained smears from affected portions of the small intestine. The presence of many vegetative Gram-positive bacilli in the smears can support the diagnosis. Isolation and typing of the bacteria and demonstration of the toxins in filtrates of the intestinal contents may be a positive diagnosis. ELISA is used to detect specific antitoxins in serum or beta toxins in the intestinal contents. Enterotoxaemia should be differentiated from salmonellosis and colibacillosis which also cause haemorrhagic enteritis in neonatal lambs or kids by demonstration of the causative organisms in intestinal contents or faeces. In addition, in colibacillosis ulceration of the mucosa is not a common features.

A hyperimmune serum is effective in the treatment of the disease if given in early. Antibiotic therapy can be effective in treating mild cases of the disease. Penicillins, oxytetracyclines and chloramphenicol can be used. Vaccination of pregnant ewes 2 months and then 2 weeks before parturition using C. perfringens type B or C toxoid to stimulate antibody production for passive protection of neonatal lambs is recommended. A booster dose should be given annually. Cross-protection between C. perfringens type B and C bacterins has been reported to occur. Polyvalent vaccines are commercially available in South Africa. When outbreaks occur, sick animals should be isolated and treated while animals at risk should be protected using a specific immunoglobulins against C. perfringens type B. Maintenance of good hygiene in the herd can greatly reduce transmission of the disease.

PULPY KIDNEY DISEASE

This is a toxaemic of sheep caused by toxin produced by Clostridium perfringens type D in the intestines and it is characterised by diarrhoea, paralysis, convulsions or sudden death. Goats are less commonly affected.

Epidemiology

The disease occurs world-wide. C. perfringens type D is an obligate parasite of the intestinal tract but under certain conditions it proliferates and produce large quantities of toxins which can be lethal. Heavy grain diet or lush pastures have been found to be favourable for the proliferation of the bacteria and occurrence of the disease. Thus, the disease commonly affects well-fed animals especially in intensive feedlot units. Factors which result in intestinal stasis or slow the of passage of the ingesta through the intestines such as heavy tapeworm infestation favour the accumulation of the toxin and occurrence of the disease. Inclement weather, coccidiosis and deworming can predispose animals to the disease. Lambs and kids of 3-12 weeks and 6-12 months old have been found to be the most susceptible groups.

Pathogenesis

C. perfringens type D organisms are abundant in the ileum and less so in other parts of the small intestine. Sudden change from low to high energy and especially starchy diets favours rapid multiplication of the saccharolytic C. perfringens type D which produces an epsilon toxin. The toxin is endotheliotropic and binds to the endothelial cells causing damage. Damage to the capillary endothelium results in increased permeability of the intestinal mucosa and this facilitate further absorption of the epsilon and other toxins. The toxin also causes capillary damage in other tissues such as kidneys, lungs and the brain resulting in oedema. Extracellular oedema in the brain is associated with nervous signs.

Clinical signs

Sudden death is the principal manifestation of the peracute disease in young animals although some of the animals may be dull, depressed and anorexic. In acute cases, there is frothy salivation, green or pasty diarrhoea, staggering, recumbency, opisthotonus, colonic convulsions, coma and death. Colic and bloat may occur. Affected adult sheep often lag behind the rest of the flock and show nervous signs as in young animals which include hypersensitivity, staggering gait, ataxia and knuckling of the fetlock. Champing of the jaws, blindness, salivation, rapid and shallow respiration, atonic rumen and pasty faeces may also be evident. In goats, the acute disease is characterised by diarrhoea or dysentery, abdominal discomfort and convulsions. Death may occur within 24-36 hours of onset of the disease. In both sheep and goats, the subacute syndrome is characterised by anorexia, intermittent diarrhoea/dysentery or presence of epithelial shreds in faeces. The chronic disease is characterised by progressive weight loss, emaciation and anaemia but goats may also be diarrhoeic. The chronic nervous form of the disease is characterised by aimless wandering, incoordination, paralysis of the masseter muscles, inappetence and ruminal atony.

Pathological features

At necropsy, the carcass is in good condition and no gross changes are observed in the peracute disease. The acute syndrome is characterised by presence of a clear straw coloured fluid in the pericardial sac which rapidly clots on exposure to air, patchy congestion of the abomasal and intestinal mucosa and, presence of custard ingesta in the intestines. Diffuse petechial haemorrhages occur on the peritoneal surface of the abomasum and intestines. Petechial or ecchymotic haemorrhages also occur in the muscles of the flank, muscular portion of the diaphragm, epicardium and in the thymus. There is rapid decomposition of the carcass and purple discoloration of hairless areas of the body. The small intestine is distended with gas. A dark congested liver with haemorrhagic spots on its surface and gelatinous or blood-tinged pericardial fluid are observed a few hours after death. The kidney has a mottled appearance, soft consistency and the cortex is jelly-like or semi-fluid (pulpy kidney). Nephrosis, congestion of the renal cortex and rupture of capillaries occur. In young animals terminal rupture of the abomasum has been reported.

In goats, the acute disease is characterised by pulmonary oedema, necrosis of the small and large intestinal walls. The intestinal contents may be green, blood-stained or mucoid and, fibrinous casts or strands may present the lumen of the large intestine. The mesenteric lymph nodes are oedematous.

In histological sections of the brain, the presence of perivascular oedema, haemorrhages and bilateral symmetrical areas of leucoencephalomalacia in the basal ganglia, thalamus, substantial nigra and cerebellar peduncles is characteristic of the nervous form of the disease (also known as focal symmetrical encephalomalacia).

Diagnosis

The diagnosis of the disease is based on the epidemiological features especially the type of diet, clinical and pathological features. Gram-positive C. perfringens D rods can be demonstrated from smears of the ingesta or intestinal lesions. Isolation of the bacteria by culturing a sample of faecal material and demonstration of epsilon toxin in intestinal contents can be highly suggestive of the disease. Protection of mice injected with toxin filtrates from the ingesta using a specific antiserum is diagnostic. An agglutination test using specific antiserum for the epsilon toxin is also used to confirm the disease. Other diagnostic tests include ELISA, counterimmunofluorescence, passive haemagglutination and radial immunodiffusion.

The differential diagnosis of pulpy kidney disease in young animals include acute ruminal impaction, polioencephalomalacia, other clostridial enterotoxaemias and acute pasteurellosis. No convulsions are observed in acute ruminal impaction and the course of the disease is longer (1-3 days) and polioencephalomalacia takes a longer course. Acute pasteurellosis can be differentiated by isolation and identification of Pasteurella spp from the affected tissues. In adult animals rabies, acute lead poisoning and pregnancy toxaemia should be considered in the differential diagnosis of focal symmetrical encephalomalacia. In rabies, there will be a history of encounter with the rabid animal or bite wounds. The presence of materials containing lead such as paints can be suggestive of lead poisoning. Pregnancy toxaemia occurs during late pregnancy in under inadequate nutrition and ketonuria is common feature at clinical pathology.

Treatment and Control

A hyperimmune serum is used in the treatment of the disease. Combining the hyperimmune serum with sulphadimidine has been found to be effective in goats. Oxytetracyline is effective in treating subacute cases. Chelating agents may be used to neutralise the toxins. Outbreaks of the disease may be prevented by vaccination of animals prior to anticipated changes in diet. Vaccination accompanied with reduction of feed intake has proved to be effective in the control of the disease. An alum precipitated, formalin-killed whole culture toxoid is commercially available. Vaccination of animals using toxins prepared in Freund's adjuvant have been found to provide immunity for up to 2 years. Oral vitamin E preparations stimulate immune response in vaccinated animals. Lambs should be vaccinated at 3 days and 4 weeks old followed by re-vaccination at 6 months. Kids are first vaccinated twice at 4 weeks interval and then re-vaccinated at 6 months. Severe anaphylactic reactions have been reported in Saanen kids following re-vaccination with the toxoid. Vaccination using a multi- component clostridial toxoid may be beneficial.

BOTULISM

This is a highly fatal motor paralysis caused by ingestion of a neurotoxin produced by a Gram-positive, spore forming anaerobic bacterium, Clostridium botulinum. Four antigenically distinct types of C. botulinum, A, B, C and D may cause the disease.

Epidemiology

Although the distribution and economic importance of botulism in sub-Saharan Africa is not well documented, the wide distribution of the causative organisms and food scarcity which commonly occur during the dry season in most of these country merits its consideration. The vegetative form of C. botulinum is commonly found in the intestinal tract of herbivores and faeces from these animals contaminate the environment. The spores which are formed are highly resistant to environmental conditions. C. botulinum has been found to proliferate only in decomposing animal carcasses or sometimes plant materials. Carrion animals may spread the organisms from one area to another. Pica caused by deficiency of protein in the diet or starvation may force animals to crave on infected carrion or decomposing plant materials and subsequent ingestion of lethal doses of the toxin. Deficiency of phosphorus in the diet lead to osteophagia and if the bones are contaminated with C. botulinum toxin animals may ingest lethal doses of the toxin. Botulinum toxin from dead rodents, birds, chicken litter or inadequately sterilised fertilisers may contaminate water sources resulting in outbreak of the disease in animals using such water sources. Warm and wet conditions are favourable for the proliferation of C botulinum and toxin production.

Pathogenesis

Proteolytic enzymes present in the alimentary tract digest the toxin and hence, ingestion of large doses of the toxin is required for a clinical disease to occur. Following ingestion, the toxin crosses the intestinal wall into systemic circulation. Presence of the toxin at the neuromuscular junctions inhibits the secretion of acetylcholine, the neuromuscular transmitter. This inhibition prevents transmission of impulses to the motor endplates resulting in flaccid paralysis. Death is caused by asphyxiation following paralysis of the respiratory muscles. A toxoinfectious form of botulism caused the neurotoxin produced by organisms already present in body tissues has been reported.

Clinical features

In initial stages, the acute disease is characterised by stiffness of muscles, incoordination and excitability. The affected animal becomes listless and, the head is raised or lowered during walking or may be held on one side. Weakness of the neck muscles may result in torticollis. Lateral bending of the tail, arching of the back, salivation, serous nasal discharges and frequent urination also occur. Abdominal respiration and flaccid paralysis are observed in the terminal stages of the acute disease. The chronic disease is characterised by ruminal and intestinal stasis.

Pathological features

No specific pathological features are associated with the disease although congestion of the intestinal mucosa and serosa, subepicardial and subendocardial haemorrhages may be observed. Presence of foreign bodies such as bones, sand and pieces of wood in the stomach or intestinal contents; catarrhal enteritis; pulmonary oedema and excess pericardial fluid may be observed. Perivascular haemorrhage in the brain and destruction of the Purkinje cells may be evident in histological sections. At clinical pathology the toxin can be demonstrated in the liver.

Diagnosis

A provisional diagnosis can be based on epidemiological features such as starvation, pica or osteophagia and clinical signs. Demonstration of large quantities of the toxin in suspected feed or intestinal tracts of dead animals is diagnostic. Occurrence of the clinical disease in unvaccinated susceptible animals fed on suspected feed and absence of the disease in vaccinated animals is confirmatory. Botulism resembles the paralytic form of rabies, but a history of a bite wound caused by a rabid animal should be highly suggestive of rabies. Plant poisoning, lead poisoning, polioencephalomalacia hypocalcaemia, hypomagnesaemia and louping ill should also be differentiated on the basis of epidemiological features and demonstration of the aetiological agents.

Treatment and Control

A hyperimmune serum given together with the antitoxin for 5 days may result in recovery. Treatment is not effective in late stages of the disease. Good nursing and supportive intravenous or stomach tube feeding is recommended for animals which cannot feed on themselves. Animals should be put on sternal recumbency to prevent bloat. Control of the disease is achieved by removing the infected feed and correcting the dietary deficiencies which predispose animals to the disease. Proper disposal of carcasses to avoid contamination of the pastures and watering points is recommended and in high risk areas, annual vaccination of animals is useful. A polyvalent toxoid containing type A, B, C and D strains is commercially available.

COLIBACILLOSIS

This is a disease of new-born lambs and kids caused by pathogenic strains of Escherichia coli and characterised by septicaemia or enteritis depending on the strains of bacteria involved.

Epidemiology

The disease is common under intensive production systems. Faeces of infected animals are the main sources of infection. Sub-clinically infected animals act as reservoirs which contaminate bedding, pens and feed or water troughs making them sources of infection. People working with animals can transmit the infection between herds or pens. Stress factors such as cold, wet or windy weather; poor hygiene in animal houses and overcrowding predispose animals to the disease. Inadequate intake of immunoglobulins through colostrum immediately after birth has also been found to increase the susceptibility of animals to the septicaemic form of the disease (colisepticaemia). Outbreaks may occur when there is mass lambing or kidding.

The losses associated with colibacillosis in small ruminants in sub-Saharan Africa are not well documented. This may probably be because, with the exception of small ruminant intensive production units in few countries such as South Africa, Kenya and Zimbabwe the majority of sheep and goats in the region are kept extensively and hence, the incidence of the disease is low. However, with increasing population pressure and decreasing land available for grazing, intensive small ruminant production systems are being adopted especially in urban or peri-urban areas. This change of management systems may be associated with an increase in incidence of the disease.

Pathogenesis

The occurrence of clinical colibacillosis depends on the type and pathogenicity of the infecting strain of E. coli, host susceptibility and presence or absence of predisposing factors. Thus, two syndromes of the disease, that is, septicaemic (colisepticaemia) and enteric colibacillosis can occur.

Colisepticaemia is caused by invasive strains of E. coli. Invasion of tissues may occur through the intestinal lumen, the umbilical vessels, nasopharyngeal mucosa and tonsillar crypts. Posses adhesive pili, resistance to antibacterial activity of serum and production of endotoxin are the factors which enhance the pathogenicity of the invasive strains of E. coli. Presence of receptors for the pili in the epithelium of intestinal mucosa also facilitates establishment of the bacteria. After successful establishment on the mucosa the bacteria produce endotoxins which pass into systemic circulation and initiate bronchoconstriction, pulmonary hypertension and pulmonary oedema. Invasive bacteria also cause tissue damage.

Enteric colibacillosis is caused by enterotoxigenic strains of E. coli which are capable to colonise, proliferate and producing an enterotoxin in the upper small intestine. The bacterial fimbriae attach on the receptor sites on the villous epithelial cells and the bacteria multiply and colonise the villous surface. The colonisation of the villi and production of enterotoxins disrupt the absorptive mechanisms on the intestinal surface resulting in the secretion of fluids and electrolytes from the systemic circulation into the intestinal lumen. This leads to electrolyte imbalance, dehydration, acidosis, hyperkalemia, circulatory failure and death.

Clinical and pathological features

Septicaemic colibacillosis is common in lambs and kids. Lambs and kids of 1-2 days and 3- 8 weeks old have been found to be the most susceptible groups. The syndrome may be peracute in which case sudden death occurs without any premonitory signs. The acute disease is characterised by stiff gait or recumbency, depression, fever, hyperaesthesia and tetanic convulsions. Animals may collapse because of acute meningitis. The chronic form of the disease is characterised by polyarthritis. The bacteria may also cause local reactions in other tissues.

No gross pathological lesions are observed in peracute septicaemic colibacillosis because of sudden death. In the acute form there are widespread subserosal and submucosal petechial haemorrhages. Enteritis and gastritis are common features. Fibrinous exudates are found in joints and in serous cavities. Fibrinopurulent meningitis and peritonitis may also be encountered. Infection through the umbilicus is associated with omphalophlebitis.

Enteric colibacillosis is manifested mainly by a haemorrhagic or mucoid diarrhoea various degrees of diarrhoea and slight fever. Other enteropathogens such as rotaviruses, salmonellae and Campylobacter spp may also be involved and complicate the clinical picture. Pathologically there are widespread haemorrhages in the intestinal mucosa and large numbers of the bacteria can be demonstrated in smears from the intestinal mucosa.

Diagnosis

The epidemiology, clinical signs, pathological features and, response to treatment may support a presumptive diagnosis of colibacillosis. Confirmation is achieved by the isolation and characterisation of E. coli from suspected animals. Bacterial culture alone is of limited use because of the presence of non-pathogenic strains of E.coli and, demonstration of specific toxins may be of great value to support the diagnosis. In the peracute form of the disease the organisms may be isolated from abdominal viscera and heart blood.

The differential diagnosis of colisepticaemia include clostridial enterotoxaemia and salmonellosis. These conditions can be confirmed by isolation and identification of the causative bacteria. The differential diagnosis of enteric colibacillosis include dietetic diarrhoea, coccidiosis and campylobacteriosis. Dietetic diarrhoea is manifested by passage of voluminous and pasty or gelatinous faeces and the animals are usually bright or alert although they may be inappetent. Other enteritides can be differentiated by isolation and identification of their aetiologic agents

Treatment and Control

In view of the diversity of strains of E. coli which are involved in the syndrome it is important to carry out drug sensitivity testing before any treatment is instituted. Trimethoprim-sulphonamide combination (15-25 mg/kg) and kanamycin (20 mg/kg) given parenterally and colistin administered at a rate of 1-2 g/kg in drinking water have been found to be effective in the treatment of the disease. Other antibiotics such as oxytetracycline, neomycin, chloramphenicol and sulphadimidine are also used.

Vaccination of dams 2-4 weeks before parturition to stimulate production of specific antibodies is recommended in order to provide passive protection bf neonatal lambs and kids through colostral immunoglobulins. Formalin-killed whole-cell vaccines are commercially available. Specific E. coli strain vaccines produced using K99+ pili antigens have been found to confer immunity to lambs and kids. Ewes have to be vaccinated twice in their first year of lambing, first at 8-10 weeks and then at 2-4 weeks before lambing. In subsequent years, one vaccination 2-4 weeks before parturition has been found to be satisfactory. Maintenance of good hygiene in the animal environment can reduce transmission and incidence of the disease. Provision of adequate colostrum to newly born kids and lambs will help to protect them from colisepticaemia.

SALMONELLOSIS

This is a disease of animals and man caused by different species of salmonellae and is characterised clinically by three major syndromes: peracute septicaemia, acute enteritis or chronic enteritis. Salmonella dublin, S. typhimurium and S. anatum are the common species associated with the disease in sheep and goats. S. abortusovis has been found to cause abortion in sheep.

Epidemiology

Salmonellae are widespread and the disease occurs world-wide. Salmonella spp are enteric bacteria and carrier animals shed the organisms in faeces thus contaminating the environment. It has been found that infection with S. dublin may result in a clinical disease or an active or passive carrier state. Active carriers constantly shed the organisms in faeces whereas, passive carrier will shed the organisms when stressed and, they may also manifest an overt disease. Recovered animals become subclinical carriers and shed the organisms in faeces. S. typhimurium may also originate from man or wild animals. Infection is acquired by ingestion of contaminated material. Animals may acquire the infection through food of animal origin and pastures contaminated with infective slurry or improperly treated fertilisers. Watering points may be contaminated with slurry from infected herds or fertilisers. Intensification of animal management favours spread of the disease from carriers animals. The organisms may be introduced in the herd via contaminated feed stuffs, formites, birds or nematodes. Stresses such as transport, starvation, parturition, overcrowding in communal grazing land, holding yards and dips activate latent infections and favour rapid spread of the disease. Disruption of the intestinal flora by factors such as antibiotic therapy, change of diet and water deprivation increases the susceptibility of the host to infection. Infection in animals occurs mainly by ingestion but in sheep it has been shown that infection may also be acquired by inhalation of infective material. Animal salmonellosis is the principal reservoir for human salmonellosis.

Pathogenesis

The ability of Salmonella spp to produce disease is facilitated by the presence of virulence factors. It has been found that pathogenic salmonellae posses adhesive pili, protective plasmids and, produce an enterotoxin, cytotoxin and lipopolysaccharide. These act together and enable the bacteria to adhere and colonise the intestinal epithelium, survive the phagocytic activity of macrophages and increase the permeability of the intestinal epithelium. The presence of bacteria on the intestinal wall also initiates an inflammatory response. After successful establishment, colonisation and disruption of the integrity of the intestinal wall, the organisms the pass through lymphatic system to mesenteric lymph nodes after which a clinical disease may occur depending on the virulence of the organisms, immune status and age of the host and, presence of intercurrent infections or other stress factors. From the mesenteric lymph nodes, the organisms invade the reticuloendothelial cells and then enter the blood stream causing septicaemia, enteritis and localisation in various tissues. Invasion of bacteria in the uterus and placenta causes abortion.

Clinical features

Enteric salmonellosis is the commonest form of the syndrome encountered in sheep and goats. The incubation period is 1-4 weeks. The syndrome is characterised by fever (40- 41°C), anorexia, listlessness, severe diarrhoea and sometimes dysentery or tenesmus. Faeces have a putrid smell, mucoid and may contain blood clots or fibrin casts. Fibrin sheets may be found in the intestinal mucosa. Shallow and fast respiration, rapid pulse and congestion of the mucosae are observed. Abortion is a common feature. There may also be dehydration, toxaemia, loss of weight, prostration, recumbency and death. New-born animals that survive the septicaemic disease develop severe enteritis characterised by diarrhoea. Polyarthritis and pneumonia are a common sequel. Does and ewes often die after abortion and lambs born alive may die subsequently. S. dublin is most common cause of the disease in goats. S. typhimurium also causes peracute septicaemia or acute enteritis.

Pathological features

Acute enteritis is characterised by muco-haemorrhagic enteritis and submucosal petechiation. In S. typhimurium infection, there is necrotic enteritis in the ileum and large intestines. The intestinal contents are putrid, mucoid, blood-tinged or may contain frank blood. The intestinal mucosa may be covered by an extensive diphtheritic membrane. The mesenteric lymph nodes are enlarged, oedematous and haemorrhagic. There is also enlargement and fatty degeneration of the liver; thickening of the gall bladder wall and presence of blood-stained fluid in the serous cavities.

The histopathological picture is characterised by necrosis, oedema, congestion and infiltration of the lamina propria and submucosa of the caecum, colon and small intestine with neutrophils, lymphocytes, plasma cells and macrophages. Focal necrosis in the mesenteric lymph nodes and thrombosis of the submucosa vessels occur. Hepatocellular necrosis and neutrophilic and mononuclear cell infiltration in the portal tracts may be evident. Necrosis and neutrophilic infiltration in the mesenteric lymph nodes and lymphoid and reticuloendothelial hyperplasia occur in protracted cases.

Diagnosis

A provisional diagnosis can be based on the epidemiological, clinical and pathological features and the disease can be confirmed by bacterial isolation and serotyping. In the acute disease the bacteria are present in heart blood, spleen, liver, bile, mesenteric lymph nodes and intestinal contents while in chronic cases, the bacteria can be isolated from the intestinal lesions or other viscera. Lymph nodes which drain the caecum and lower intestine have been found to be rich in the bacteria. The organisms can be easily demonstrated in a thick smear made from the wall of the gall bladder. Selective media such as MacConkey agar, brilliant green agar, triple sugar iron agar and xylose-lysine deoxycholate medium are used in the isolation of Salmonella spp. Species-specific antibodies may be used to diagnose the disease but cross-reaction do occur.

Coccidiosis, campylobacteriosis and parasitic gastroenteritis should be considered in the differential diagnosis of salmonellosis. Unlike the above conditions, salmonellosis is often manifested by a more acute and often fatal enteritis. High faecal oocyst and demonstration of developmental stages of Eimeria on the intestinal wall may be highly suggestive of coccidiosis whereas, high faecal egg and worm burdens may be highly suggestive of parasitic gastroenteritis. These features are not observed in salmonellosis except when they occur as intercurrent infections. Campylobacteriosis can be differentiated by demonstration of Campylobacter spp in faeces.

Salmonellosis can be treated using chloramphenicol (20 mg/kg) infused intravenously at 6 hours interval for 3 days. Other drugs include trimethoprim-sulphadoxine combination, sulphadimidine, framomycin, ampicillin and amoxycillin. Oral nitrofurazone daily for 5 days mixed in the feed or as a drench is commonly used in mass medication during outbreaks. The recommended treatment regime is to combine oral and parenteral therapy. It is important to remember that oral antimicrobial therapy may disrupt the normal intestinal flora and increase host susceptibility to the disease. Supportive fluid therapy to alleviate the effects of dehydration and electrolyte loss is beneficial. In some countries, treatment of animals against salmonellosis has led to selection for drug resistant strains thus complicating the effectiveness of treatment of human cases of the disease. Salmonellosis can be controlled by avoiding faecal contamination of feed or water and maintaining good hygiene in the animal houses. Animals should be purchased from herds which are known to be free from the disease. Regular testing should be carried out to identify carriers which should be culled. Infected premises should be properly disinfected and the infective materials should be destroyed. Personnel from infected herds should not be allowed to come into contact with disease- free animals. Vaccination of small ruminants against salmonellosis is not widely practised.

MASTITIS

Mastitis refers to the inflammation of the mammary gland and is characterised enlargement of the udder and abnormal milk secretion with or without fever. The disease has a multiple aetiology but Staphylococcus aureus and Streptococcus agalactiae are the commonest bacteria isolated from cases of mastitis in small ruminants. Other bacteria encountered in include Corynebacterium pyogenes, Klebsiella spp, Mycobacterium spp and Brucella spp.

Epidemiology

Reports on clinical mastitis in small ruminants are available from South Africa, Kenya and Nigeria and, information from other countries is limited. This lack of information is probably be related to the fact that the indigenous small ruminants are kept primarily for meat and, hence little attention has been paid to the economic significance of mastitis. However, with recent introduction of dairy goats and intensification of management systems, mastitis may become an important disease entity worth attention.

Un-hygienic conditions in animal houses and poor milking hygiene are important predisposing factors. Mechanical or surgical wounds in the teats or udder facilitate penetration of the bacteria. Most often, Mycobacterium spp and Brucella spp spread systemically and lodge in the mammary tissue causing mastitis.

Pathogenesis

After entry through the teat canal the bacteria colonise and multiply in the mammary tissue. Some bacteria produce enzymes and toxins which cause inflammation and damage to the mammary tissue, Pyogenic bacteria cause abscessation and suppuration. These inflammatory changes are associated with abnormalities in milk. The severity of infection is determined by the virulence of the organism, extent of mammary tissue damage, stage of lactation and efficiency of host defence mechanisms in the mammary tissue.

Clinical features

The clinical signs of acute staphylococcal mastitis in goats include restlessness, elevated pulse (up to 144 per minute) and respiratory rate (up to 80 per minute) rates, hot, painful and enlarged mammary glands. Gangrenous necrosis of the mammary tissue may occur. On palpation there is marked diffuse induration of the mammary glands and enlargement of the supramammary lymph nodes. The milk shows a thick yellowish discoloration or may be blood-stained.

Pathological features

The affected mammary glands are enlarged and hard on palpation. The teat orifices may be blocked. Abscesses may be present in different sections of the mammary tissue.

Diagnosis

A tentative diagnosis is based on the clinical signs especially presence of abnormalities in milk and pathological lesions. Confirmation is achieved by isolation or demonstration of the causative agents in smears prepared from pus or milk secretions. Cell counts and California mastitis test are also used in the diagnosis. Mastitis in goats' may also be caused by Mycoplasma agalactiae and Candida albicans and these should be considered in the differential diagnosis of the disease. Other mammary abnormalities such as oedema, passive congestion and haematomata are usually not associated with abnormalities in milk.

Treatment and Control

Bacterial mastitis can be treated by penicillin, streptomycin, oxytretracycline and gentamycin either as intramammary infusions or parenterally in systemic cases. Combination of systemic and intramammary antibiotic therapy is beneficial where there is systemic involvement. Some strains of S. aureus are resistant to Penicillins, hence drug sensitivity testing is recommended before the use of these drugs in the treatment of mastitis. Proper herd and milking hygiene is the most effective means of controlling mastitis.

Other bacteria such as Mycobacterium spp, Listeria spp, Actinobacillus spp and Actinomyces spp cause disease syndromes in small ruminants, the clinical and pathological features are similar to those observed in cattle.

Abu-Samra, M.T. (1978) Zbl Veterinary Medicine, 25: 641-651.

Abu-Samra, M.T. and Walton, G.S. (1981) Journal of Comparative Pathology, 91: 317- 328.

Abubakr, M.I., Elfaki, M.E., Abdalla, S.A. and Kamal, S.M. (1981) Bulletin of Animal Health and Production in Africa, 29: 85-94.

Adesiyun, A.A., Ezeokoli., C.D., Kumi-Diaka, J. and Udechukwu, A.L. (1983) Bulletin of Animal Health and Production in Africa, 33: 11-16.

Addo, P.B. (1978) Bulletin of Animal Health and Production in Africa, 26: 37-41.

Addo, P.B., Chineme, C.N. and Eid, F.I.A. (1980) Bulletin of Animal Health and Production in Africa, 28: 225-231.

Ameh, J.A., Addo, P.B., Adekeye, J.O and Gyang, E.O. (1993) Preventive Veterinary Medicine, 17: 41-46.

Amin, J.D. and Silsmore, A.J. (1993) Bulletin of Animal Health and Production in Africa, 41: 123-128.

Anonymous (1993) Capricone, 6: 24-28.

Bagadi, H.O. (1974) Veterinary Bulletin, 44: 385-388.

Bagadi, H.O. and M.M.H. Sewell (1973) Research in Veterinary Science, 15: 49-53. Bagadi, H.O. and M.M.H. Sewell (1973) Research in Veterinary Science, 15: 54-61. Bekele, T., Kasali, O.B. and Tekelye-Bekele (1990) Bulletin of Animal Health and Production in Africa, 38: 23-25.

Blasco, J.M., Garin-Bastuji, B., Marin, C.M., Gerbier, G., Fanlo, J. and Jimenez-de-Bagues, M.P. and Cau, C. (1994) Veterinary Record, 134: 415-420.

Blood, D.C. (1994) Pocket Companion to Veterinary Medicine. Balliere Tindall, London. Blood, D.C. and Radostitis, O.M. (1989) Veterinary Medicine. A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses. Seventh Edition. Balliere Tindall, London.

Bwangamoi, O. (1969) Bulletin of Epizootic Diseases of Africa, 17: 185.

Bwangamoi, O. (1976) In: D.H. Llyod and K.C.Sellers (Editors) Dermatophilus Infection in Animals and Man. Proceedings of a Symposium held at the University of lbadan, Nigeria, 1973. Academic Press, London, pp 49.

Chartier, C. (1992) Bulletin of Animal Health and Production in Africa, 40: 277-283. Chatterjee, A. (1989) Skin Infection in Domestic Animals. Moitri Publication. Calcultta, India.

Cheyne, I.A., Edelsten, R.M., Cartwright, C.F., Pegram, R.G. and Wooldridge, R.L. (1994) Livestock Diseases in the Northern Regions of Somalia. Report of the British Veterinary Team, 1969-1972. Vetaid, Centre for Tropical Veterinary Medicine, Edinburgh.

Chukwu, C.C. (1985) Bulletin of Animal Health and Production in Africa, 33: 193-198.

Chukwu, C.C. (1987) Bulletin of Animal Health and Production in Africa, 35: 92-98.

Edelsten, R.M., Bell, R.A. Gourlay, R.N. and MacOwan, K.J. (1987) Bacterial Diseases. In: A. Robertson (Editor) Handbook of Tropical Veterinary Diagnosis. Section 5. Centre for Tropical Veterinary Medicine, University of Edinburgh.

Edelsten, R.M., Bell, R.A. Gourlay, R.N. and MacOwan, K.J. (1990) Diseases caused by Bacteria. In: M.M.H.Sewell and Brocklesby, D.W. (Editors) Handbook on Animal Diseases in the Tropics. Balliere Tindall, London.

Falade, S. (1977) Bulletin of Animal Health and Production in Africa, 25: 393-395. Falade, S. and Ezenwane, E. (1984) Bulletin of Animal Health and Production in Africa, 32:43-51.

Falade, S., Nwufoh, J.K. and Nmezi, L.J. (1981) Bulletin of Animal Health and Production in Africa, 29: 197-201.

Falade, S., Ojo, M.O. and Sellers, K.C. (1974) Bulletin of Epizootic Diseases of Africa, 22: 335-337.

Fensterbank, R. (1987) Brucellosis in Cattle, Sheep and Goats: Diagnosis, Control and Vaccination. Comprehensive Report. Office International Des Epizooties. Technical Series No. 6. Monnaie, France. pp 9-34.

Fison, T.W. (1987) Report on Investigations Carried Out By The Veterinary Investigation Centre, Naliendele near Mtwara, Southern Tanzania, 1984-1986. ODA, London.

Garin-Bastuji, B. (1992) Sciences Veterinaires Medicine Comparee, 94: 187-206.

Glynn, T. (1993) Australian Veterinary Journal, 70: 7-12.

Hyslop, N.S.G. (1980) Comparative Immunology and Microbiology of Infectious Diseases, 2: 389-404.

Ikede, B.O. (1977) Bulletin of Animal Health and Production in Africa, 25: 49-59. Kaminjolo, J.S. (1988) Bulletin of Animal Health and Production in Africa, 36: 81-82. Kaya, O. (1992) Veterinarium, 3: 13-18.

Kuria, J.K.N. and Ngatia, T.A. (1990) Bulletin of Animal Health and Production in Africa, 38: 15-18.

Mahlau, E.A. and Hammond, J.A. (1962) Bulletin of Epizootic Diseases of Africa, 10: 511-516.

Mahlau, E.A. (1967) Bulletin of Epizootic Diseases of Africa, 15:373-378.

Mgassa, M. N. (1987) Bulletin of Animal Health and Production in Africa, 35: 162-166.

Mgassa, M.N. and Arnbjerg, J. (1993) Small Ruminant Research, 10: 63-67.

Ministry of Agriculture, Fisheries and Food (1986) Manual of Veterinary Parasitological Techniques. Reference Book 418. Her Majesty's Stationary Office, London. Momotami, E., Inui, S., Ishikawa, Y. and Azuma, R. (1984) Journal of Comparative Pathology, 94: 33-34

Munz, E. (1976) In: D.H. Llyod and K.C.Sellers (Editors) Dermatophilus Infection in Animals and Man. Proceedings of a Symposium held at the University of Ibadan, Nigeria, 1973. Academic Press, London, pp 57-65.

Ndarathi, C.M. and Waghela, S. (1991) Indian Journal of Animal Sciences, 61: 156-157.

Ngatia, T.A., Kimberling, C.V., Johnson, L.W., Whitelaw, C.E. and Lauerman, L.H. (1989) Bulletin of Animal Health and Production in Africa, 37: 13-19.

Office International Des Epizooties (1987) Dermatophilosis, Veterinary Training in Africa, Pan African Rinderpest Campaign, Animal Health Status. Proceedings of the 7 th Conference of the OIE Regional Commision for Africa, 19-22 January, Cairo, pp 211-231.

Ojo, MO. (1976 Tropical Animal Health and Production, 8: 85-89.

Okewole, P.A., Eze, E. N., Okoh, A.E.J., Oyetunde, I.L. and Vyver, F.H. (1988) Bulletin of Animal Health and Production in Africa, 36: 251-254.

Okoh, A.E.J. (1980) Tropical Animal Health and Production, 12: 11-14.

Okoh, A.E.J. (1981) Bulletin of Animal Health and Production in Africa, 29: 355-359.

Oppong, E.N.W.(1991) Epizootiology of dermatophilosis. Paper presented at the Second International Symposium on Dermatophilosis held in Vom, Plateau State, Nigeria, 4-9 November, 1991. pp l-37.

Osborne, H.G. (1958) Australian Veterinary Journal, 34: 301-304.

Plommet, H. (1992) Proceedings of the International Seminar organised by CIHEAM, CEC, MINAG (Malta), Valetta, Malta, 28-30 October 1991. CIHEAM Publication No. 1. Pudoc Scientific Publishers. Wageningen, Netherlands.

Quinn, P.J., Carte, M.E., Markey, B. and Markey, G.R. (1994) Clinical Veterinary Microbiology. Mosby Yearbook Europe Limited, London.

Rhaymah, M.S., Yousif, Y.A. and Sawa, M.I. (1993) Iraqi Journal of Veterinary Sciences, 6:111-113.

Ribeiro, L.L.M., Herr, S., Chapparo, F. and Vyrer, F.H. (1990) Onderstepoort Journal of Veterinary Research, 57: 143-145.

Roberts, D.S. (1965) British Journal of Experimental Pathology, 46: 635-642.

Roberts, D.S. (1967) Veterinary Bulletin, 37: 513-521.

Schwartzkoff, C.L., Lehrbach, P.R., Ng, M.L. and Poi, A. (1993) Australian Veterinary Journal, 70: 127-129.

Singh, K.P., Parihar, N.S. and Tripathi, B.N. (1992) Indian Journal of Animal Sciences, 62:611-615.

Smith, O.B. and Jansen, H.J. (1983) Nigerian Veterinary Journal, 12: 52-55.

Soltys, M.A. (1979) Introduction to Veterinary Microbiology. Pernbit University Pertaninan Malaysia. Serdang, Selangor, Ipon, Malaysia.

Sutherland, S.S., Ellis, TM. and Masters, A.M. (1991) The development of and evaluation of vaccines against ovine dermatophilosis. Paper presented at the Second International Symposium on Dermatophilosis held in Vom, Plateau State, Nigeria, 4-9 November 1991, pp 1-12.

Tuah, A.K. (1988) In: K.O. Adeniji (Editor) Proceedings of the Workshop on the Improvement of Small Ruminants in West and Central Africa, 21-25 November 1988, Ibadan, Nigeria, pp 137-148.

Tuchili, L.M., Pandey, G.S., Sinyangwe, P.G. and Kaji, T. (1993) Veterinary Record, 132: 487.

Ugochukwu, E.I. (1985) Bulletin of Animal Health and Production in Africa, 33: 235-239.

Ugochukwu, E.I. (1985) Bulletin of Animal Health and Production in Africa, 33: 303-306.

Wachira, J.W. and Shavulimo, R.S. (1986) Proceedings of the 5th Small Ruminants Collaborative Research Workshop, Kabete, Kenya. pp 108-112.

Waghela, S. (1976) Bulletin of Animal Health and Production in Africa, 21: 53 -59.

Wallach, J.C., Miguel, S.E., Baldi, P.C., Guarnera, E., Goldbaum, F.A. and Fossati, C.A. (1994) Immunology and Medical Biology, 8: 49-56.

Wandera, J. (1987) Proceedings of the Workshop of the Sixth Kenya Veterinary Association/Small Ruminant CRSP Workshop, Kabete, Kenya. pp 192-194.

Ware, J.K.W., Scrivener, C.J., Vizard, A.L. and Webb-Ware, J.K. (1994) Australian Veterinary Journal, 71: 88-89.

Yeruham, I., Elad, D. and Perl, S. (1994) Israel Journal of Veterinary Medicine, 49: 161- 164.