Bovine petechial fever is a rickettsiosis of cattle characterized by high fever, hemorrhages, and edema. Its occurrence has been confirmed in the highlands of Kenya and Tanzania at altitudes >5,000 ft (1,500 m), although it is considered likely to occur in neighboring countries with similar topography. The importance of bovine petechial fever lies in its threat to dairy development in the highlands of eastern Africa, but no outbreak has been reported for over a decade.

Etiology and Epidemiology

The disease 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, impala, Thomson's gazelles, and wildebeest, and hence, probably in most domestic and wild ruminants. E ondiri is believed to be endemic in wild ruminants, particularly bushbuck, and it sporadically overspills into domestic cattle grazing forest edges or 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 residual population of bushbuck and duiker, the 2 wild ruminants believed to be the main amplifying and reservoir hosts. It occurs sporadically throughout the year in imported breeds of cattle. It is not known how the disease is transmitted. As in other rickettsial infections, an arthropod vector is suspected, but extensive attempts to incriminate ticks, biting insects, and mites have failed.

Pathogenesis

The route of infection is not known, but E ondiri 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, and it may be free in capillary lumens in the heart. It is believed that E ondiri initially multiplies in the spleen, with subsequent spread to other areas. Damage to the vascular endothelium would explain the hemorrhages and edema, as in many other rickettsial infections.

Clinical Findings

The disease is characterized by a high fluctuating fever, apathy, lowered milk yield, and widespread petechiation of mucous membranes. After an incubation period of 4–14 days, animals develop a high fever; 2–3 days later, most animals appear dull, and petechiae may be seen on mucous membranes, particularly the lower surface of the tongue and the vaginal mucosa. These hemorrhages enlarge over several days and then regress as the animal begins to recover. Marked conjunctival edema and hemorrhage (“poached egg eye”) are characteristic in some severe cases. The conjunctival sacs are swollen and everted around a tense and protruding eyeball, and there may be blood in the aqueous humor. Pregnant cows may abort, most likely from the high fever. Other clinical signs are absent. The case mortality rate in untreated cases can be as high as 50% in imported animals or in animals newly introduced to the area. Latent infections develop after recovery in some animals, especially in indigenous stock and in bushbuck. Following recovery from the disease, affected cattle are immune against experimental challenge for ~2 yr.

Lesions

Typically, eosinopenia and lymphopenia are marked, followed by an equally pronounced neutropenia. Anemia is characteristically a sequela, and organisms can be demonstrated in Giemsa-stained smears of blood or spleen. At necropsy, widespread serosal and mucosal hemorrhages and edema are accompanied by lymphoid hyperplasia. Organs frequently affected include the heart, alimentary tract from the forestomach to the colon, liver, gall bladder, kidneys, and urinary bladder. The edema is characterized by gelatinous fluid in the intermuscular connective tissue, lymph nodes, and abomasum. No characteristic histologic abnormalities have been described, but there is vascular proliferation with prominent endothelial swelling and mild mononuclear infiltration.

Diagnosis

In areas where the disease 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 stains blue with Giemsa and can be seen as small bodies (0.4 μm), larger bodies (1–2 μm), groups of small and large bodies, and groups or morulae of small bodies. They are seen in cytoplasmic vacuoles and are most commonly seen in neutrophils. Tissue suspensions (spleen) can also be inoculated into susceptible cattle or sheep. Blood smears from the recipient animal should be made daily for up to 10 days, by which time E ondiri should be detectable in neutrophils. The disease is difficult to differentiate from other hemorrhagic diseases of cattle such as Rift Valley fever, acute trypanosomosis (hemorrhagic Trypanosoma vivax), acute theileriasis, heartwater, hemorrhagic septicemia, and bracken fern poisoning.

Treatment and Control

Dithiosemicarbazone and tetracyclines have been used successfully to treat early experimental cases but are ineffective in advanced cases. The former is said 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.

Last full review/revision March 2012 by Basil O. Ikede, BVetMed, DVM, PhD, FCVSN