CHAPTER 5: DISEASES CAUSED BY VIRUSES

The common viral infections of goats and sheep in sub-Saharan Africa are peste des petits ruminants (PPR), contagious ecthyma, goat/sheep pox and Nairobi sheep disease. Other viral diseases are Rift Valley fever and blue tongue.

PESTE DES PETITS RUMINANTS

This is a contagious viral disease of goats and less commonly sheep and it is characterised by fever, erosive stomatitis, enteritis, pneumonia and death. The disease is caused by a PPR virus of the genus Morbillivirus and family Paramyxoviridae which closely resembles the rinderpest virus.

Epidemiology

PPR is endemic and is considered to be the most serious infection of small ruminants in West and Central Africa. The disease has recently been encountered in small ruminants in the eastern part of the continent ( Ethiopia ). An infection rate of 22.0-51.0% has been estimated in Nigeria and heavy mortalities associated with the disease have been reported. No sero- evidence of PPR so far has been reported in Africa south of the Equator, however, uncontrolled movement of livestock between countries is a potential danger to the spread of the disease.

The source of infection is the sick or sub-clinically infected animal and the virus is discharged in milk, saliva, urine or faeces. The disease spreads primarily by inhalation but the virus can also be acquired by ingestion and penetration through the conjuctival mucosa. Animals may acquire the infection by licking or muzzling each other. Bedding, feed and water troughs can be sources of infection. Goats are highly susceptible to PPR compared to sheep, and kids under one year are most susceptible. In West Africa, the dwarf breeds of goats have been found to be more susceptible than the Sahelian breeds. Presence of other diseases and other stress factors precipitate the occurrence of the disease. Severe outbreaks can occur when naive animals are moved into an endemic area. In West Africa, the incidence of PPR is reported to increase during the rainy season and during the cool harmattan winds.

Pathogenesis

After infection, the PPR virus multiplies in the regional lymph nodes which is followed by viraemia. The virus then infects and causes cytopathic changes in epithelial cells which are associated with the clinical signs and lesions observed.

Clinical features

Acute and subacute forms of PPR occur. The incubation period of acute PPR is about 7 days and the syndrome is characterised by severe depression, pyrexia, sneezing, dyspnoea, coughing, serous or mucopurulent occulo-nasal discharges which lead to matting of eyelids and blockage of nostrils. There may be crackling lung sounds which are clearly audible. Focal necrotic stomatitis, halitosis, anorexia, profuse mucoid diarrhoea or dysentery and sometimes tenesmus are prominent features. Abortion occurs and there may be superficial erosions on vulva or prepuce. Death of severely affected animals occur in about 7 days after the onset of clinical signs. Mortalities of 71-100 % are not uncommon.

Subacute PPR is the commonest form of the disease in sheep. Clinically, it resembles the acute syndrome of goats except that clinical signs are milder. Intercurrent infections with contagious ecthyma is common and secondary bacterial infection often aggravates the severity of PPR. Solid immunity develops in recovered animals and passive maternal immunity protects kids under 4 months.

Pathological features

The gross pathological picture include an emaciated and dehydrated carcass, soiled hind quarters, matted eyelids and nostrils are blocked with exudate. Focal necrotic lesions in the oral mucosa, pharynx, upper oesophagus, abomasum and small intestines are evident. Zebra striping of the large intestinal mucosa, oedema and congestion of mesenteric lymph nodes occur. The nasal cavity and larynx are filled with mucopurulent exudate and presence of froth in the trachea and pulmonary oedema are common features. Secondary bacterial infection results in bronchitis, tracheitis, atelectasis and interstitial pneumonia.

The histopathological picture includes lymphocyte depletion in lymphoid tissues, picnosis and karyorrhexis of lymphocytes in the cortex of lymph nodes. Multinucleated giant cells, eosinophilic intracytoplasmic and intranuclear inclusion bodies can be demonstrated in epithelial cells which also show hydropic degeneration and necrosis. The lamina propria of the small intestine is infiltrated with lymphocytes, macrophages and eosinophils. There is also necrosis of the epithelium of the abomasal and intestinal glands, villous atrophy and accumulation of necrotic debris in glandular pits. The alveoli and terminal bronchi are infiltrated with giant cells containing intracytoplasmic and intranuclear inclusion bodies. There may be hepatic necrosis and glomerulonephritis. The clinical pathology of PPR is dominated by leucopenia and lymphopenia.

Diagnosis

A tentative diagnosis of PPR is based on the epidemiology, clinical and pathological features. The virus in swabs from tissue excretions, buffy coat or tissue suspensions can be isolated by inoculation in primary kid or goat kidney cells. Chilled pieces of the spleen, lungs, lymph nodes and gut mucosa can transported to the laboratory for virus isolation.

Inoculation of tissue suspensions from affected or suspected cases in susceptible animals elicits a severe disease in goats, a mild disease in sheep and a subclinical disease in cattle.

The virus neutralisation test, ELISA, complement fixation test, immune electrophoresis, monoclonal and polyclonal antibodies detection are the common serological methods employed in the diagnosis of PPR. Serum neutralisation test and DNA probes are used to differentiate PPR from rinderpest. Agar gel immunodiffusion, counterimmunodiffusion and DOT-ELISA are used to demonstrate virus antigens from ocular and nasal discharges, pharynx, faeces and lymphoid tissues.

The differential diagnosis of PPR include rinderpest, contagious ecthyma, goat/sheep pox, Nairobi sheep disease, blue tongue, CCPP, pneumonic pasteurellosis, salmonellosis, colibacillosis and parasitic gastro-enteritis. PPR and rinderpest are differentiated by serum neutralisation test. In contagious ecthyma, lesions in the alimentary tract are not common except in secondary infections. Nairobi sheep disease is not very severe in goats and no oral lesions are observed. Furthermore, NSD is restricted to areas where the vector tick, R. appendiculatus is found. CCPP is primarily a disease of the respiratory system affecting goats and no mucosa lesions or diarrhoea are observed in uncomplicated cases. FMD and bluetongue can be differentiated by close examination of the feet lesions and diarrhoea is not a feature of these diseases. Salmonellosis and colibacillosis can be differentiated by isolation of the causative bacteria whereas, in parasitic gastroenteritis, demonstration of high egg or worm burdens precludes PPR.

Control

Treatment of secondary bacterial pneumonia using broad spectrum antibiotics may be effective in the early stages of the disease. A hyperimmune serum produced from cattle hyperimmunised against rinderpest can be used. Fluid therapy is recommended to alleviate the effects of diarrhoea/dysentery. Good nursing of the sick animals may facilitate recovery. Control of the disease can be achieved by preventing the contact between susceptible animals and clinically or sub-clinically affected ones. Affected animals should be isolated and infected premises disinfected. If an outbreak occurs, quarantine measures should be imposed and supported by vaccination of the population at risk.

Vaccination using tissue culture rinderpest vaccine starting at 3-4 months of age is the commonest method of control of PPR in endemic areas. Although the PPR homologous vaccine and attenuated tissue culture vaccines are not widely, used they are showing promising results.

RINDERPEST

This is a disease of ruminants characterised by fever, erosive stomatitis, severe diarrhoea or dysentery, dehydration and death. It is caused by a rinderpest virus of the genus Morbillivinis and family Paramyxoviridae which closely resembles the PPR virus. The epidemiology and pathogenesis of rinderpest in sheep and goats is similar to that of PPR. Small ruminants may suffer an inapparent, subacute or acute form of rinderpest. However, the mild form is more common in field infections. The acute disease is characterised by fever, depression, inappetence, arched back, serous nasal and lacrimal discharges which may become mucopurulent and may block the nostrils or mat the eyelids. In late stage, a foetid diarrhoea may occur. Death may occur in 6-7 days after the onset of the clinical disease although recovery may occur within 2 weeks. The subacute disease is mainly characterised by transient fever.

Congestion of the crest of the longitudinal folds in the rectal mucosa result in characteristic zebra striping lesions. The diagnostic methods are similar to PPR. The two viruses can be differentiated by virus neutralisation test and monoclonal antibodies.

CONTAGIOUS ECTHYMA

Contagious ecthyma (contagious pustular dermatitis or orf) is a highly infectious disease of goats and sheep characterised by pustular and scabby lesions on the muzzle, commissures of the lips and nostrils. The disease is caused by a contagious ecthyma virus of the genus Parapoxvirus and family Poxviridae and, it also affects man.

Epidemiology

Contagious ecthyma is endemic in most African countries. The sero-prevalence of the disease in goats has been reported to be 3.0-19.0 % in the humid zone of Nigeria, 1.6 % in Mali, 14.0 % in Kenya and 14.0% in Tanzania. The disease has also been encountered in small ruminants in Sudan, Ethiopia, Uganda and Malawi.

All breeds of goats and sheep are affected with contagious ecthyma but the disease is chiefly confined to kids and lambs of 3-6 months old. The source of infection is the affected animal or contaminated inanimate objects and, transmission occurs by contact. The contagious ecthyma virus cannot penetrate the intact skin, hence abrasions of the skin caused by spiky plants, hypodermic needles and surgical operations facilitate the penetration of the virus. The contagious ecthyma virus is highly resistant to desiccation and can survive in dry scabs for years.

Pathogenesis

Initial multiplication of the virus occurs at the site of primary infection. Viraemia develops and is followed by subsequent localisation of the virus in the epithelial cells of the Malphigian layer of epidermis of the target organs especially the head, extremities and udder. Cells of the genital tract, lungs and liver can also be infected. The cytopathic effects of the virus in the infected cells include the development of papules, vesicles, pustules and scabs.

Clinical features

Contagious ecthyma is characterised initially by appearance of erythema which later develop into papules and pustules. When the pustules rupture, the pus forms a thick layer of grey crust and later on result in discrete and thick scabs which are crumbly but adherent to the underlying tissues. Lesions usually begin at the oral commissures and then spread to the lips, muzzle, nostrils, ears and sometimes to the buccal and nasal mucosae. Lesions may also occur on the coronet, interdigital cleft, skin of the udder and teats, vulva, preputial orifice, perineal area, thighs and axillae. Adjoining scabs coalesce and form continuous plaques. Fissures which occur between scabs cause soreness. The lesions may become malignant. Invasion of the virus into respiratory and alimentary tracts may occur leading to pneumonia and gastroenteritis. Morbidity may reach 70-90 % but mortality is rare although it may be considerable if secondary bacterial infection occurs. Spontaneous recovery occurs in 2-3 weeks. Lesions along the alimentary tract interfere with feeding and result in considerable weight loss and emaciation.

Pathological features

At gross pathology, contagious ecthyma is characterised scabby lesions on the affected areas and in malignant cases there are ulcerative lesions in the nasal cavity, trachea, oesophagus, abomasum and small intestine. Inflammation and oedema of the affected dermis is evident in histopathological sections. Parakeratosis, acanthosis, and ballooning degeneration occur in keratinocytes. Nuclear pyknosis and oesinophilic intracytoplasmic inclusion bodies in the affected cells are common features. The virus can be demonstrated in ultra-thin sections of the affected tissue by examination under electron microscope.

Diagnosis

Clinical signs and lesions of contagious ecthyma are quite characteristic. Confirmation of the disease can be achieved by electron microscopy, tissue culture and transmission experiments. Complement fixation, virus neutralisation and gel diffusion tests are the common serological methods used in the diagnosis of the disease.

Contagious ecthyma has to be differentiated from dermatophilosis, bluetongue, goat/sheep pox and ulcerative dermatosis. Lesions caused by dermatophilosis are small, light and yellowish in colour and can be easily removed unlike the thick greyish black tenacious scabs of contagious ecthyma and, distortion of the lips and muzzle is not observed in dermatophilosis. Dermatophilosis can be confirmed by demonstration of Gram-positive mycelial-like D. congolensis in impression smears made from the under surface of the lesions. Bluetongue is commonly associated with the presence of vector midges (Culicoides spp) and is characterised by a systemic reaction; excoriation, ulceration and necrosis of the lips and buccal mucosa; lesions in the coronet and high mortality which are not features of contagious ecthyma. The presence of distinctive pox lesions, a febrile reaction and high mortality are features that can be used to distinguish goat/sheeppox from contagious ecthyma. Ulcerative dermatosis is manifested by pyo-ulcerative lesions with thin, brown and bloody scabs. However, isolation and characterisation of the causative viruses is important in order to confirm the above diseases.

Control

Antiseptic ointments such as Lugol's iodine are used to protect secondary bacterial infection on lesions. Parenteral antibiotics are useful in the treatment of systemic secondary bacterial infections. Good nursing such as provision of soft diet to severely affected cases may enhance recovery. Local autogenous live-virus vaccines prepared from vesiculo-pustular material are effective. Attenuated virus vaccines are commercially available. In endemic areas, annual vaccination of 6-8 week kids or lambs is recommended.

GOAT AND SHEEPPOX

This is an acute, febrile and highly contagious disease of goats and sheep which is characterised by fever, cutaneous nodular or visceral eruptions. Goat and sheep pox are caused by the goat and sheep pox viruses of the genus Capripoxvirus and family Poxviridae. The viruses closely resemble each other although they are antigenically different. A Kenya sheep and goat pox virus which is closely related to the lumpy skin disease virus also causes the disease in both goats and sheep.

Epidemiology

Goat and sheep pox is endemic in some sub-Saharan countries especially north of the Equator. Morbidity rates of 25 % in Nigeria, 18 % in Mali and 83% in Tanzania have been reported. Information regarding the occurrence of goat/sheeppox in southern Africa is lacking.

Goat and sheep pox affects animals of all ages although kids and lambs are most susceptible. The disease is highly contagious and transmission occurs mainly by inhalation but animals can also be infected by drinking contaminated milk or by direct contact. Cuts and abrasions on the skin facilitate entry of the virus into the body. The virus can be spread mechanically by insects, birds and personnel. Transplacental transmission has been demonstrated. Congregation of animals in communal grazing lands, markets, dips and the dry and dusty environments are favourable for the transmission of the disease because the virus can be excreted through nasal and conjuctival discharges. Such husbandry conditions were considered to be important epidemiological factors for the outbreak of the disease in northern Tanzania in 1983.

Pathogenesis

Following infection the virus is carried through the lymphatic system to the blood circulation. Viraemia develops and is followed by localisation of the virus in the skin and mucous membranes and appearance of pox lesions.

Clinical features

The incubation period of goat/sheeppox is about 2 weeks. The disease is more severe in sheep than goats and in young than adult animals. In sheep, the disease is characterised by depression, pyrexia (40-41 °C), anorexia, laboured breathing, ocular and nasal discharges. Cutaneous nodules normally appear on hairless areas of the body such as lips, nostrils, udder, vulva, scrotum and under the tail but they may also occur on hairy areas. Severely affected animals may die before pox lesions appear. The nodules progress through vesicles, pustules and finally become scabs. Severe erosive and ulcerative plaques may be found on the buccal, oesophageal and tracheal mucosae. Lesions in the alimentary tract may lead to diarrhoea whereas, those in the genital tract can cause abortion. A 70% morbidity of sheep pox is common and mortality varies from 5% to 50 %. Secondary bacterial pneumonia and mastitis are common sequelae.

In goats, lesions occur mainly on lips, eyes, scrotum, udder and medial aspects of the limbs. Severe infections in goats may extend to the neck, thoracic and abdominal organs as hard intracutaneous nodules. A 51 % case fatality in goats was reported in an outbreak of goatpox in Nigeria in 1982. Recovered animals become immune for life.

Pathological features

At necropsy, reddish circular nodules or confluent plaques are observed on the skin. Marked greyish-white subpleural nodules are present in the lungs. The superficial lymph nodes are swollen and oedematous. Erosions and ulcers may be present in the mouth pharynx, oesophagus and trachea. There may also be haemorrhagic gastroenteritis.

Histopathologically, there is hyperplasia of epidermal cells, local oedema and cell degeneration or coagulative necrosis. Vasculitis and thrombosis can also be present. Bronchitis and alveolitis may be observed in the lungs. Intracytoplasmic inclusion bodies are observed in infected cells. The presence of vacuolated nuclei in infected cells is highly diagnostic.

Diagnosis

The pox lesions are characteristic and highly suggestive of the disease. The demonstration of eosinophilic intracytoplasmic inclusion bodies in cells which show a clear vacoule is pathognomonic. In dead animals, the virus can be isolated from the skin and mouth lesions, lungs and liver tissue suspensions by inoculating in lamb kidney cells or other cell lines whereas, in live animals the virus can be isolated in blood collected during the viraemic stage of the disease. Electron microscopy of the negatively stained preparations of skin and mucous membrane sections show typical infected cells. Virus neutralisation and indirect fluorescent antibody tests are the serological methods commonly used in the diagnosis of goat and sheeppox.

Goat and sheeppox has to be differentiated from contagious ecthyma, FMD, blue tongue, peste des petits ruminants and mange. The pox lesions are quite diagnostic and are different from those observed in contagious ecthyma. The diseases can also be differentiated by electron microscopy or serologically. Foot lesions are used to distinguish goat/sheeppox from FMD. PPR and bluetongue can be distinguished by their oral lesions and mange can be confirmed by demonstration of mange mites on skin scrapings.

Control

No treatment is available for the disease. Goat/sheep pox is a notifiable disease and quarantine measures should be imposed immediately if an outbreak occurs to minimise its spread. The affected flock should be destroyed and infected premises properly disinfected. Commercially available single- or mixed-virus cell culture-derived vaccines are used to vaccinate animals in countries where the disease is endemic.

NAIROBI SHEEP DISEASE

Nairobi sheep disease (NSD) is a tick-borne infection of sheep and goats which is characterised by fever, nasal discharges, dyspnoea, haemorrhagic gastroenteritis, abortion and high mortality. It is caused by a Nairobi sheep disease virus of the genus Nairovirus and family Bunyaviridae.

Epidemiology

The disease is endemic among goat and sheep populations in East and Central Africa. It has also been reported to occur in Ethiopia, Somalia, Zaire and Mozambique. The disease is considered to have a more wider serological distribution in Africa, than the available reports.

All breeds of sheep and goats are affected with Nairobi sheep disease. The disease is transmitted by R. appendiculatus ticks. Both transstadial and transovarial modes of transmission occur. Other ticks considered to be involved in the transmission of the disease include R. pulchellus, R. sinus and A. variegatum. Ticks can harbour the virus for a long time. The distribution of Nairobi sheep disease in East Africa is closely linked with the distribution of R. appendiculatus and the incidence of the disease increases with increased tick activity. Animals in endemic areas tend to be immune but naive animals introduced in such areas suffer a severe disease. Outbreaks may also occur when there is a breakdown of tick control measures. Goats are less susceptible than sheep and adult sheep and goats suffer a more severe disease than lambs or kids.

Pathogenesis

The virus is introduced into the host's through bites infected ticks. Viraemia develops and is followed by localisation of the virus in the liver, spleen, lungs and other organs of the reticuloendothelial system. The NSD virus has a particular predilection in the vascular endothelial cells in which the cytopathic effects include endothelial swelling, oedema and necrosis. The necrosis of the vascular endothelial cells of the mucous membranes of the abomasum, small intestine, gall bladder and female genital tract results in congestion, haemorrhagic and catarrhal inflammation and finally desquamation of the necrotic epithelium.

Clinical features

The incubation period for NSD is about 4-6 days. The disease is characterised clinically by fever (41-42 °C), dullness, anorexia, mucopurulent and blood-stained nasal discharges, ocular discharges, conjunctivitis, dyspnoea and groaning. Straining, severe, mucoid and foetid diarrhoea or dysentery and, abortion occur. Deaths may occur 3-9 days after the onset of the acute disease or after 11 days in less acute cases: The clinical signs are less severe in goats. The case fatality rate may reach 90 %.

Pathological features

At necropsy the carcass is dehydrated with soiled hind quarters. Dry crusts are observed on the nostrils and may occlude the nasal passages. The mesenteric lymph nodes are enlarged and oedematous. There may be splenomegaly and swelling of superficial lymph nodes. There is marked haemorrhagic inflammation of the abomasal and intestinal mucosa which present as multiple haemorrhages especially on the longitudinal folds of the abomasum, distal ileum, ileo-caecal valve, caecum and proximal colon. Haemorrhages on the colon and caecum appear as longitudinal striations or lines of ecchymoses extending from the cranial part of the caecum to the rectum. Haemorrhages also occur in the subserosa of the gall bladder, below the kidney capsule and, in the genital and lower respiratory tracts. Pulmonary congestion and alveolar oedema may be evident. The heart becomes pale, flaccid and contains unclotted blood. Epicardial petechiae and endocardial ecchymoses are present. The bone marrow of the long bones become gelatinous and bright red. Dermal haemorrhages are evident in the foetus of dead pregnant ewes.

The histopathological picture is characterised by myocardial and glumerulo-tubular necrosis, degeneration of tubular epithelium, accumulation of hyaline material and cellular casts in the tubuli. Coagulative necrosis of the gall bladder may occur.

Diagnosis

The clinical and pathological features of Nairobi sheep disease are highly suggestive. Recent introduction of animals in an endemic area is an important epidemiological factor to be considered. The liver, lungs, spleen, mesenteric lymph nodes contain high titres of the virus and the virus may be isolated by inoculation of the affected tissue suspensions in several cell lines and infant mouse brain. The virus can also be isolated from whole blood or serum taken from animals during the febrile stage of the disease. Inoculation of susceptible sheep with suspensions from the affected organs or blood and subsequent development of clinical disease is the most sensitive method of diagnosis. Viral antigens may be detected in the spleen, lung tissue and mesenteric lymph nodes using NSD-virus specific hyperimmune serum. Complement fixation, virus neutralisation, agar gel immunodiffusion, ELISA, indirect haemaglutination and immunofluorescence tests are common employed in the serological diagnosis of the disease.

The differential diagnosis of Nairobi sheep disease include peste des petits ruminants, rinderpest, Rift Valley fever, heartwater and salmonellosis. Virological and serological tests are necessary to differentiate NSD from the other viral diseases. Hepatic necrosis which occurs in RVF is diagnostic. However, inoculation of blood or tissue suspensions from suspected animals into susceptible sheep and subsequent development of a clinical disease is considered to be the most sensitive method for confirmation of NSD. Demonstration of C. ruminantium in the cytoplasm of endothelial cells of blood vessels or in Giemsa-stained lymph node or brain biopsy smears will confirm heartwater. Salmonellosis can be confirmed by isolation and characterisation of Salmonella spp from the intestinal lesions or contents.

Control

No effective treatment is available for NSD. Fluid therapy is recommended in diarrhoeic or dysenteric cases. Sick animals should be isolated and well nursed. Control of ticks by dipping or spraying of susceptible flocks can reduce the transmission and incidence of the disease. Vaccination of susceptible risk groups such as naive animals before being introduced into endemic area is recommended. Modified live-virus or inactivated-virus vaccines are available. However, vaccination is very not commonly practised in endemic areas because animals tend to be immune and losses sporadic.

BLUETONGUE

This is an arthropod-borne disease of ruminants particularly sheep which is characterised by catarrhal stomatitis, haemorrhages, enteritis, cyanosis of the oronasal cavity, laminitis, oedema of the head and neck and, torticollis. Bluetongue (BT) is caused by a blue tongue virus of the genus Orbivirus and family Reoviridae.

Epidemiology

Blue tongue is endemic among sheep and goat populations in Africa. Reports of outbreaks are available from Ghana, Nigeria, Guinea, Kenya and South Africa. Biting midges (Culicoides spp) are the principal vectors of the disease and Culicoides imicola is considered to be the main species involved in the transmission of the disease in Africa. The infected midges can remain infective for life. Mechanical transmission by the sheep ked (Mellophaga ovinus), ticks (A. variegatum and Ornithodorus coviaceus) and blood sucking flies such as Stomoxys spp and Tabanus spp may also occur. The incidence and distribution of the disease is related to the environmental and climatic factors which affect the survival and distribution of the vectors. Sheep are more susceptible than goats and young animals are more severely affected that adult ones. Introduction of naive animals into an endemic area may result in an outbreak of a severe disease. Recovered sheep harbour the virus for some months. Cattle and wild animals may acts as reservoirs of the virus.

Pathogenesis

Following infection the virus is carried through the lymphatic vessels to the blood circulation and viraemia develops. Replication of the virus also occurs in lymphoid tissues and is followed by localisation of the virus in the vascular endothelial cells resulting in the destruction of the vessel walls. Haemorrhages, exudation, oedema, stasis and occlusion of the blood vessels give rise to hypoxia and other lesions epithelial lesions. It has been observed that exposure of the affected animals to sunlight and other stress factors exacerbates the disease. The presence of the virus in semen causes structural changes in the spermatozoa. The virus can cross the placental barrier/ invade the foetus and cause death because of hepatic necrosis and suppression of the foetal haemopoietic system.

Clinical features

Acute and chronic forms of the disease occur. The acute disease is characterised by fever (41-42 °C); hyperaemia of the buccal mucosa, muzzle, eyes, ears; increased salivation (which may become blood-stained due to excoriations of the buccal mucosa); conjunctivitis with ocular discharges and serous, mucopurulent or blood-stained nasal discharges which form crusts that may interfere with breathing. Oedema of the tongue, lips, face, eyelids, ears and submandibular region occur. Erosions and petechial haemorrhages of the muco-cutaneous junction of the lips, muzzle, buccal, nasal and conjuctival mucosae are evident. There is anorexia, cyanosis of the tongue which may protrude out of the mouth (blue tongue), necrosis of the buccal mucosa, foetid breath, ruminal stasis and occasionally vomiting and terminal diarrhoea or dysentery.

Foot lesions are characterised by hyperaemia of the coronary band, warm and painful feet, reluctance to move or severe lameness which may be manifested by walking on the knees. A dark-red to purple band in the skin above the coronet is diagnostic. Later on the hoof sloughs off. Muscle degeneration and cachexia are common features with degeneration of the neck muscles resulting in torticollis. The clinical signs are less severe in endemic areas.

Pathological features

The post-mortem picture is characterised by mucosal and skin lesions, generalised oedema, hyperaemia, haemorrhage and necrosis of the skeletal and cardiac muscles. Petechial or ecchymotic haemorrhages at the base of the pulmonary artery is a distinctive feature.

Haemorrhages and hyaline degeneration of muscles occur. Copious froth in the trachea, hydrothorax and oedema of the lungs are common features. Aspiration pneumonia may be observed. The nasal, pharyngeal and tracheal mucosae become petechiated and oedematous. Hyperaemia, petechiation, erosion or ulceration on of papillae of the fore stomachs, rumenal pillars, reticular folds, oesophageal groove and abomasal mucosae may be evident. Catarrhal or haemorrhagic enteritis, hyperaemia, oedema and cyanosis of the mucous membranes are features. The inside of the lips, dental pads, cheeks and tongue become excoriated and ulcerated. Pharyngeal, cervical and thoracic lymph nodes become oedematous and swollen. There may be splenomegaly, epicardial haemorrhages and hydropericardium with fibrin clots. Generalised hyperaemia and malformations are observed in foetuses.

Histopathologically, there is hyaline degeneration, necrosis and mineralisation of muscle fibres. The muscles are infiltrated with neutrophils, macrophages and lymphocytes. Lesions in the foetus include generalised hyperaemia, focal haemorrhages and symmetrical bilateral leucoencephalomalacia.

Diagnosis

Epidemiological, clinical and pathological features may be suggestive of the disease. The virus can be isolated from blood or scarified tissue suspensions by intravascular inoculation in 10-12 days old embryonated hen's egg or in mouse brain after passage of the virus in the hen's egg. The virus can also be isolated in BHK21, Vero and mouse L-cells. Inoculation of blood from suspected animals into susceptible sheep and subsequent development of a clinical disease is diagnostic. Fluorescent antibody test, indirect or competitive ELISA and gel immunodiffusion are the serological methods used in the diagnosis of bluetongue. Virus neutralisation and plaque reduction or plaque inhibition tests are used for serotyping. DNA probes are used for diagnosis in advanced laboratories.

Bluetongue should be differentiated from foot and mouth disease, foot rot, polyarthritis, contagious ecthyma, sheep/goat pox, heartwater and pulpy kidney disease. Unlike FMD, bluetongue has a seasonal pattern of distribution which is closely related to the activity of Culicoides spp and, cyanosis of the mucous membranes is not a feature of FMD. Goat/sheeppox has characteristic pox lesions and is highly fatal compared to bluetongue. Contagious ecthyma and ulcerative dermatosis have characteristic lesions. The reproduction of a clinical disease followed by production of neutralising antibodies and resistance to subsequent challenge by susceptible sheep inoculated with blood from suspected cases is diagnostic. The virological and serological methods described above are also useful to differentiate bluetongue from other viral diseases. Heartwater, foot rot, pulpy kidney disease and polyarthritis can be confirmed by demonstration of the causative organisms.

Control

There is no effective treatment for blue tongue. Good nursing of sick animals is recommended. Control can be achieved by restriction of entry of animals from endemic areas. Control of the midges and blood sucking insects will reduce the transmission of the disease. In endemic areas, it is recommended to vaccinate the susceptible stocks one month before the predicted occurrence of the disease. A polyvalent attenuated virus vaccine is produced in South Africa. A modified live virus vaccine is also available. Vaccination of ewes between 4-8 weeks of pregnancy has been associated with deformities in lambs.

RIFT VALLEY FEVER

Rift Valley Fever (RFV) is a mosquito-borne peracute or acute disease of ruminants which is characterised by fever, necrotic hepatitis, haemorrhages, abortion and high mortality in young animals. The disease, which is also a serious zoonosis is caused by a Rift Valley fever virus of the genus Phlebovirus and family Bunyaviridae.

Epidemiology

RVF is widespread in Africa and serious outbreaks have been encountered in both animals and man in Egypt, Sudan, Kenya, South Africa, Zimbabwe, Zambia and Senegal. The disease has also been encountered in Guinea, Nigeria, Burkina Faso, Gabon, Central African Republic, Zaire, Uganda, Tanzania, Mozambique and Angola.

Sick or carrier animals are the sources of infection. The virus is transmitted by mosquitoes and Aedes mcintoshi is considered to be the main vector. Aedes dentatus, Culex spp and Anopheles spp can also transmit the disease. Hyalomma truncatum ticks have also been incriminated to play part in the transmission of the disease. The incidence of the disease increases with increase in vector activity. The disease is common in areas with dense vegetation and heavy rainfall which are favourable for the multiplication of the mosquitoes. It has been observed that floods may be followed by outbreaks. Body secretions except milk do not contain the virus. The virus may also be present in aborted foetuses. Sheep are more susceptible than goats and lambs and kids are more severely affected than adult animals. Man is infected by penetration of the virus through abrasions on the skin or mucosa when handling infective materials or by inhalation of infective aerosols.

Pathogenesis

After injection of the virus in tissues, initial replication occurs at the site of infection followed by viraemia and localisation of the virus in the target organs especially the liver, spleen and kidneys. Further replication of the virus in these organs amplifies the viraemia. Severe destruction of the hepatic cells which is caused by the cytopathic effects of the virus or immunopathological mechanisms results in hepatic insufficiency. Damage to the blood vessel walls causes vasculitis and widespread haemorrhages in the affected tissues. Abortion is caused by placentitis or foetal death following invasion of virus to the gravid uterus.

Clinical features

The incubation period of RVF in neonatal lambs is 24-36 hours. The disease is characterised by high fever (41°C), listlessness, rapid respiration, abdominal pain, staggering gait and recumbency. Death in severely affected animals can occur 36 hours after the onset of clinical signs. Mortality in neonatal lambs and kids may be over 90%.

Lambs and kids over 2 weeks old and adult sheep and goats are much less susceptible but may develop a peracute, acute or inapparent infection. The acute disease, with an incubation period of 1-3 days is the commonest form of field infection. It is characterised by high fever (up to 42°C) which may last for 1-4 days, anorexia, weakness, listlessness, staggering gait and increased respiration. There may also be melaena or diarrhoea and blood-stained mucopurulent nasal discharges. The ingesta may be regurgitated. Jaundice is commonly observed in adult animals. Abortion of autolysed foetuses at any stage of pregnancy may occur. Salpingitis, purulent metritis and placental retention usually occur and are followed by a high rate of infertility. Congenital anomalies may occur in lambs or kids born from infected dams. During outbreaks the mortality may reach 50% in goats and 60% in sheep while an abortion rate of 80-100% has been reported.

Pathological features

Peripheral and visceral lymph nodes are enlarged, oedematous and petechiated. The liver shows a bright yellow or yellowish-brown discoloration with congestion and haemorrhages in the parenchyma. Greyish-white necrotic foci occur throughout the liver parenchyma (mottled appearance). Fibrinous peri-hepatitis and haematomas may be evident. The gall bladder wall becomes haemorrhagic and oedematous. Petechial or ecchymotic haemorrhages are observed on the abomasal mucosa and in neonatal lambs chocolate-brown blood is found in the abomasum. There are also widespread subcutaneous, serosal and visceral haemorrhages. The body cavities may contain blood-tinged, fluid and in lambs, haemoperitoneum may be observed. The lungs are congested and oedematous. The hepatic lesions are also present in aborted foetuses.

Severe coagulative centrilobular necrosis with the loss of the hepatic architecture is the most characteristic histopathological feature. The necrosis is diffuse in lambs and multi-focal in adult animals. Some hepatocytes contain acidophilic intracytoplasmic and oval or rod-like intranuclear inclusion bodies. Hyaline material accumulates in the cytoplasm of necrotic hepatocytes. In the new-born lambs or kids there is pyknosis and karryorrhexis of lymphocytes, cloudy swelling and hydropic degeneration of epithelial cells of the convoluted tubules and glomeruli. Multi-focal necrosis and haemorrhage of the adrenal cortex may also be evident. Nephrosis with severe tubular degeneration, hyaline casts in the tubular lumen and fibrin deposits in the glomeruli are features of the disease in adult animals. The clinical pathology is characterised by severe leucopenia.

Diagnosis

The epidemiology, clinical signs and post mortem features may be suggestive of the disease. Histopathological features are pathognomonic. The virus can be isolated from blood, plasma or serum collected from the affected live animals during the viraemic phase of the disease or from the liver, kidneys, spleen, lymph nodes and the heart of dead animals by inoculation in Vero cells; BHK 21; mosquito line cells; primary calf, lamb and goat kidney or testis cells. The virus may also be isolated from suckling and weaned hamster inoculated intraperitoneally or intracerebrally. Viral antigens in tissue suspensions may be detected by immunofluorescence, complement fixation, immunodiffusion and in tissue sections by immunoperoxidase staining. ELISA, virus neutralisation and reverse haemagglutination tests are used to detect viral antigens in serum. Antibodies can also be detected by complement fixation, virus neutralisation, immunodiffusion, ELISA, radio-immunoassay and by haemagglutination inhibition tests.

The characteristic hepatic lesions distinguishes RVF from other diseases with similar clinical signs such as Wesselsbron disease which is common in southern Africa, peste des petits ruminants, Nairobi sheep disease, enterotoxaemia and plant poisoning. In addition, abortion and mortality rates observed in RVF are higher than in Wesselsbron disease. Stomatitis and buccal mucosal lesions which are features of PPR are not observed in RVF. The occurrence of NSD is closely associated with distribution and activity of R. appendiculatus ticks. A recent history of grazing on poisoning plants will help to different RVF from plant poisoning. Clostridial enterotoxaemia can be confirmed by isolation and characterisation of the causative bacteria or fluorescent antibody test. Abortion caused by brucellosis and salmonellosis can be confirmed by isolation and identification of the causative bacteria. Other serological and microbiological tests applicable to the different diseases should be carried out to confirm them.

Control

There is no effective treatment for the disease. Control can be achieved by restriction of entry of animals from endemic into non-endemic areas. Vaccination of newly introduced animals is recommended. The modified live Smithburn vaccine is cheap and stimulates a long lasting immunity but, the organisms can revert to virulence and induce abortion or teratology of the foetus. The formalin-inactivated cell culture vaccine is expensive and elicits a short lasting immunity but does not induce abortion or teratology of the foetus. Control of mosquitoes by spraying with insecticides and destroying their breeding habitats can reduce the transmission and incidence of the disease in endemic areas.

OVINE PROGRESSIVE PNEUMONIA (MAEDI/VISNA)

This is an insidious disease of sheep mainly characterised by progressive weight loss and dyspnoea. It is caused by an ovine progressive pneumonia virus of the subfamily Lentivirinae and family Retroviridae.

Epidemiology

The disease has been reported to occur world-wide. It is mainly encountered in adult sheep over 3 years of age. Housing and close confinement facilitate transmission of infective droplets. The virus can also be transmitted mechanically by biting insects, fleas, lice and surgical equipment. Infection through contaminated water may occur.

Pathogenesis

The pathogenesis of the disease is not well elucidated but it has been demonstrated experimentally that after infection the virus multiplies in the regional lymph nodes. Viraemia develops and the virus spreads to the target organs.

Clinical features

The course of the disease takes about 3-8 months but it may be shortened when animals are exposed to stress factors such as inclement weather, poor nutrition and intercurrent diseases especially Pasteurella spp pneumonia. The affected animals lag behind the flock, the nostrils are flared and inspiration is associated with rhythmic jerking of the neck. There may be nasal discharges or coughing. The animal progressively losses condition although it remains alert and maintains its appetite. Severe dyspnoea which is exacerbated by exercise develops in arid the animal spends most of the time lying down. Chronic suppurative arthritis of the carpal and tarsal joints and mastitis are often associated with OPP.

A nervous form of the syndrome (visna) may occur. It has a shorter incubation period than the pulmonary syndrome and it is characterised initially by weakness of the hind limbs, straggling and stumbling or falling without any apparent cause. Progressive weight loss and trembling of the facial muscles may occur. There may also be ataxia, paresis, paraplegia and quadriplegia. There is no fever and the animal remains alert.

Pathological features

At necropsy, OPP is characterised by a marked extensive consolidation of the lungs, multi- focal grey foci on the surface and marked enlargement of the bronchial and mediastinal lymph nodes. At histopathology, there is hyperplasia of the fibrous tissue and muscles of the alveolar septa and, mononuclear cell infiltration.

In visna, there may be myogenic muscle atrophy and minimal lung abnormalities but the histopathological picture is dominated by a de-myelinating leucoencephalomyelitis, mononuclear cell infiltration, perivascular cuffing and neuronal necrosis. Demyelination and the malacic lesions are scattered throughout the central nervous tissue.

Clinical features and pathological features may support a provisional diagnosis of the disease. ELISA, complement fixation, gel diffusion and plaque reduction tests are used for the serological diagnosis of the disease. Monoclonal antibodies are also employed in specialised laboratories. The differential diagnosis of OPP include chronic bacterial, fungal and mycoplasmal pneumonia and, parainfluenza- or adenovirus infections. The neurological form of the disease can be differentiated from hypomagnesaemia, copper, selenium or and vitamin E deficiency by consideration of the feeding history and clinical pathology. Cl. perfringens enterotoxaemia, listeriosis and brain abscesses can be confirmed by demonstration of the causative bacteria and, rabies can be differentiated on the basis of history and confirmation by serological tests. In neonatal animals, polyarithitis caused by Chlamydia spp and bacterial infection through the umbilicus can be differentiated by isolation of the causative organisms. Mastitis caused by Staphylococcus ssp and Streptococcus spp can be differentiated by isolation of the bacteria. Serological tests are also used. Control of the disease is achieved by culling of clinically affected animals or positive reactors on serological tests.

Other viral infections of sheep and goats such as pulmonary adenomatosis (jaagsiekte) and caprine arthritis encephalitis are not common in sub-Saharan Africa, but there is a danger for their introduction with exotic breeds of goats and sheep from endemic other area.

RABIES

This is a highly fatal disease of the central nervous system affecting animals and man which is characterised by abnormal behaviour and paralysis. It is caused by a neurotropic rabies virus of the genus Lyssavirus and family Rhabdoviridae.

Epidemiology

Rabies is endemic in Africa and reports of fatal human and animal cases of rabies are available from most countries. Different antigenic variants of the rabies virus have been isolated from different geographical locations. The rabies virus is sensitive to most disinfectants, heat and irradiation. Animals or human beings become infected through bite wounds caused by a rabid animal. For example, stray dogs and cats are the major sources of livestock and human rabies in Tanzania. Infection may also occur by inhalation of infective aerosols. Wild animals such as foxes, wolves, and vampire bits can be reservoirs and source of the disease to livestock or human beings.

Pathogenesis

Infective saliva is deposited in the wound or abrasions during a bite by a rabid animal. Initial replication of the virus occurs in the muscle or subepithelial tissue cells at the site of infection. When a sufficient concentration of the virus is reached it binds to acetylcholine or other receptors at the motor or sensory nerve endings. The virus passively moves centripetally along the peripheral nervous system to the spinal cord and the brain. The presence of the virus in the nervous system results in nervous dysfunction. Replication of the virus in the limbic system is associated with the furious form of the disease. Further replication and spread of the virus to the neocortex causes the dumb form of the disease. After replication in the central nervous system the virus spreads centrifugally to other tissues such as adrenal cortex, pancreas and salivary glands. The furious form of the disease coincides with a high concentration of the virus in the saliva.

Clinical signs

The incubation period is about 14-90 days but sequestration of the virus in striated muscles before ascending through the peripheral nervous to the central nervous system may delay the onset of clinical signs. The clinical signs of rabies in different animals species are similar with only slight variations. Two clinical syndromes; furious and paralytic rabies progressing through the prodromal, excitation and paralytic phase occur. The prodromal phase is characterised by the animal refusing to eat or drink and drop in production.

The furious syndrome is more common in goats and is characterised by aggressiveness and continuous bleating while in sheep, the paralytic form of the disease which is characterised by inability to swallow, excessive salivation, posterior paralysis, convulsions and respiratory arrest. Some animals, however, may show aggressiveness and sexual excitement. In the terminal stages the animal becomes comatose and dies within 5-7 days after the onset of clinical signs.

Pathological features

There are no significant gross features associated with the disease and at histopathology there may be a moderate mononuclear cell infiltration.

Diagnosis

A history of being bitten by a rabid animal and the clinical signs may support a presumptive diagnosis of the disease. A rabies-suspected animal should be confined and the clinical course closely monitored. If the animal survives for more than 10 days then the presence of rabies is ruled out. In live animals the virus may be isolated from saliva or brain biopsies. Sometimes the virus can be demonstrated in impression smears made from the cornea. In dead animals, the presence of intracytoplasmic inclusion bodies (Negri bodies) in neurones of formalin-fixed and paraffin-embedded brain tissue sections particularly in the cerebellum and brain stem is pathognomonic. The fluorescent antibody test has been used to confirm the disease for many years. Intracerebral inoculation of suckling or weaning mice with 10% brain suspensions from a suspected animals will result in nervous signs and presence of the virus in cells in 14-18 days. The virus can be isolated by inoculation of tissue suspensions onto monolayers or mouse neuroblastoma cells after incubation for 1-4 days, and then confirmed by fluorescent antibody test. ELISA is also a reliable method of diagnosis especially when facilities for fluorescent antibody test are lacking. Other serological tests include radioimmunossay, passive haemagglutination and indirect fluorescent antibody tests radioimmunossay. Brain material for laboratory examination should be kept in cold packs and transported in crush resistant containers.

Rabies should be differentiated from other disease manifested by nervous signs such as enterotoxaemia and pregnancy toxaemia and choke. Enterotoxaemia can be differentiated by identification of the causative bacteria and toxins in the intestinal tract, whereas pregnancy toxaemia can differentiated on the basis of pregnancy status and nutritional status of the animal and, marked ketonemi or ketonuria. Choke can be confirmed by location of a foreign body in the pharyngeal or oesophageal regions.

Control

In endemic areas, all dogs and cats should be vaccinated and all stray dogs and cats should be destroyed. Vaccination of valuable stock at risk such as breeding animals may be necessary. People who are at risk such as veterinarians and animal attendants should be immunised. People who have been bitten with pets or livestock whose vaccination history is unknown should be seek medical advice immediately. Tissues or secretions from rabid animals such as meat and milk should not be used for human consumption. Co-operation between the veterinary and medical professionals is of paramount importance in the control of the disease both in livestock and man.

FOOT AND MOUTH DISEASE (FMD)

This is a highly infectious disease affecting cloven-hoofed animals caused by a foot and mouth disease virus of the genus Aphthovirus and family Picornaviridae and characterised mainly by fever, stomatitis, lameness and fall in production.

Epidemiology

FMD is enzootic in Africa and other parts of the world and is characterised by considerable losses especially in the dairy cattle industry. Of the seven serotypes which are associated with the disease (A, O, C, SAT-1, SAT-2 and SAT-3), only serotypes SAT-1, SAT-2 and SAT-3 are commonly associated with the disease in the sub-Saharan region. The FMD virus is easily destroyed by sunlight, boiling, autoclaving under pressure and 1-2 % formalin but it is resistant to other disinfectants and environmental conditions. The virus can be present in saliva, milk, blood, urine, faeces and vesicular fluid which become sources of infection to in- contact susceptible animals. Cattle, sheep and goats may harbour the virus for up to 6 months. Camels and buffaloes are said to be asymptomatic carriers.

Inhalation of infective aerosols is the main method of transmission although the virus can also be acquired through ingestion of contaminated food and water, inoculation with contaminated vaccines and insemination with infected semen. The virus can be carried by wind to distant places. Movement of animals and people between herds can transmit the disease. After infection, initial multiplication occurs at the site of entry resulting in the formation of primary vesicles. Viraemia then develops and is followed by spread of the virus to target tissues where further replication occurs resulting in a large number of secondary vesicles. The FMD virus is epitheliotropic and the mucus membranes and the skin are the main target organs. Damage to the mucous membranes or skin facilitates penetration of the virus.

Clinical features

In goats the disease is characterised by formation of vesicles in the coronary band and interdigital cleft. Vesicles may also occur on the lower lip, commissures of the lips and buccal mucosa. Rupture of vesicles causes small fissures. In sheep, small vesicles appear on the feet resulting in lameness, although they may also be encountered on the udder and vulva. Immunity develops after recovery but animals may be infected with other serotypes or subtypes....[text missing in original hard copy]...ever, acute stomatitis, anorexia, lameness and marked fall formation of vesicles in the mouth and foot, fall in production and lameness.

Diagnosis

In live animals, the virus can be demonstrated in vesicular fluid, epithelial tissues from the edge of ruptured vesicles, pharyngeal and oesophageal secretions, and blood collected in anticoagulant. The virus can be isolated following inoculation in monolayers of bovine thyroid, suckling mice, baby hamster, lamb and calf kidney cells. In dead animals, the virus can be isolated from lymph nodes, thyroids, and heart. Samples should be frozen or kept in glycerol buffer (pH 7.6) during transit to the laboratory. The serological tests used for the diagnosis of the disease include ELISA, complement fixation, virus neutralisation and use of monoclonal antibodies. FMD in sheep and goats should be differentiated from other causes of lameness such as bluetongue, polyarthritis and traumatic injury. Bluetongue in sheep is more severe than FMD and cyanosis of the mucous membranes is not observed in FMD. Serological tests can be employed to distinguish these diseases. Polyarthritis and foot rot can be differentiated by isolation of the causative bacteria.

Control

FMD is a notifiable disease. Vaccination of animals is the main method of control of the disease in endemic areas. Restriction entry of animals and animal products from endemic areas has been used to prevent entry of the disease in disease-free countries. If an outbreak occurs strict quarantine measures should be instituted and accompanied with vaccination of animals at risk. Destruction of affected population is used in some countries. Commercial vaccines for FMD are available.

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