Bovine Petechial Fever

Bovine petechial fever is caused by Ehrlichia ondiri, an intracellular rickettsia that resides in cytoplasmic vacuoles of circulating leukocytes. The organism can multiply after experimental infection in cattle, sheep, goats, bushbuck, duiker and impala antelopes, Thomson’s gazelles, wildebeest; and hence, probably in most domestic and wild ruminants. E ondiri is believed to be endemic in wild ruminants, particularly bushbuck; sporadic infection spreads to domestic cattle grazing forest edges or bush lands (scrubs).

The disease is restricted to scrub or forest edge areas that have heavy shade, a thick litter layer that provides high relative humidity, and a resident population of bushbuck and duiker antelopes, the two wild ruminant species believed to be the main reservoir and amplifying hosts. It is seen sporadically throughout the year in imported breeds of cattle. Breeds native to Kenya, such as Zebu (Bos indicus) are more resistant to infection. The method of disease transmission is not known. As for other rickettsial infections, an arthropod vector is suspected; however, extensive attempts to implicate ticks, biting insects, and mites have failed.

The route of infection with E ondiriis not known; however, the organism can be seen in circulating granulocytes (neutrophils and eosinophils) and monocytes while cattle are ill and in the spleen at necropsy. Electron microscopic studies have shown that E ondiri can also infect endothelial and Kupffer cells of the liver, and may also be detected in capillary lumens in the heart. It is believed that E ondiri initially multiplies in the spleen, with subsequent spread to other regions of the body. Damage to the vascular endothelium would explain the petechial hemorrhage and edema, as for many other rickettsial infections.

Bovine petechial fever is characterized by a high, fluctuating fever, signs of depression, decreased milk production, and widespread petechial hemorrhages affecting mucous membranes. Fever develops after an incubation period of 4–14 days, animals 2–3 days later most animals appear depressed with petechiae on mucous membranes, particularly the ventral surface of the tongue and the vaginal mucosa. The petechiae enlarge over several days and then resolve as the animal begins to recover. Marked conjunctival edema and hemorrhage (“poached egg eye”) are characteristic in some severe cases. The conjunctivae are swollen and everted surrounding a turgid and protruding eyeball, and there may be blood in the aqueous humor. Pregnant cows can abort, likely due to the high fever.

The mortality rate in untreated cases can be as high as 50% in imported animals or animals newly introduced to affected areas. Latent infections develop after recovery in some animals, including in bushbuck. After recovery, affected cattle are immune against experimental infection for ~2 years.

In areas where bovine petechial fever is endemic, a history of movement to forest edge areas, coupled with clinical signs and postmortem lesions, allows for a presumptive diagnosis. Definitive diagnosis requires demonstration of the causal organism in Giemsa-stained smears of blood or spleen or by electron microscopy. E ondiri appears blue with Giemsa stain and can be seen as small bodies (diameter, 0.4 mcm), larger bodies (diameter, 1–2 mcm), groups of small and large bodies, and groups or morulae of small bodies. Organisms are present in cytoplasmic vacuoles, most commonly in neutrophils. Tissue suspensions (spleen) can also be inoculated into susceptible cattle or sheep. Blood smears from the recipient animal should be evaluated daily for up to 10 days, at which time E ondiri should be detectable in neutrophils.

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Dithiosemicarbazone and tetracyclines have been used successfully to treat experimental cases early in the disease course but are ineffective in advanced cases. The former is suggested to be more effective. In endemic areas, the disease can be prevented by avoiding areas associated with previous cases. However, this may not always be practical.