Page 1508 - Small Animal Internal Medicine, 6th Edition

1480 PART XIV Infectious Diseases

lymphadenopathy and splenomegaly are not as common as because infection with nonpathogenic SFG agents can induce
in dogs with ehrlichiosis. Petechiae, epistaxis, subconjunc- cross-reacting antibodies. Demonstration of R. rickettsii by
VetBooks.ir tival hemorrhage, hyphema, anterior uveitis, iris hemor- inoculating affected tissues or blood into susceptible labora-
tory animals or by documenting the organism in endothelial
rhage, retinal petechiae, and retinal edema occur frequently.
Cutaneous manifestations can include hyperemia, petechiae,
a definitive diagnosis of RMSF but is not clinically practi-
edema, and dermal necrosis. Hemorrhage likely results from cells by using direct fluorescent antibody staining leads to
vasculitis, thrombocytopenia from consumption of plate- cal. PCR assay can be used to document the presence of R.
lets at sites of vasculitis, thrombocytopenia from immune rickettsii DNA in blood, other fluids, or tissues and docu-
destruction, and, in some dogs, disseminated intravascular ment infection. But results from naturally occurring cases
coagulation. CNS signs include vestibular lesions (nystag- are rarely positive in PCR panels. In experimentally infected
mus, ataxia, head tilt); seizures; paresis; tremors; changes in dogs, R. rickettsii DNA was inconsistently amplified from
mentation; and hyperesthesia (Mikszewski and Vite, 2005). the blood of the dogs one to four times between day 5 and
Fatal RMSF is generally secondary to cardiac arrhythmias 13 after tick infestation (Levin et al., 2015). As with other
and shock, pulmonary disease, acute renal failure, or severe vector-borne testing recommendations, the combination of
CNS disease. serology and PCR assay should be used in dogs with sus-
pected RMSF (Maggi et al., 2014).
Diagnosis
Clinicopathologic and radiographic abnormalities are Treatment
common but do not definitively document RMSF. Neutro- Supportive care for gastrointestinal tract fluid and electrolyte
philic leukocytosis, with or without a left shift and toxic cells, losses, renal disease, disseminated intravascular coagulation,
is found in most clinically affected dogs. Platelet counts are and anemia should be provided as indicated. Overzealous
variable, but in one study 14 of 30 dogs had less than 75,000 fluid therapy may worsen respiratory or CNS manifestations
platelets/µL without evidence of disseminated intravascular of disease if vasculitis is severe.
coagulation (Gasser et al., 2001). Leukocytosis and throm- Tetracycline derivatives, chloramphenicol, and quino-
bocytopenia were the most common laboratory findings in lones are the antirickettsial drugs used most frequently.
experimentally infected dogs (Levin et al., 2015). In some Doxycycline (5-10 mg/kg PO q12h for 21-28 days) is the
naturally infected dogs, hemostatic abnormalities consistent preferred treatment. In one study of experimentally infected
with disseminated intravascular coagulation occur. Anemia dogs, treatment for 16 days resulted in temporary clinical
occurs in some dogs, primarily from blood loss. Increased improvement in one dog that then relapsed (Levin et al.,
activities of alanine aminotransferase, aspartate aminotrans- 2014). In one study of 30 dogs with RMSF, all dogs survived
ferase, and alkaline phosphatase, as well as hypoalbumin- and no apparent differences in response rate occurred among
emia, occur frequently. Because R. rickettsii does not result tetracycline, doxycycline, chloramphenicol, or enrofloxacin
in chronic intracellular infection as does ehrlichiosis, hyper- (Gasser et al., 2001). Fever, depression, and thrombocytope-
globulinemia is rare. Renal insufficiency in some dogs causes nia often begin to resolve within 24 to 48 hours after starting
azotemia and metabolic acidosis. Serum sodium, chloride, therapy. Administration of prednisolone at anti-inflammatory
and potassium concentrations decrease in many dogs with or immunosuppressive doses in combination with doxycy-
gastrointestinal tract signs or renal insufficiency. Compared cline did not potentiate RMSF in experimentally infected
with dogs with chronic ehrlichiosis, chronic proteinuria dogs. The prognosis for canine RMSF is fair; it has been
from glomerulonephritis is rare. Positive direct Coombs test estimated that death occurs in less than 5% of affected dogs.
results occur in some dogs.
CNS inflammation usually causes increased protein con- Zoonotic Aspects and Prevention
centrations and neutrophilic pleocytosis in cerebrospinal Because RMSF has not been reported twice in the same dog,
fluid; some dogs may have mononuclear cell pleocytosis or permanent immunity is likely. Providing strict tick control
mixed inflammation. No pathognomonic radiographic can prevent infection. Human beings probably do not acquire
abnormalities are associated with RMSF, but both experi- R. rickettsii from contact with dogs, but dogs may increase
mentally and naturally infected dogs commonly develop human exposure to RMSF by bringing ticks into the human
unstructured pulmonary interstitial patterns. environment. People can also be infected when removing
A presumptive diagnosis of canine RMSF can be based ticks with activated R. rickettsii from the dog by hand. Two
on the combination of appropriate clinical, historic, and dogs and the owner all died of RMSF in one study (Elchos
clinicopathologic evidence of disease; serologic test results; and Goddard, 2003). As in dogs, RMSF in people is most
exclusion of other causes of the clinical abnormalities; and commonly diagnosed from April to September when most
response to antirickettsial drugs. Documentation of sero- of the tick vectors are most active. However, in areas endemic
conversion or an increasing titer 2 to 3 weeks after initial for R. rickettsii and Rhipicephalus sanguineus, RMSF could
serologic testing suggests recent infection. Positive serum be diagnosed year round. RMSF can be fatal in some infected
antibody test results alone do not prove RMSF because sub- people, particularly if treatment is not started soon after
clinical infection is common. In addition, positive serum clinical signs are recognized (Drexler et al., 2017; Helmick
antibody tests do not document infection by R. rickettsii et al., 1984).