[3] Potomac horse fever is currently endemic in the United States but has also been reported with lower frequency in other regions, including Canada, Brazil, Uruguay, and Europe.

[5] PHF has a fatality rate of approximately 30%, making this condition a concern for horse owners in endemic regions.

[5] N. risticii is typically acquired in the middle to late summer near freshwater streams or rivers, as well as on irrigated pastures.

[6] This is a seasonal infection because it relies on the ingestion of an arthropod vector, which is more commonly found on pasture in the summer months.

[6] Individual organisms are small, pleomorphic (coccoid to ellipsoidal) gram negative aerobes that lack LPS and peptidoglycan in their cell walls.

[17] Once phagocytized by the monocyte, the pathogen prevents lysosomal fusion with the phagosome thus escaping the host defense mechanism.

Neorickettsia risticii is the infectious cause of equine neorickettsiosis, or the colloquially termed Potomac horse fever (PHF).

[7] N. risticii is able to stay inside these trematodes through their development stages, and can also be transmitted to future generations through a transovarial transmission route.

[5] This disease can cause horses to become feverish, experience liquid diarrhea, show a quiet demeanor and go off their food, which can lead to colic and laminitis.

[5] Intestinal lesions previously seen with PHF include pronounced enterocolitis with ulcerative erosions and evident reduction in villus projections.

[20] However, it could be argued that N. risticii requires more research in this area, and could be a more common cause of equine abortion than was previously thought.

Neorickettsia risticii is detected in the blood using an indirect immunofluorescent antibody (IFA) test or by PCR identification.

[21] The IFA serological test detects the presence of IgG and IgM antibodies against N. risticii in the blood, however does not differentiate whether an animal is actively infected or has had previous exposure.

[1] N. risticii is an obligate intracellular microorganism and as such is more technically difficult to culture, isolate, and ship to a diagnostic laboratory.

Timely diagnosis and treatment of PHF is important for preventing the disease from progressing and causing clinical signs such as laminitis, endotoxemia and colic.

[24] When treatment is delayed until after the onset of clinical signs, additional therapy with doxycycline, demeclocycline or rifampin has been associated with higher antibody titer levels than those of untreated animals.

[26] In addition to antimicrobial treatment, supportive therapy for pain management, dehydration and gastrointestinal function should also be utilized to treat laminitis, endotoxemia and colic, respectively.