CHAPTER 6: DISEASES CAUSED BY PROTOZOA AND RICKETTSIA

Coccidiosis and trypanosomosis are the clinically and economically most important protozoan diseases of goats and sheep in sub-Saharan countries. Toxoplasmosis is associated with reproductive wastage in small ruminants but the extent of the problem and the economic significance in the sub-Saharan region is not well documented. Babesia spp infection in goats and sheep is an inapparent infection but it may cause a mild or serious disease in exotic or immunosuppressed animals.

COCCIDIOSIS

This is an enteric disease affecting particularly kids and lambs and it is characterised by debility, malaise, inappetance, diarrhoea or sometimes dysentery, dehydration and death in untreated animals.

Aetiology

Coccidiosis in goats and sheep is caused by protozoa of the genus Eimeria. The common species of Eimeria affecting goats in sub-Saharan countries are E. alijevi, E. arloingi, E. ninakohlyakimovae and E. christenseni. Other species are E. hirci, E. caprovina, E. jolchijevi and E. aspheronica. E. arloingi, E. christenseni and E. ninakohylakimovae are considered to be the most pathogenic species of Eimeria in goats.

The species affecting sheep include E. crandallis, E. ahsata, E. faurei, E. intricata and E. ovina. Other species are E. ovinoidalis, E. pallida and E. parva. E. ovinoidalis, E. crandallis, E. ovina and E. ahsata are known to be pathogenic in sheep.

Epidemiology

Coccidiosis is widespread among small ruminants and has been reported in all sub-Saharan countries. Outbreaks of clinical Coccidiosis with mortality up to 86% have been reported in Nigeria. Studies carried out in Senegal, Ghana, Kenya, Tanzania, Zimbabwe and Botswana have indicated that Coccidiosis is an important subclinical disease which may be associated with significant economic losses in the small ruminant industry. The prevalence of Coccidiosis among goats and sheep range between 40-90%.

Animals acquire the infection by ingestion of contaminated feed and water. Non-grazing lambs and kids can acquire infection from infected udders or the wool of their dams. Sub- clinically infected animals continuously shed the oocysts and contaminate the environment. Overstocking and poor hygiene favour rapid transmission and built-up of coccidial infections in animals whereas, stress factors such as weaning, inclement weather, confinement and intercurrent diseases precipitate the occurrence of a clinical disease. Clinical coccidiosis is frequently encountered in intensively managed animals than in extensively managed ones. Coccidiosis is likely to become a more important disease of small ruminants in sub-Saharan countries in future as the increasing land scarcity is forcing people to adopt more intensive management systems.

Temperature, moisture and oxygen tension are the main factors which determine the survival and development of coccidial oocysts to the infective stage. The optimum temperature for the sporulation of most Eimeria spp oocysts of sheep and goats is 28-31 °C while temperatures below -40 and above 40 °C are considered to be lethal. Sporulated oocysts are resistant to heat and desiccation and; at 0-5 °C oocysts may remain viable for up to 10 months in faecal sediments and moist pellets. Sunlight and low oxygen tension are detrimental to the oocysts. The climatic conditions of the humid tropics are favourable for the survival and development of coccidial throughout the year.

Transmission

The unsporulated oocysts are voided in faeces of infected hosts and under optimum conditions of temperature, moisture and oxygen tension they sporulate and become infective in 2-5 days. The sporulated oocysts are ingested by goats or sheep followed release of sporozoites in the intestine. Sporozoites penetrate the intestinal wall and become trophozoites. The latter subdivide to form schizonts (meronts). The schizonts rupture and release merozoites which infect new intestinal cells. Asexual (schizogony) or sexual (gametogony) development may occur. During gametogony microgametocytes and macrogametocytes develop into microgametes and macrogametes respectively. Microgametes fertilise intracellular macrogametes and oocysts (zygotes) are produced. When the host cell ruptures, the oocysts are released into the intestinal lumen and are passed out in faeces.

The average prepatent period for Eimeria spp of goats and sheep is 2-3 weeks. Variations in prepatent periods between different Eimeria spp occur. For example, it has been found that the prepatent periods of E. ninakohlyakimovae, E. alijevi and E. christenseni range between 15-20 days whereas, the prepatent period of E. intricata, E. pvina and E. \veybridgensis range between 20-33 days. Eimeria spp are host-specific and cross-transmission between hosts rarely occur.

Pathogenesis

The pathogenesis of the disease is dependent on the effect of developmental stages of the parasite in various regions of the intestine. The number of oocysts ingested, species of Eimeria present, age and immune status of the host, location of the parasite in tissues and number of host cells destroyed determine the severity of the disease. Severe damage to the intestinal mucosa is caused by the second generation meronts and sexual stages of Eimeria. Destruction of capillaries in the intestinal mucosa may lead to hypoproteinaemia and anaemia. Secondary bacterial infection can occur and cause severe enteritis. The changes in the intestinal mucosa cause increased the rate of peristalsis, malabsorption and diarrhoea. Diarrhoea is followed by dehydration, acidosis, anaemia and terminal shock. Coccidiosis is mainly a disease of kids and lambs up to 4-6 months of age and in adult animals the disease is usually asymptomatic or mild. The clinical disease occurs when young non-immune animals are exposed to massive challenge with sporulated oocysts.

Clinical features

Diarrhoea which may be mucoid or bloody, abdominal pain, tenesmus, inappetence, debility, loss of weight and dehydration are the common features associated with coccidiosis. Anaemia may also be encountered. In the acute disease, there may be fever, ocular and nasal discharges. Subclinical coccidiosis is associated with reduced feed intake, poor weight gains and poor food utilisation. Coccidiosis is self-limiting, however, other enteropathogens can complicate the clinical picture. Exposure to low-grade challenge results in development of strong immunity against the disease. Successive infections in young animals may cause animals to excrete large numbers of oocysts with subsequent heavy contamination of houses, pastures or watering places.

Pathological features

The gross pathological picture includes a thickened, oedematous and sometimes haemorrhagic intestinal wall. Necrosis, greyish-white nodular lesions and polyp-like growths may be seen on the mucosa. The intestinal contents become fluid, dark brown or haemorrhagic.

Denudation of the intestinal epithelium resulting in the shortening or disappearance of the villi occur. Sometimes there may be hyperplasia of the intestinal villi and proliferative lesions on the epithelium. There is hypertrophy and hyperplasia of glandular epithelium are evident. Various developmental stages of Eimeria spp can be demonstrated in various sections of the intestinal wall depending on the species of the infecting Eimeria. Submucosal oedema and subacute enteritis may also be observed.

Diagnosis

This is based on history, clinical signs, necropsy features and microscopic examination of intestinal mucosa and faeces. The developmental stages of Eimeria spp in the intestinal cells can be demonstrated in Giemsa-stained intestinal smears or scrapings and, in haematoxylin eosin stained histological sections. The demonstration of various developmental stages of Eimeria spp and the denudation of the intestinal epithelium in dead or sacrificed animals is considered to be a positive diagnosis for coccidiosis.

Faecal oocyst counts can support the diagnosis but they are usually not very reliable because most animals will excrete the oocysts in the absence of the disease and acute coccidiosis may occur before the oocysts are demonstrable in faeces. Furthermore, Eimeria species vary in their pathogenicity. However, the presence of very high numbers of oocysts in faeces together with clinical signs may be highly suggestive of the disease. Clinical coccidiosis has been demonstrated in lambs experimentally infected with 100,000-800,000 oocysts of E. christenseni and 50,000-500,000 oocysts of E. ninakohlyakimovae. Serum antibody quantification is a common serological method for the diagnosis of coccidiosis.

The differential diagnosis of coccidiosis include colibacillosis, salmonellosis, cryptosporidiosis, lamb dysentery and helminthosis. The confirmation of these conditions can be achieved by isolation and identification of the causative agents from faecal specimens and other affected tissues. Coccidiosis and helminthosis commonly occur together and they can be differentiated on the basis of faecal oocyst or egg counts and demonstration of various developmental stages of coccidial in the intestinal mucosa and/or worms in the mucosa or lumen of the gastrointestinal tract.

Treatment and Control

Coccidiosis can be treated using decoquinate (0.5 mg/kg) and lasolacid at a daily intake of 4.3 mg/kg body weight. Sulphonamides such as sulphadimidine, sulphamerazine, sulphamethazine and sulphaquinoxaline at dosage rates of 50-100 mg/kg for 4 days are effective against coccidiosis in small ruminants. Amprolium in feed is also used to treat the disease in goats (100 mg/kg) and sheep (50 mg/kg). Nitrofurazone given orally (10-20 mg/kg) is also effective. Other drugs include monensin (20 g/ton of feed), toltrazuril and dicrlazuril.

Coccidiostats in drinking water or feed are commonly employed to control the disease in intensive production systems. Decoquinate (0.3 -4.0 mg/kg) in feed mixtures is a safe and very effective coccidiostat in goats and sheep. Monensin fed prophylactically at 10-30 mg per ton of feed controls shedding of oocysts and increases feed conversion. However, high levels of monensin render the feed unpalatable and toxic.

Proper hygiene in the house and minimisation of predisposing factors are important factors to be considered in the control strategies of coccidiosis. Provision of adequate nutrition enhances the resistance of animals to coccidiosis.

TRYPANOSOMOSIS

Trypanosomosis is a debilitating disease of animals which is characterised by parasitaemia, intermittent fever, anaemia, loss of condition, reduced productivity and mortality.

Aetiology

A haemoflagellate protozoan, Trypanosoma spp is the cause of the disease. T. congolense and T. vivax are the main species associated with clinical trypanosomosis in small ruminants in the sub-Saharan region. T. brucei and T. simiae are frequently encountered as asymptomatic infections in goats although the latter can cause an acute and fatal disease in sheep.

Epidemiology

The distribution of trypanosomosis in goats and sheep in sub-Saharan Africa is closely related to the ecology and distribution of the vector tsetse flies of the genus Glossina. Increased tsetse fly activity particularly during the rainy season is associated with increased incidence of the disease. Clinical caprine trypanosomosis has been reported in Mozambique, Tanzania, Kenya, Uganda, Nigeria and Zambia. Infection rates with T. congolense and T. vivax in goats varying from 3.5% to 5.0% have been reported in Nigeria and Kenya. The wide distribution of tsetse flies in the sub-Saharan region (15°N-30°S) suggests a more extensive distribution of the disease.

Tsetse flies (Glossina spp) are the principal vectors of trypanosomosis in sub-Saharan Africa and G. morsitans and G. pallidipes are the most commonly involved in the transmission of the disease. Other blood sucking flies such as Stomoxys spp and Tabanus spp may also transmit the disease. Wild animals such as bush pigs, bush bucks, kudus, warthogs and buffaloes act as reservoirs of the infection in endemic areas. Stress favours such as malnutrition, intense heat and intercurrent infections have been shown to render animals more susceptible to the disease. Animals in endemic areas show some trypanotolerance while exotic breeds are much more susceptible.

Pathogenesis

Following introduction into the body by an insect bite, the trypanosomes initially multiply and cause inflammation at the site of infection. The parasites are then carried through the lymphatic channels to the blood circulation. During the parasitaemic stage, trypanosomes release haemolysins and enzymes such as phospholipases, proteases and neuraminidases which cause damage of the cell membranes of erythrocytes. Damage to the red blood cells is followed by disseminated intravascular coagulation. The trypanosomes may also block capillaries causing ischaemia and anaemia.

Clinical features

T. congolense is the most pathogenic species in goats causing an acute, subacute or chronic disease. T. simiae can induce a highly acute and fatal disease in sheep. T. vivax is less pathogenic while T. brucei may affect goats causing an inapparent infection. Thus, the severity of the disease is determined by the pathogenicity of the strain of trypanosome.

The incubation period of acute trypanosomosis caused by T. congolense is 5-10 days. The disease is characterised by depression, anorexia, rigidity of the hind limbs, drooping ears, increased heart rate (up to 250 per minute), increased respiratory rate (up to 45 per minute), watery salivation and flaccidity of the tail. The temperature may be subnormal or may reach 41 °C. Mucous nasal discharges, mild conjunctivitis, enlarged superficial lymph nodes, lethargy and recumbency are also evident. Later on, the animal becomes unresponsive to external stimuli and pallor of the mucous membranes become apparent. Death may occur 4- 6 weeks post-infection.

The subacute syndrome lasts for 6-12 weeks and is characterised by enlargement and oedema of the superficial lymph nodes (especially the prescapular lymph node), pallor of the mucous membranes and marked jugular pulsation. Other superficial lymph nodes may also be enlarged and oedematous. Animals may recover or die in 10-12 weeks. The course of chronic trypanosomosis in goats takes 12-24 weeks and is characterised by progressive weight loss, rough and dull hair coat, anaemia, weakness and paresis in terminal stages. It has been observed that trypanosomosis grossly impairs the fertility of the affected animals.

Pathological features

Acute trypanosomosis is manifested grossly by a pale and dehydrated carcass; petechial and ecchymotic haemorrhages in the serosal surfaces; enlarged and oedematous lymph nodes and congestion of the liver. The spleen is also enlarged and dark red.

Chronic trypanosomosis is characterised by an oedematous and pale carcass; enlarged lymph nodes; gelatinous fatty degeneration of the heart and kidneys; ascites, hydrothorax and hydropericardium; enlarged and flabby heart and, hepatomegaly. The bone marrow becomes yellowish and gelatinous. Testicular degeneration and, atrophy and, oedema of the choroid plexus may also be observed.

At histopathology, trypanosomes are demonstrable in the lumina of blood vessels in which they may cause thrombosis. The acute disease causes intravascular coagulation. Capillary dilatation and oedema, perivascular mononuclear cell infiltration,.hemosiderosis, and hyperplasia of lymphoid tissues are common features. Macrophages, lymphocytes and plasma cells infiltrate the myocardium, kidneys, thyroids, adrenals and gonads. The clinical pathology of trypanosomosis is characterised by a marked fall in the packed cell volume, normocytic anaemia and leucopenia.

Diagnosis

The epidemiology, particularly the presence of tsetse flies in the area, clinical and pathological features may be useful in a provisional diagnosis of the disease. Wet blood smears are useful in field diagnosis of the disease but they may be unreliable for the detection of light infections. Air-dried thin or thick blood smears stained with 10% Giemsa for 20 minutes are used for specific diagnosis of trypanosomes. In light infections with T. congolense and T. vivax, the trypanosomes can be concentrated by centrifugation and demonstrated by examination of cells at the leucocyte/plasma interface of heparinised blood by dark ground illumination. This is considered to be the most sensitive method of diagnosis of trypanosomosis. If EDTA is used as anticoagulant, trypanosomes can be demonstrated in Giemsa stained smears of cells from the buffy coat region.

The common serological methods of diagnosis are indirect haemaglutination test and ELISA. Monoclonal antibodies against T. congolense, T. vivax and T. brucei are available. DNA probes are being developed in some specialised laboratories. The differential diagnosis of trypanosomosis includes haemonchosis and malnutrition. Demonstration of trypanosomes in blood circulation is required to rule out helminthosis.

Treatment and Control

Homidium bromide (1 mg/kg), quinapyramine methyl sulphate (5 mg/kg) and diminazene aceturate (3.5 mg/kg) are used for the treatment of T. congolense and T. vivax infections in small ruminants. Chemoprophylaxis is an important control strategy in endemic areas and isometamidium (0.5 mg/kg) and pyrithidium bromide (2 mg/kg) are the drugs commonly used in small ruminants. Control of the disease depends on the prevention of contact between susceptible animals and vectors particularly tsetse flies. The methods of control of tsetse flies include bush clearing, spraying of animals and habitats with effective insecticides and the use of tsetse fly traps. The use of trypanotolerant breeds of goats and sheep is also being adopted in some countries. Avoidance of stress factors such as malnutrition, intense heat and intercurrent infections can reduce the incidence of clinical cases in endemic areas.

BABESIOSIS

Babesiosis is an infectious tick-borne disease of livestock characterised by high fever, haemoglobinuria, anaemia and prostration. The disease in goats and sheep is mainly caused by an intra-erythrocytic protozoan, parasite, Babesia motasi. B. ovis causes inapparent infections.

Epidemiology

Babesia spp infections are widespread among goat and sheep populations in Africa. Babesiosis is transmitted by ticks. Boophilus, Rhipicephalus, Hyalomma, Ixodes and Haemaphysalis spp are involved in the transmission of different species of Babesia. Both transovarial and transstadial transmissions occur. Increased tick activity which is associated with high humidity results in increased incidence of the disease. Babesia spp affecting goats and sheep may be maintained in non-susceptible hosts such as wild animals. Presence or absence of intercurrent infections and differences in breed susceptibility determine the incidence and severity of the disease. Movement of naive animals from non-endemic into endemic areas may result in outbreaks.

Pathogenesis

The pathogenesis of babesiosis is related to the damage of erythrocytes and the production of pharmacologically active substances following activation of the kallikrein and complement systems. These substances destroy erythrocytes resulting in intravascular haemolysis. The haemolytic anaemia subsequently result in hypoxia and death.

Clinical features

B. motasi can cause an acute or chronic disease in goats or sheep. The acute disease is manifested by anorexia, fever, fast and audible heart beats, pallor of the mucous membranes, icterus and haemoglobinuria. Other features include abdominal pains, diarrhoea, prostration and death. The chronic disease is manifested mainly by emaciation but coughing and oedema may be features.

Pathological features

The necropsy features include widespread subcutaneous and intramuscular oedema, icteric carcass, thin and watery blood, yellow and gelatinous fat. The urinary bladder contains dark urine. The spleen is enlarged and the splenic pulp is soft. The gall bladder is distended and contains thick and dark bile.

The histopathological picture includes centrilobular necrosis of the liver; haemosiderin deposits in Kupffer cells, congestion of the lungs, heart, spleen and kidneys. The germinal layers of the spleen and lymph nodes are depleted and the reticular tissue is hyperplastic with large numbers of macrophages containing haemosiderin. Haemosiderosis is also evident in other tissues. The clinical pathology is one of marked reduction in packed cell volume and haemoglobin concentration.

Diagnosis

Clinical features can support a provisional diagnosis of the disease. The demonstration of Babesia in thin or thick smears made from peripheral blood and stained with Giemsa is confirmatory. Thick smears are recommended in light infections. B. motasi occur singly or in pairs and in the latter form the angle formed between them is acute while B. ovis often occur singly. Indirect haemagglutination and complement fixation tests are the serological methods used in the diagnosis of the disease.

Treatment and Control

Babesiosis can be treated using diminazene aceturate (2.0-3.5 mg/kg), imidocarb (2.0 mg/kg) three times at 24 hours interval and amicarbilide (10 mg/kg). Quinuronium is also used. The control of the disease depends on effective control of ticks by dipping or spraying animals at risk with recommended acaricides. In small herding units, ticks can be manually removed from the bodies of infested animals. Rotational grazing is employed to control ticks in some commercial or institutional farms.

HEARTWATER

Heartwater is a tick-borne rickettsial disease of ruminants which is characterised clinically by pyrexia, nervous signs, diarrhoea and death and; at necropsy by hydropericardium, hydrothorax and oedema of the lungs and brain. The disease is caused by a pleomorphic rickettsia, Cowdria ruminantium.

Epidemiology

Heartwater is endemic in many parts of Africa affecting both domestic and wild ruminants. The disease has been reported in Madagascar, Nigeria, Kenya, Tanzania, South Africa, Reunion and Sao Tome islands.

The disease is transmitted by Amblyomma spp ticks. In most parts of Africa A. variegatum is the principal vector. A. hebraeum is an important vector of the disease in the Republic of South Africa while A. gemma and A. lepidum have been reported to be involved in the transmission of heartwater in East Africa. Wild animals maintain the vector ticks and are asymptomatic carriers of the disease. Transmission occurs mainly trans-stadially whereas, transovarial transmission rarely occurs. Increased tick activity which is associated with increased humidity especially during the rainy season may be associated with increased incidence of the disease. Outbreaks occur when susceptible animals from tick-free areas are moved into endemic areas. Different strains of C. ruminantium with differences in virulence exist and animals which are immune to one strain may succumb to others. Kids and lambs possess innate resistance in the first week of their life although sometimes they may succumb to a clinical disease. Goats are more susceptible to heartwater than sheep and the Angora goats are particularly very susceptible. Black Head Persian sheep posses some degree of natural resistance to the disease.

Pathogenesis

The organisms are introduced in the body through the saliva of the infected ticks. Initial multiplication in the regional lymph nodes is followed by colonisation of the endothelial cells of blood vessels in all organs. C. ruminantium has a distinct predilection in the endothelial cells of the brain cells. Invasion and colonisation of the endothelial cells causes vascular damage resulting in increased vascular permeability, transudation and effusion of fluids into the body cavities and subsequent development of oedema and hypovolaemia. C. ruminantium also produces an endotoxin which, together with increased cerebrospinal fluid pressure are considered to be involved in the pathogenesis of the brain lesions. Progressive pulmonary oedema and hydropericardium results in asphyxia and cardiac insufficiency which terminate into death. Severe renal ischaemia and nephrosis has been reported to occur in goats. The severity of the disease varies depending on the virulence of the infecting organism, breed, age and immune status of the host.

Clinical features

The incubation period of heartwater in goats and sheep is 1-5 weeks and the course of acute disease takes 3-6 days. A peracute, acute, subacute or chronic disease may occur. The peracute syndrome is characterised by sudden death without premonitory signs. Sometimes, animals with a peracute disease may exhibit high fever, prostration and paroxysmal terminal convulsions. The case fatality rate in peracute cases is 100%. The acute disease is characterised by pyrexia, dullness, anorexia and nervous signs. The nervous signs include unsteady or high-stepping gait, ataxia, circling or galloping movements, chewing movements and aggression. Other signs include dullness, bleating, nystagmus, twitching of the tail, blindness, opisthotonus, droopy ears, lowering of the head, increased urination and forced respiration. Convulsions, prostration and lateral recumbency are observed in terminal stages of the disease. The case fatality rate of the acute disease is 50-90%.

Subacute heartwater develops in 7-10 days and the clinical signs are less pronounced than in the acute syndrome. They include listlessness, inappetence, loss of weight and hair/wool, recumbency, fall in temperature and ruminal atony. The chronic disease which is common in indigenous breeds of goats and sheep may be characterised by transient fever. Natural recovery and subsequent re-infection may be observed.

Pathological features

Little changes are seen in the peracute disease although petechial haemorrhages may be observed in the endocardium and pericardium. The gross pathological features of the acute disease include ascites, hydrothorax and hydropericardium. The fluid in the pericardial sac is turbid, light yellow and clots on exposure to air. Congestion of the liver and distension of the gall bladder occur. Subserosal haemorrhages, splenomegaly and lymphadenopathy are common features. The trachea and bronchi are filled with a serofibrinous foam, congested and have petechiated and ecchymotic mucosae. The lungs are oedematous and a frothy fluid exudes from the cut lung surface. The mediastinal and bronchial lymph nodes are oedematous. There is also oedema of the brain and, the meninges are swollen, congested and odematous. The choroid plexus is dull greyish in colour.

At histopathology there is perivascular infiltration of organs/tissues with macrophages and lymphocytes. Nephrosis, perirenal oedema and petechiation of the renal cortex occur. Lesions in the brain include foci of necrosis and microcavitation in the cerebral cortex, oedema of the axon sheaths, necrotic degeneration and formation of PAS positive granules and globules in the cytoplasm of neurocytes and accumulation of the latter in the perivascular space. Parasitised endothelial cells are distended. C. ruminantium colonies can be demonstrated in the cytoplasm of endothelial cells of the brain, lungs and kidneys. At clinical pathology there is oesinophilia, neutrophilia, lymphocytosis, lowered packed cell volume and haemoglobin concentration and, normocytic, normochromic anaemia.

Diagnosis

Presumptive diagnosis can be based on the epidemiological, clinical and pathological features. Demonstration of C. ruminantium in the cytoplasm of the endothelial cells of blood vessels or in Giemsa-stained smears of lymph node or brain biopsy samples is confirmatory. In dead animals, the organisms can be demonstrated in brain crush smears prepared from the hippocampus or cerebral cortex. The brain crush smears are air-dried, fixed in methanol for 1 minute and then stained with 10% Giemsa for 30 minutes or 50% Giemsa for 10 minutes. C. ruminantium appear as clusters of bluish-purple to reddish-purple cocci in the cytoplasm of vascular endothelial cells. The organisms may also be demonstrated in histological sections of the endothelial cells of renal glomeruli or capillaries of the grey matter of the cerebral cortex.

Other methods of diagnosis include the inoculation of blood from suspected animals in susceptible animals in which reproduction of a clinical disease is a positive diagnosis. Indirect fluorescent antibody test and ELISA are the common serological methods of diagnosis.

Sudden death in peracute heartwater should be differentiated from anthrax and while the nervous signs can also occur in bacterial meningoencephalitis, tetanus, plant and heavy metal poisoning. Demonstration of the causative organisms is necessary in order to differentiate the disease from anthrax, tetanus and bacterial meningoencephalitis. The nervous symptoms observed in tetanus are more severe than those encountered in heartwater. A recent grazing history and presence of poisonous plants or heavy metal contaminants in the animals' environment can be highly suggestive of poisoning. Hydropericardium and hydrothorax may also be observed in bluetongue and pulpy kidney disease. Bluetongue is can be differentiated by the mouth and feet lesions and hydropericardium is not a feature. Virological and serological tests can also be used to differentiate heartwater and bluetongue. Characteristic lesions in the kidney and isolation of C. perfringens type D and demonstration of the epsilon toxin will confirm pulpy kidney disease.

Treatment and Control

Treatment of the peracute cases is usually untimely because of sudden death. However, if correctly diagnosed in early stages, the disease can be treated with oxytetracycline (10-20 mg/kg) given parenterally and repeated after 24 hours. Other drugs used include doxycycline (2 mg/kg), rifamycin (0.2 mg/kg) and sulphadimidine. Supportive treatment with diuretics such as furosemide (1 mg/kg) 2-3 times per day for one or two days is recommended to reduce oedema formation.

Control of heartwater depends on effective control of the vector ticks. Live virulent vaccines have been developed but their effectiveness is hampered by the diversity of the strains of C. ruminantium in different areas. The infection and treatment method with oxytetracycline is used in some farms in South Africa.

Chemoprophylactic treatment of susceptible animals in endemic areas with oxytetracycline (3 mg/kg) at day 10, 20, 30, 45 and 60 has also been adopted in some commercial production units. When the protocol is adopted, animals are not dipped until day 60. Alternatively, a regime using long acting oxytretracycline (10-20 mg/kg) at day 7, 14 and 21 can be used. The costs involved in chemoprophylactic treatment do not justify adoption of the protocol in the traditional herds.

ANAPLASMOSIS

Anaplasmosis is a mild rickettsial infection of goats and sheep which is characterised in immunosuppressed animals by weakness, anaemia, icterus and respiratory distress. The disease is caused by Anaplasma ovis. A. marginale can cause latent infections in small ruminants.

Epidemiology

Anaplasmosis is transmitted by ticks. Rhipicephalus evertsi and Hyalomma spp and Ornithodorus spp have been found to be the main vectors of the disease in Africa. Biting insects or inoculation of blood into susceptible animals can also transmit the disease. Recovered animals become carriers. Splenectomy, intercurrent infections such as trypanosomosis, babesiosis, eperythrozoonosis and heavy parasitism lower the resistance of the animals and render them more susceptible to the disease. Other stress factors such as malnutrition and pregnancy also increase the susceptibility of animals to anaplasmosis. Goats have been shown to be more susceptible to A. ovis than sheep.

Pathogenesis

The presence of Anaplasma spp in erythrocytes induces physical and chemical damage to the cells culminating into erythrocytophagocytosis. It has also found that the sensitised erythrocytes produce antierythrocytic autoantibodies. Damage to the erythrocytes result in anaemia. The organisms cause a mild disease under natural infections but a clinical and sometimes fatal disease may occur in immuno-compromised animals. Thus, the clinical manifestations of the disease are precipitated by splenectomy, intercurrent infections and other stress factors.

Clinical features

Listlessness, anorexia, weakness, ruminal stasis, respiratory distress, pallor of the mucous membranes, increased heart and respiratory rates are the main clinical signs. Constipation, oedema of the submandibular region and ventral side of the neck and, abortion may occur.

Pathological features

The carcass becomes pale and icteric with thin and watery blood. There is anasarca and presence of straw-coloured fluid in body cavities. The lungs become pale and oedematous; the liver becomes enlarged and yellowish while the gall bladder is filled with yellowish-green bile. Lymphadenopathy and nephrosis may be features.

Histolopathological features include erythrophagocytosis, oesinophilia, reticulocytosis, anisocytosis and haemosiderosis of reticuloendothelial cells. Basophilic stippling, centrolobular necrosis of the liver and degenerative changes in the cells of the convoluted tubules occur. The clinical pathology is manifested by a marked fall in the haematocrit.

Diagnosis

A presumptive diagnosis of anaplamosis is based on clinical features, haematological changes and demonstration of the organisms in erythrocytes. Blood smears prepared on grease-free slides, fixed with methanol and stained with Giemsa show the parasite as a round, uniformly stained black or dark purple body in the cytoplasm of erythrocytes. Reproduction of a clinical disease by inoculation of suspected blood in splectomised susceptible animals is a diagnostic but it is an expensive and time consuming method. The serological methods of diagnosis include rapid card agglutination, capillary tube agglutination, complement fixation, direct and indirect fluorescent antibody tests.

Anaplasmosis should be differentiated from haemonchosis, trypanosomosis, babesiosis, eperythrozoonosis, copper poisoning and other conditions which are manifested with loss of condition, listlessness, mild fever and anaemia. The demonstration of high nematode egg and worm burdens in anaemic animals can be highly suggestive of haemonchosis. Trypanosomosis can be distinguished from anaplasmosis by the demonstration of Trypanosoma spp in blood circulation. Babesia spp can be easily demonstrated in erythrocytes of the affected animals while Eperythrozoon spp is an extraerythrocytic parasite and much smaller than Anaplasma spp. Haemoglobinuria which is common in chronic copper poisoning is not a feature of anaplasmosis.

Treatment and Control

Long acting oxytetracycline (20 mg/kg) repeated one or two times after 7 or 14 days has been shown to be effective in the treatment of anaplasmosis in sheep. Chlortetracycline and imidocarb (5 mg/kg) are also used. Control of the disease depends on effective control of vector ticks and insects. Asepsis during mass vaccination and surgical procedures can prevent mechanical transmission of the disease. Vaccination is not practised and is not justifiable under natural conditions because of the asymptomatic nature of the disease.

ERYTHROZOONOSIS

This is an arthropod-borne subclinical disease of sheep and sometimes goats caused by a rickettsial Eperythrozoon ovis and is characterised by mild fever, anaemia and icterus in immunosuppressed animals.

Mosquitoes and stable flies are the main vectors of the disease although the disease can also be transmitted by inoculation of blood from affected animals into susceptible animals or infection through surgical procedures such as castration, docking and shearing. Placental infection may also occur. Occurrence of the clinical disease is exacerbated by stress factors. The organism induces erythrophagocytosis resulting in anaemia and icterus.

Clinical signs include anorexia, mild fever, depression, debility, loss of weight, exercise intolerance, pallor of the mucosae and icterus. At necropsy, the carcass is pale or icteric. The kidney becomes reddish-brown and there may also be fatty degeneration of the liver, subcutaneous oedema and hydropericardium. Haemoglobinuria may be encountered. Haemosiderosis in the liver, kidney and spleen are common histopathological features. The clinical pathology is characterised by a fall packed cell volume and haemoglobin concentration, leucopenia and hypoglycemia.

The epi-erythrocytic E. ovis can be demonstrated in the Giemsa-stained thick smears as pale- or reddish-purple rings, rods or clusters of organisms around the erythrocytes. ELISA, complement fixation, indirect haemagglutination, direct and indirect immunofluorescent tests are the serological methods used in the diagnosis of the disease. Fluorescent microscopy is also employed. The disease should be differentiated from anaplasmosis, helminthosis, malnutrition and chronic copper poisoning. The mild nature of the disease does not justify treatment, but iminocarb can be effective.

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