Synonyms: Piroplasma kochi, Piroplasma parvum, Theileria kochi.
Disease: East Coast fever, bovine theileriosis, African Coast fever, Rhodesian tick fever, Rhodesian redwater.
Hosts: Ox, zebu, water buffalo, African buffalo (Syncerus caffer).
Location: Lymphocytes, erythrocytes.
Geographic Distribution: East, Central and South Africa.
Prevalence: East Coast fever is one of the most important cattle diseases in the regions where it is found. According to Neitz (1959), it occurs enzootically in the Belgian Congo, Uganda, Kenya, Tanganyika, Nyasaland, Zanzibar and Swaziland. It has been eliminated from most parts of South Africa.
Morphology: The forms in the erythrocytes are predominantly (over 80%) rod-shaped, and measure about 1.5 to 2.0 by 0.5 to 1.0 u. Round, oval and comma-shaped forms also occur. When stained with a Romanowsky stain, they have a red nucleus at one end and blue cytoplasm. Several parasites are often found in a single host erythrocyte.
The multiplying forms occur in the lymphocytes and occasionally in the endothelial cells. They are found especially in the lymph nodes and spleen, where they are usually very numerous. They are known as Koch's blue bodies or Koch's bodies, and are circular or irregularly shaped bodies averaging 8 u in diameter and ranging up to 12 u or more. They may be intracellular or free in the gland or spleen juice. When stained with a Romanowsky stain, their cytoplasm is blue and they contain a varying number of red chromatin granules.
Two types of these schizonts are recognized. Macroschizonts (sometimes called agamonts) contain chromatin granules 0.4 to 2.0 u in diameter with a mean of 1.2 u and produce macromerozoites 2.0 to 2.5 u in diameter. Microschizonts (sometimes called gamonts because they are thought to produce sexual stages) contain chromatin granules 0.3 to 0.8 u in diameter with a mean of 0.5 u and produce micromerozoites 0.7 to 1.0 u in diameter.
Life Cycle: The life cycle of this species has been studied more than that of other members of the family, but its details in the tick are still uncertain. The most important vector is Rhipicephalus appendiculatus. Other vectors are R. ayrei, R. capensis, R. evertsi, R. jeanelli, R. neavei, R. simus, Hyalomma excavatum, H. dromedarii and H. truncatum. Transmission is stage-to-stage in all cases, and not thru the egg. R. appendiculatus, for instance, acquires the infection as a larva and transmits it as a nymph, or acquires the infection as a nymph and transmits it as an adult. The parasite will not survive in the ticks thru more than 1 molt.
Reichenow (1940), who made a careful study of the life cycle in cattle and in R. appendiculatus, said that the great majority of parasites die in the tick intestine. A few succeed in passing thru the intestinal wall into the body cavity and thence to the salivary glands, where they invade the secretory cells. Here they lie dormant until after the tick has dropped off its host, molted, attached itself to a new host and started to suck blood. The parasites then begin to multiply by repeated binary fissions, filling the interstices between the secretory droplets. They continue to multiply, and finally the host cell is greatly enlarged and filled with something over 30,000 tiny parasites. This requires 15 successive binary divisions. Very few secretory droplets remain. The host cell ruptures, and the parasites are released into the lumen of the salivary ducts and are injected into the host when the tick sucks blood. It takes 3 days for the developmental process to be completed in nymphs and 4.5 days in adult ticks.
The above process is completely asexual. Gonder (1910, 1911), however, thought that there was a sexual stage in the tick, and described a process of syngamy. Cowdry and Ham (1932) also thought that sex was involved, altho they admitted they found no proof of it. According to their account of the life cycle, two types of parasite, large and small, emerge from the erythrocytes in the tick's gut and become applied to the surface of the gut epithelial cells. Cowdry and Ham thought that fertilization probably takes place here. They said, "Very careful search was made for fertilisation stages without conspicuous success. Large and small parasites were, however, occasionally observed in contact, but it was difficult to tell whether this was merely optical superposition or whether actual union was taking place. Such appearances were detected in 0.1 per cent or less of the parasites."
The parasites then enter the intestinal cells, the small forms disappear, and the large forms grow and give rise to a stage without distinct nuclei which they called a zygote. The zygote grows, a nucleus reappears in it, and also a central concentration of material. This central concentration becomes more marked and turns into a large, elongated, nucleated organism which they called an ookinete. The ookinete breaks out of the zygote into the gut cell, enters the body cavity, makes its way to the salivary glands, and enters a salivary gland cell. Here it rounds up and grows, surrounded by a colorless halo of host cell cytoplasm, becoming so large that it distends the host cell. Buds appear about its periphery which Cowdry and Ham called sporoblasts; the parent cell they called a sporont. The sporoblasts develop rapidly and produce sporozoites about their periphery. These are discharged into the lumen of the salivary gland acinus and are introduced into the animal when the tick feeds on it.
Reichenow (1940) criticized the work of Cowdry and Ham (1932) severely. He said that the bodies in the intestinal cells (the "zygotes"), could be found in both infected and clean ticks and were therefore not a stage in the parasite's life cycle. He found no structures which resembled ookinetes. He considered the "sporonts" to be degenerated tissue cells phagocytized by the salivary gland cells, and the "sporoblasts" to be masses of coalesced droplets secreted by the salivary gland cells. Gonder's work has been discredited not only by Reichenow but also by Cowdry and Ham, Wenyon (1926) and others. According to Cowdry and Ham, Gonder did not distinguish between Theileria and the symbionts which are present in all ticks, and substantiating details in his account were conspicuous by their absence. Wenyon said that his "account was so obscured by such theoretical bias that it is difficult to separate fact from theory."
A definitive study is badly needed to clear up the life cycle of T. parva, and one may hope that 20 more years do not pass before someone carries it out. In the meantime, Reichenow's account is the most convincing.
Pathogenesis: T. parva is highly pathogenic. From 90 to 100% of affected cattle die, altho the mortality is lower in endemic areas. In East Africa, for instance, immature cattle are more resistant than adults, and the mortality among calves varies from 5 to 50%. In Kenya, the mortality varies considerably among calves, but adults usually die.
The incubation period following tick transmission is 8 to 25 days, with a mean of 13 days. The disease itself lasts 10 to 23 days, with a mean of 15 days. Acute, subacute, mild and inapparent forms of the disease have been described, of which the acute type is the usual one.
In the acute form, the first sign is fever. The body temperature varies from 104 to 107 F; it may continue high or it may decrease after 7 to 11 days and then increase again. Other clinical signs usually appear a few days after the initial rise in temperature. The animals cease to ruminate and to eat. Other signs are a serous nasal discharge, lachrymation, swelling of the superficial lymph nodes, sometimes swelling of the eyelids, ears and jowl region, rapid heart beat, general weakness, decreased milk production, diarrhea, frequently with blood and mucus in the feces, emaciation, coughing, and sometimes icterus. Breathing becomes rapid and dyspnea is pronounced just before death. An oligocythemic anemia is present, but there is no hematuria in uncomplicated cases.
In the subacute form, which is often encountered in calves and sometimes in adults in the endemic areas of East Africa, the signs resemble those in the acute form but are not so pronounced. Affected animals may recover, but it takes them several weeks to return to normal.
In the mild form, little is seen but a relatively mild fever lasting 3 to 7 days, listlessness and swelling of the superficial lymph nodes. An inapparent form of the disease has been produced by injection of blood, coarsely ground spleen and lymph node emulsions or suspensions from partially engorged, infected ticks.
The lymph nodes are usually marked swollen, with a variable degree of hyperemia. The spleen is usually enlarged, with soft pulp and prominent Malpighian corpuscles. The liver is enlarged, friable, brownish yellow to lemon yellow, with parenchymatous degeneration. The kidneys are either congested or pale brown, with a variable number of hemorrhagic "infarcts" or greyish white lymphomatomata. The meninges may be slightly congested. The heart is flabby, with petechiae on the epicardium and endocardium. The lungs are often congested and edematous. There may be hydrothorax and hydropericardium, and the kidney capsule may contain a large amount of serous fluid. There may be petechiae in the visceral and parietal pleura, adrenal cortex, urinary bladder, and mediastinum. There are characteristic ulcers 2 to 5 mm or more in diameter in the abomasum, and similar ulcers together with red streaks or patches may be present thruout the small and large intestines. These ulcers consist of a central, red or brown necrotic area surrounded by a hemorrhagic zone. The Peyer's patches are swollen, and the intestinal contents are yellowish.
Immunity: Animals which recover from T. parva infections are solidly immune. The parasites disappear completely, and there is no premunition. There is no cross-immunity between T. parva and Gonderia mutans, but there is partial cross-immunity between T. parva and G. lawrencei.
Diagnosis: Diagnosis is based upon finding the parasites in the erythrocytes in stained blood smears or in stained smears made from the lymph nodes or spleen. Differential diagnosis between East Coast fever and the gonderioses is not always easy, however, and depends upon knowledge of the geographic distribution of the parasites, symptomatology, pathology, pathogenicity, degree of parasitemia, epidemiology and results of cross-immunity tests. The last is the best test in case of doubt.
Cultivation: Tsur-Tchernomoretz, Neitz, and Pols (1957) cultivated T. parva up to 15 days in ox spleen, liver or lymph node tissue cultures. The Koch bodies developed during the first 10 days but then died out. Brocklesby and Hawking (1958) also grew T. parva in tissue cultures, but could not maintain them more than 14 days. The parasites occurred mostly in lymphoid cells.
Treatment: No drug is effective against T. parva once signs of disease have appeared. However, chlortetracycline and oxytetracycline seem to prevent clinical disease if given repeatedly during the incubation and reaction periods, and treated animals become solidly immune (Neitz, 1957; Barnett, 1956).
Prevention and Control: These depend upon tick control and quarantine measures. Immunization by intravenous injection of a suspension of spleen and lymph node material from affected animals was practiced in South Africa around 1912 to 1914, but was then discontinued.
Repeated, regular dipping of cattle in arsenical dips has been found effective, even tho some arsenic-resistant strains of ticks have appeared. Other dips, such as lindane and toxaphene, have also been used.
Quarantine measures are also effective in preventing the spread of East Coast fever. In isolated outbreaks, the whole herd may be slaughtered and the farm kept free of cattle for 18 months before restocking.