Horses affected with PHF usually develop acute depression,
fever (102-107ºF) and anorexia. After 24-48 hours, the horse often develops
profuse, watery diarrhea without blood, characteristic odor, or leukocyte
excretion. The diarrhea may be present for up to 10 days but, in most cases,
only lasts 1-5 days. However, not all horses have diarrhea or diarrhea may be
transient in nature. Laminitis, a frequent sequel to PHF, occurs most commonly
within three days of the onset of diarrhea. Other clinical signs include colic
and subcutaneous edema of the legs and ventral abdomen. Borborygmal sounds are
typically decreased or absent in the early stages of the disease. Although
horses show different hematologic signs, most horses with PHF have leukopenia
characterized by neutropenia, lymphopenia, and eosinopenia. In addition, some
horses may develop thrombocytopenia and, rarely, petechiation. Acid base and
values are typical of most horses with acute diarrhea,
namely metabolic acidosis, hyponatremia, hypokalemia, and renal azotemia.
Since the clinical signs closely resemble those of
salmonellosis, multiple samples of fecal matter should be submitted to a
laboratory for culture. In addition, colitis X, antibiotic-associated
diarrhea, endotoxic shock, and peritonitis should be ruled out as differential
diagnoses for horses with acute diarrhea. The characteristic epidemiologic
features including the seasonal nature, the sporadic occurrence on farms
located near rivers, and lack of Salmonella isolation renders PHF a more
Currently, the most convenient way to diagnose PHF is by
indirect fluorescent antibody test (IFA). The IFA detects antibodies in sera
to the causative agent E. risticii. Most horses have detectable
antibody titers at the onset of clinical signs although a rapid rise in
antibody titer after the first few days of infection with E. risticii merits paired serum samples. Though significant changes in titer of affected
horses can occur in 2-3 days, paired serum samples should be taken at least two
weeks apart. Nonetheless, the presence of antibodies of the IFA does not
indicate that the horse has clinical PHF, only that the horse was exposed to E.
risticii sometime in the past. At least a four-fold increase in antibody
titer has been suggested as a criterion for serologic diagnosis.
A definitive diagnosis of PHF is made by isolation of E.
risticii from the peripheral blood of a clinically affected horse. The
organism is best isolated in macrophages in tissue culture media without
antibiotics. In addition, electron microscopic examination of peripheral blood
monocytes can be done as a definitive diagnosis by using Giemsa stain to
demonstrate the organism in dried blood or buffy coat smears.
The gross lesions at necropsy may be minimal affecting
primarily the cecum and colon and, to a lesser degree, the small intestines.
Affected segments are distended with fluid mixed with ingesta and the fluid is
pale brown and fetid. Very little hemorrhage or damage of the mucosal surface
is evident, except for some patchy hyperemia (approximately 4-8 cm of the small
intestine affected and approximately 5-20 cm of the cecum or colon.) In
contrast to large areas of necrosis and ulceration with some cases of
Salmonellosis, the scattered mucosal erosions and ulcers present in the mucosa
from horses with PHF are less frequent. In addition,
splenomegaly and ventral edema may be present at necropsy.
Microscopically, the mucosa of the cecum and colon is
reduced in thickness due to the loss of surface epithelium, a marked decrease
in the number of intestinal crypts, and collapse of the lamina propria. The
denuded surface epithelium may be covered by a pseudomembrane focally, which
consists of necrotic cells, fibrin, and bacteria. Capillaries and veins of the
mucosa are engorged with blood. The remaining intestinal crypt cells have
intact epithelium. The lamina propria is hypercellular, especially at the base
of the crypts. The submucosa is edematous. Both lamina propria and submucosa
contain macrophages with clusters of the infectious agent. These clusters of E.
risticii are demonstrated using a modified Steiner's or Dieterle's silver
stain. The germinal centers of the lymphoid follicles are depleted of
lymphocytes and contain karyorrhectic nuclei.
Treatment of horses with PHF includes antibiotics, fluid
and electrolyte replacement therapy for animals exhibiting diarrhea, and
nonsteroidal anti-inflammatory drugs for the relief of pain in cases of colic
Vaccines are available for protection against PHF.
However, protection may be short-lived and incomplete because, in many cases,
vaccination has been shown to reduce clinical signs, rather than provide
complete protection. Nonetheless, vaccination may be necessary for horses
residing in or traveling to endemic areas.
The prognosis for survival of PHF has increased to over
85% in recent years with the heightened awareness of the disease among
veterinarians and horse owners. The greatest percentage of mortality is
attributed to complications of laminitis. Outbreaks of PHF will decline in the
future with vaccination, increased awareness, and initiating diagnosis and
treatment at the early stages of the disease.
-by Ashley Armstrong, Class of 2006
-edited by Dr. Dinesh Singh, ADDL Graduate student
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