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Identity Pathogen/s Distribution Distribution Map for Africa Distribution Table for Africa Host Animals Systems Affected Epidemiology Impact: Economic Pathology Disease Course Disease Treatment Table Disease Treatment Vaccines Prevention and Control References Links to Websites Images
Preferred Scientific Name
East Coast fever
International Common Names
Corridor disease, Fortuna disease, January disease, Theileria parva infections, theileriosis in ruminants - exotic, theileriosis, Zimbabwe, Zimbabwe theileriosis, Zimbabwean theileriosis
Bovine theileriosis is also known as East Coast Fever (ECF), Egyptian fever, Tropical theileriosis, Mediterranean Coast fever and Corridor disease. East Coast fever is essentially present in central and eastern Africa. Mediterranean Coast fever is present in northern Africa, southern Europe, Middle East and central Asia.
During 2011, ten countries reported 1,942 outbreaks of bovine theileriosis to the AU-IBAR, with 28,427 cases and 2133 deaths (AU-IBAR, 2011). The number of outbreaks recorded was highest in 2011 compared to previous years. The disease was reported mainly in the eastern part of the continent. Kenya recorded the highest number of outbreaks (1,356), Tanzania, the highest number of cases (14,700) and Zambia, the highest number of deaths (1,444). The table below shows details of the reporting countries with the related quantitative data.
Countries reporting theileriosis to the AU-IBAR in 2011
= Present, no further details = Widespread = Localised
= Confined and subject to quarantine = Occasional or few reports
= Evidence of pathogen = Last reported... = Presence unconfirmed
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further information for individual references may be available in the Animal Health and Production Compendium. A table for worldwide distribution can also be found in the Animal Health and Production Compendium.
|Country||Distribution||Last Reported||Origin||First Reported||Invasive||References||Notes|
|Botswana||Localised||Norval et al., 1992|
|Burundi||Widespread||Tama, 1989; Norval et al., 1992|
|Central African Republic||Present||Norval et al., 1992|
|Congo||Localised||Norval et al., 1992|
|Kenya||Localised||Kariuki, 1989; Norval et al., 1992; Duffus, 1977|
|Malawi||Widespread||Chinombo et al., 1989; Norval et al., 1992; Moodie, 1977|
|Mozambique||Present||Mazibe & Lopes, 1989; Norval et al., 1992; Travassos Santos Dias, 1977|
|Rwanda||Widespread||Norval et al., 1992; Kiltz, 1977|
|Sudan||Localised||Norval et al., 1992; Shommein, 1977; Julla et al., 1989|
|Swaziland||Localised||Norval et al., 1992|
|Tanzania||Localised||Norval et al., 1992; Semuguruka, 1977|
|-Zanzibar||Present||Shambwana, 1989; Norval et al., 1992; Hofstedt, 1977|
|Uganda||Widespread||Otim, 1989; Norval et al., 1992; Oteng, 1977|
|Zimbabwe||Present||Munatswa, 1989; Norval et al., 1992|
|Bos indicus (zebu)||Domesticated host|
|Bos taurus (cattle)||Domesticated host|
|Capra hircus (goats)|
|Ovis aries (sheep)|
Blood and Circulatory System - Large Ruminants
Digestive - Large Ruminants
Mammary Glands - Large Ruminants
Multisystem - Large Ruminants
Nervous - Large Ruminants
Reproductive - Large Ruminants
Respiratory - Large Ruminants
Skin - Large Ruminants
Urinary - Large Ruminants
R. appendiculatus, the major field vector of T. parva inhabits wooded and shrubby grassland from South Sudan through East and Central Africa to South Africa (Norval et al., 1992). Its role and the role of the two other field vectors of T. parva, R. zambeziensis and R. duttoni, in the epidemiology of T. parva is discussed by Norval et al., (1991, 1992). Other species of tick can transmit T. parva experimentally, but are not known as field vectors (Norval et al., 1992). Molecular tools, using nucleic acid-based hybridization techniques, are helping to clarify the taxonomic identities and relationships of ticks (Sparagano and Jongejan, 1999) and detect pathogens within ticks (Figueroa and Buening, 1995; Sparagano and Jongejan, 1999; Sparagano et al., 1999).
Protective immunity to T. parva infections
Protection against T. parva appears to be mediated primarily by CD8 major histocompatibilty complex class I restricted cytotoxic lymphocytes (Mc Keever et al., 1999), with CD4T cells and g d -T-cells helping to contain infection by lyzing schizont-infected lymphocytes and producing parasite-inhibitory cytokines. A degree of resistance in young calves under conditions of endemic stability suggests a role for innate immune mechanisms.
Many factors are involved in assessing the economic impact of tick-borne diseases such as the theilerioses (Mukhebi, 1992). The economic impact of T. parva and its control in Eastern and Central Africa are estimated to be US$ 168 million per annum (Mukhebi, 1992). Eradication of T. parva from South Africa is calculated to have cost US$ 137 million (at the 1989 exchange rate) (Mazibe and Lopes Pereira, 1989).
At death, cases of East Coast fever (ECF) most commonly show evidence of pneumonia and pulmonary oedema with froth in the trachea, bronchi and nostrils (Brown, 1990a). The post-mortem findings in acute, lethal cases of ECF have been described (Irvin and Mwamachi, 1983; Levine, 1985; Lawrence et al., 1994b) (see pictures). The most dramatic pathological changes occur in the respiratory organs. In acute cases, animals may die before mucosal lesions become apparent in the gastrointestinal tract. In prolonged cases, following necrosis of the lymphoid tissue, ulceration may be seen in the Peyer's patches of the small intestine (Irvin and Mwamachi, 1983). The condition of the lymphoid organ may vary between infections caused by different parasite stocks and depending on the duration of disease reaction (Brown, 1990a). There may be generalized hyperplasia of the lymph nodes, spleen and lymphoid tissue in the liver, kidneys and gut or, despite aberrant lympho-proliferation, the nodes and spleen may be exhausted, the nodes oedematous, and the spleen dry and aplastic.
The general post-mortem findings are:
Carcasses: often a frothy exudate around the nostrils, emaciation, and dehydration in protracted cases.
Lymph nodes: in acute cases, oedematous, hyperaemic and may be greatly enlarged. In protracted cases they may be shrunken and necrotic.
Thymus: atrophy, with necrosis common in young animals.
Heart: petechial and ecchymotic haemorrhages are common on the epicardium and endocardium. There may be a serous fluid in the pericardium.
Trachea and bronchi: may be full of white, frothy exudate.
Lungs: interlobular oedema, emphysema and hyperaemia.
Pleural cavity: petechial and ecchymotic haemorrhages on the serosal surfaces. Serous fluid.
Spleen: mushy or dry, swollen or shrunken. Subcapsular ecchymotic haemorrhages are common.
Liver: usually normal although it may be enlarged and mottled.
Gall bladder: is usually normal.
Kidneys: petechial haemorrhages are common on the surface. Greyish-red or white 'pseudoinfarcts' of lymphoid tissue can be seen in the renal cortex and the cortex may be congested.
Bladder: small haemorrhagic lesions on the mucosal and serosal surface.
Peritoneum and viscera: petechial and ecchymotic haemorrhages are common on the serosal surfaces.
Abomasum: ecchymotic and larger haemorrhages (up to 1cm) with ulceration common on the mucosa.
Small and large intestines: petechial haemorrhages on mucosal surfaces throughout.
Peyer's patches: may be swollen.
Nervous system: changes are rarely obvious. There may be some hyperaemia.
Bladder: small haemorrhagic lesions on the mucosal and serosal surfaces. There may be haemorrhages in the muscles, subcutaneous tissues and in the myelin sheath of nerves.
The pathogenic mechanisms associated with East Coast fever have been described in detail by Lawrence et al., 1994b, in particular the role of the coagulation cascade, the complement cascade and the vasoactive components. Non regenerative anaemia and icterus are sometimes seen in T. parva infections but evidence of an haemolytic process is lacking (Lawrence et al., 1994b).
There is increasing evidence for a pathogenic role of immune responses in bovine theilerioses. T. annulata and T. parva schizont-infected cells activate autologous lymphocytes non-specifically in vitro (Pearson et al., 1979, 1982; Campbell et al., 1995), if such activation occurs in vivo, it could cause a cascade of detrimental cytokine-related effects. The failure of animals undergoing primary infection with T. parva to mobilize protective cytotoxic CD8+ T-cells and to control infection has been attributed to the down-regulation of type 1 T-cell responses by interleukin-10 (IL-10) produced by the schizont-infected lymphocytes (McKeever et al., 1997). The extensive lymphocytolysis and leucopenia seen in the late stages of East Coast fever may be due to the marked non-specific lytic activity observed in the peripheral blood mononuclear cells at this time.
T. parva is highly pathogenic to cattle, causing the lympho-proliferative diseases known as East Coast fever (Jura and Losos, 1980; Irvin and Mwamachi, 1983; Lawrence et al., 1994b), Corridor disease (Jura and Losos, 1980; Lawrence et al., 1994c) and January disease (Lawrence et al., 1994d).
East Coast fever (ECF)
The parasites causing East Coast fever (ECF) are mostly maintained by cattle-tick transmission (Lawrence et al., 1994b). Infection is subclinical or mild in African buffalo, which serve as a maintenance host in some areas. In the Asian buffalo, the disease resembles that seen in oxen. ECF is fatal in cattle of European origin (Bos taurus). African zebu or Sanga cattle (predominantly Bos indicus) respond variably to infection. Significant numbers of clinical cases occur in endemic areas only when susceptible cattle, particularly improved dairy or beef breeds, are introduced and become infested with ticks.
ECF is a non-contagious, febrile disease of cattle that is characterized by high fever, leucopenia and severe damage to the lymphoid system (Brown, 1990a). The disease may occur as a mild, per-acute, acute or sub-acute form (Lawrence et al., 1994b). In susceptible cattle, acute lethal disease normally lasts about three weeks, with a pre-patent period of five to twelve days after infection with sporozoites. Pronounced clinical symptoms develop as the schizont-infected cells disseminate rapidly.
The early clinical signs of ECF are pyrexia, leucopenia, listlessness, loss of appetite, deterioration of bodily condition and milk production, enlargement of lymph nodes draining the site of inoculation of the parasite, palpable enlargement of and heat in other nodes. As the disease progresses, appetite and rumination cease, and bodily condition degenerates rapidly. Emaciation follows cachexia, lethargy, weakness and recumbency increase. Animals are reluctant to move, tucked up and hang their heads. Constipation, lacrimation and photophobia occur. The mucous membranes are unaffected, animals become slightly hyperaemic or even anaemic, petechial haemorrhages are common under the tongue and on the vulva of infected animals. During the later stages, if disease is prolonged, diarrhoea and dysentery may develop and blood may appear in the faeces. Anaemia and icterus may occur and nodular skin lesions may develop. In the terminal stages, animals undergo severe respiratory distress, with a watery cough due to pulmonary oedema. As oedema increases, watery frothy fluid runs from the mouth and nostrils, animals become recumbent; copious quantities of fluid may pour from the nostrils and death is normally due to asphyxiation following pulmonary oedema.
Death may follow within a week. More commonly, the clinical phase lasts about two to three weeks. Symptoms other than hyperthermia and lymphadenopathy are rare (Brown, 1990a). In per-acute cases, animals may die before marked respiratory symptoms arise. Pregnant animals may abort during the pyrexic stage or recovery stage. Animals that develop severe respiratory or nervous symptoms rarely recover, those that survive often fail to regain normal levels of productivity. Sub-lethal acute disease may be followed by complete recovery or persist for months leading to chronic, often irreversible emaciation. Mortality among indigenous cattle may be negligible, but the disease significantly reduces growth and productivity.
Corridor disease and January disease
Corridor disease (Jura and Losos, 1980; Lawrence et al., 1994c) is an acute usually fatal disease of cattle that occurs sporadically wherever ticks transmit T. parva from infected African buffaloes to cattle. The 'buffalo-adapted' parasites causing this disease are usually non-pathogenic to African buffaloes, but they are not well adapted to cattle. The schizonts are fewer and smaller than in ECF and usually fail to develop to piroplasms. January disease, Zimbabwe theileriosis or Fortuna disease (Lawrence et al., 1994d) is an acute, strictly seasonal, frequently fatal disease of cattle caused by T. parva in the high and low areas of Zimbabwe. Its occurrence (December to May) coincides with the seasonal distribution of adult R. appendiculatus. Schizonts and piroplasms, when present, are scanty. Primary outbreaks are associated with new additions to the herd. Corridor disease and January disease have the same clinical signs as ECF, but the clinical symptoms last only a few days after the first onset of signs. Emaciation and diarrhoea are not seen in Corridor and January disease. Turning sickness of cattle (Lawrence et al., 1994e) is an aberrant form of infection characterized by the sudden onset of nervous signs caused by an accumulation of parasitized lymphoblasts in the cerebral blood vessels, leading to thrombosis and infarction. In East Africa, it is caused by T. parva and in South Africa by T. taurotragi.
|Drug||Dosage, administration and withdrawal times||Life stages||Adverse affects||Drug resistance||Type|
|buparvaquone||Two doses of 2.5 mg/kg body weight (48 hours apart). Given intramuscularly. Withdrawal times: For milk- 2 days For meat- 42 days Always seek veterinary advice before administering treatment.||All Stages||Toxic||No||Drug|
|halofuginone lactate||Two doses of 1.2 mg/kg bodyweight (repeated administration) given orally. Withdrawal time: For milk- 8 days For meat- 24 days Always seek veterinary advice before administering treatment.||All Stages||Toxic||No||Drug|
|infection and treatment method||Cryopreserved stabilate of an infectious dose of sporozoites (prepared from ground up ticks). If virulent, an antibiotic is given simultaneously; if avirulent, no antibiotic. Eastern Zambia: local strain of sporozoites administered with long acting oxytetracycline (20 mg/kg) given simultaneously. Tanzania, Uganda: cocktail of East African stocks. Kenya: experimentally using Marikebuni stock from Kenyan coast. Zimbabwe: Local 'Boleni' avirulent strain used with or without antibiotic treatment.||All Stages||Patent clinical disease: if necessary treat as above.||No||Vaccine|
|parvaquone||Two doses of 10 mg/kg milk bodyweight (48 hours apart). Given intramucularly. Withdrawal times: For milk- 14 days For meat- 28 days Always seek veterinary advice before administering treatment.||All Stages||Toxic||No||Drug|
Chemotherapy of Theileria annulata and Theileria parva infections
The napthoquinones, parvaquone (Hawa et al., 1988; Gill et al., 1981; McHardy et al., 1983) and buparvaquone (McHardy et al., 1985; McHardy, 1989; McHardy, 1991), and the febrifuginone, halofuginone lactate (Schein and Voigt, 1979, 1981), will cure clinical disease resulting from infection with T. annulata or T. parva. However, the therapeutic dose of halofuginone (1.2 mg/kg) often produces side effects (Schein and Voigt, 1979). Parvaquone does not affect a parasitological cure and recovered animals may take several months to return to a normal level of productivity (Dolan, 1986).
Buparvaquone is a safe and effective drug, which can be used both prophylactically (during prepatent/incubation period) and therapeutically (during patent disease) against T. annulata (McHardy et al., 1985; Dhar et al., 1987, 1988, 1990; McHardy, 1991; Sharma and Mishra, 1990; Singh et al., 1993) and T. parva (McHardy et al., 1985; McHardy, 1991; Dolan et al., 1992). However, in young calves haematopoiesis stimulating drugs must be applied together with buparvaquone to avoid the deleterious effects of severe anaemia (Dhar et al., 1988).
Tetracyclines are effective against the schizonts of T. annulata (Gill et al., 1978; Jagdish et al., 1979; Pipano et al., 1981; Mallick et al., 1987) and of T. parva (Dolan, 1981), but only when used in large doses during the prepatent/incubation period of infection (Hashemi-Fershaki and Shad-Del, 1974).
The 8-aminoquinolones - pamaquin and primaquine- are active against the piroplasms of T. annulata (Zhang, 1987, 1997; Luo and Lu, 1997). Extracts of the plant Perganum harmala have a marked suppressive effect on natural infections of T. annulata (Hu et al., 1997).
|Vaccine||Dosage, Administration and Withdrawal Times||Life Stages||Adverse Affects|
|infection and treatment method||Cryopreserved stabilate of an infectious dose of sporozoites (prepared from ground up ticks). If virulent, an antibiotic is given simultaneously; if avirulent, no antibiotic. Eastern Zambia: local strain of sporozoites administered with long acting oxytetracycline (20 mg/kg) given simultaneously. Tanzania, Uganda: cocktail of East African stocks. Kenya: experimentally using Marikebuni stock from Kenyan coast. Zimbabwe: Local 'Boleni' avirulent strain used with or without antibiotic treatment.||-Cattle & Buffaloes: All Stages||Patent clinical disease: if necessary treat as above.|
Immunization against T. parva infections responsible for East Coast fever, January disease and Corridor disease depends on the infection and treatment method (Radley et al., 1975; Cunningham, 1977; Irvin et al., 1989: Lawrence et al., 1994b; Pegram et al., 1996; McKeever et al., 1999). In this method, cattle are infected with a dose of viable sporozoites and infection is then deliberately blocked by chemotherapy. This method albeit costly has proved successful in a number of field trials in several different African countries (Robson et al., 1977; Uilenberg et al., 1977; Dolan et al., 1980, 1987; Morzaria et al., 1987, 1988; Musisi et al., 1989; Berkvens, 1991). The avirulent 'Boleni' stock from Zimbabwe (Irvin et al., 1989) may serve as a suitable vaccine in the absence of chemotherapy. On farms where T. parva is a serious problem, immunization coupled with a strategic dipping programme could be economically attractive (Pegram et al., 1996). To avoid importing new strains into an area and because of the strain specificity of T. parva (McKeever et al., 1999), sporozoites should be prepared from local stocks. Details of vaccine preparation are summarised in Lawrence et al., 1994b. Immunization against T. parva by cell line vaccines is not feasible as 108 cells in 100 ml diluent are required for successful protection (Lawrence et al., 1994b) because schizonts fail to transfer easily to the host's lymphocytes (Innes et al., 1989). Efforts are therefore being directed towards developing sub-unit vaccines (McKeever et al., 1999; Hall et al., 2000). Molecular tools are proving useful in analysing the biological impact of introducing live vaccines of T. parva on population dynamics (Morzaria et al., 1999).
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Date of report: 03/06/2013
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