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Human granulocytic ehrlichiosis (HGE) was first
recognized as a clinical illness in 1994. The etiological agent of HGE is still unknown;
however, evidence suggest that a single Ehrlichia species closely related to E.
equi is the causative agent. The DNA sequences of 16S rDNA from the blood of naturally
infected horses in Sweden, dogs in Minnesota and Wisconsin, and horses in Connecticut are
identical with HGE and differ only slightly from the published 16S rDNA sequence for E.
equi. Furthermore, when infected human blood from HGE patients is injected into
horses: HGE infection develops in the gorses, can be transmitted to other horses, and
induces protection against subsequent E. equi challenge.
HGE has been diagnosed in human patients in Arkansas, California, Connecticut, Florida, Maryland, Massachusetts, Minnesota, New Jersey, New York, Rhode Island, Pennsylvania and Wisconsin. There is evidence that the western blacklegged tick Ixodes pacificus (a closelsy related species to Ixodes scapularis) transmits E. equi to horses in California. Elsewhere in the United States, I. scapularis has been implicated as the vector of HGE. Ixodes scapularis collected in Wisconsin in 1982 and 1991 were infected with HGE. Also, an engorged tick was removed from a patient with HGE in the same area, and HGE DNA was amplified from the salivary glands. Similarly, PCR-amplified DNA of HGE was detected in 50% of I. scapularis collected in Connecticut. The demonstration that blood from a high proportion of deer in Wisconsin contained HGE suggest that deer might be an important reservoir. However, studies also suggest that meadow voles, Microtus pennsylvanicus, and white-footed mice, Peromyscus leucopus, are naturally infected with a granulocytic ehrlichia.
Follow this link for more information about Human Ehrlichiosis including symptoms and treatment.
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