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| December 2000 |
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| LEPTOSPIROSIS |
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Leptospirosis continues to be a significant clinical presence in canine medicine
since its resurgence this past decade. In addition to an increased number of cases, more diverse
clinical presentations are being recognized. Selection of appropriate vaccines and interpretation
of serologic results in the presence of vaccinal titers are emerging issues in clinical practice.
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| Epidemiology |
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Leptospirosis is caused by a spirochete, a motile spiral-shaped bacteria.
Distribution is worldwide. Two species of leptospires are primarily responsible for disease
in dogs. Leptospira interrogans includes the serovars bratislava, autumnalis, icterohemorrhagiae,
pomona, canicola and hardjo. A second species, Leptospira kirschneri contains the serovar
grippoty-phosa. Each serovar has a known reservoir host of one or more species. These reservoir
hosts may be subclinically infected and shed organisms for months to years.
When other susceptible species, or incidental hosts, become infected with that serovar they become
acutely ill. For example, reservoir hosts for L. kirschneri, serovar grippotyphosa are the vole,
raccoon, skunk and opossum. When dogs are infected with this serovar as incidental hosts they become
ill. Dogs, however, are the reservoir hosts for L. interrogans, serovar canicola which can cause
clinical disease in horses, cows and pigs. Although reservoir hosts may develop illness, disease in
incidental hosts is more severe, shedding periods are shorter, and transmission between animals is
less likely.
Infection occurs by direct contact with leptospires from infected animals. Infected urine,
venereal contact, bite wounds and ingestion of infected tissues are all possible routes of
transmission. Indirect spread from contact with contaminated soil and food may also result in
infection. The organism may survive for days to months in warm, moist environments.
Seropositive cats have been identified, but little clinical disease has been reported in this
species, as cats appear to be relatively resistant to leptospirosis.
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| Pathogenesis |
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Once infected animals become bacteremic, leptospires multiply in the kidney, liver,
spleen, central nervous system, ocular tissue and genital tract. In dogs, serovars canicola and
grippotyphosa result in more renal dysfunction, whereas serovars icterohemorrhagiae and pomona
produce more hepatic damage. Reservoir hosts may be subclinically infected and shed organisms for
months to years after recovery. Dogs with protective titers may have mild, inapparent illness or no
clinical signs. In susceptible animals, however, the acute phase of illness may result in acute renal
failure. Leptospiral toxins result in hepatic necrosis and subsequent cholestasis and hyperbilirubinemia.
Vascular endothelial damage during the bacteremic phase can result in disseminated intravascular coagulation
and thrombocytopenia. Although hemolysis is uncommon in dogs, a case of refractory hemolytic anemia with
positive leptospires serology responded to treatment for leptospirosis. Cattle infected with L. interrogans,
serovar pomona frequently develop hemoglobinemia and hemoglobinuria from a hemolytic toxin produced by that
serovar.
Although dogs appear to make a full recovery with appropriate treatment, chronic disease can be a sequela of
acute leptospirosis. Compensated chronic renal failure may follow acute renal failure. Hepatocellular damage and
altered hepatic immune response may lead to chronic hepatitis.
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| Clinical Signs |
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Dogs with leptospirosis commonly present with fever, anorexia, polydipsia, vomiting and
dehydration. Hyperesthesia may result from renal, muscle or meningeal pain. Coagulopathies may lead to
epistaxis, petechiae, hematemesis or melena. It is important to recognize that leptospirosis may be
subclinical, or that it may present as chronic illness. Thus, leptospirosis should be included in the
differential diagnosis in dogs with fever of unknown origin or with renal or hepatic disease of unknown
etiology. Two dogs presenting for evaluation of polyuria and polydipsia without concurrent signs of illness,
one four months old and one middle-aged, tested positive for leptospirosis and responded to treatment. Clinical
awareness and appropriate test selection led to a resolution of their disease; but these animals could easily
have been misdiagnosed as having congenital renal disease or interstitial nephritis.
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