Update on babesiosis, leptospirosis in dogs

Update on babesiosis, leptospirosis in dogs

Reviewing means of transmission, latest diagnosis and treatment protocols
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Jul 01, 2008

Q: Please provide a review on canine babesiosis and canine leptospirosis.

A. Dr. Douglass K. Macintire lectured on Diagnosis and Treatment of Canine Babesiosis and Canine Leptospirosis at the 2007 American College of Veterinary Internal Medicine Forum in Seattle. Here are some relevant points from his presentation:

Canine babesiosis is an emerging infectious disease in North America. Historically, the disease has been classified either as "large babesia" (B. canis) or "small babesia" (B. gibsoni) on the basis of the size of intraerythrocytic forms. There are three subspecies of the "large" babesia: B. canis vogeli (found in the United States), B. canis canis (found in Europe) and B. canis rossi (found in South Africa). Large babesia piroplasms appear as bi-lobed, pear-shaped organisms in the red blood cells.


Johnny D. Hoskins DVM, PhD, Dipl. ACVIM
There are at least three genetically distinct, but morphologically indistinguishable, small piroplasms that can infect dogs. Babesia gibsoni was first diagnosed in Asian dogs but now is reported worldwide. It is being diagnosed in epidemic proportions in American Pit Bull Terriers throughout the United States. A second small babesia was reported in dogs from California in 1991. Although the organism was initially thought to be B. gibsoni, subsequent PCR analysis has reclassified the piroplasm as a Theilena species. A third small piroplasm, a babesia microti-like organism has been found in dogs in northwest Spain as a newly emerging pathogen.

Babesiosis can cause severe, life-threatening signs in some dogs, while others show no outward signs of disease. Common findings in affected dogs include hemolytic anemia, thrombocytopenia, hemoglobinuria, icterus, pallor, splenomegaly, lymphadenopathy and fever. Clinical signs resemble those associated with immune-mediated hemolytic anemia, immune-mediated thrombocytopenia or other tick-borne diseases. It is important to identify the correct diagnosis, as early recognition and appropriate treatment are important for reducing associated morbidity and mortality.

Transmission, diagnosis

The vectors known to transmit babesiosis include Rhipicephalus species, Haemaphysalis species and Dermacentor species. The tick must feed for two to three days for transmission to occur from the salivary glands of the infected tick to the dog's bloodstream. The parasites enter red blood cells, causing extravascular and intravascular hemolysis. Autoagglutination and secondary immune-mediated destruction of red blood cells may occur.


Correct diagnosis is key: Babesiosis can cause severe, life-threatening signs in some dogs, while others show no outward signs. That's why early, correct identification of the disease is important.
Diagnosis can be confirmed by finding the organism on a blood smear or by PCR testing. Only the PCR test can identify species or subspecies, and it is more sensitive in detecting subclinical carrier animals than a blood smear. Serologic titers >1:64 are considered positive, but they do not differentiate clinical exposure from active infection, and there is cross-reactivity between species. Dogs with a positive babesia titer should not be used as blood donors.

Other means of transmission besides arthropod vectors include blood contamination through poor kennel practices, such as sharing needles or surgical instruments, dog fighting and blood transfusions. Vertical transmission from dam to offspring is suspected as a means of transmission among American Pit Bull Terriers and Greyhounds. About 50 percent of American Pit Bull Terriers surveyed have a positive PCR test for B. gibsoni, and most have subclinical infections.

Treatment is recommended even in subclinically infected dogs to reduce the natural reservoir for transmitting the disease to arthropod populations. Aggressive control measures to eradicate the vector are key to eliminating spread of the disease.

The most commonly used treatment is imidocarb dipropionate, 6.6 mg/kg IM or SC once, repeated in seven to 14 days. Pretreatment with atropine (0.04 mg/kg IM or SC 30 minutes prior to imidocarb) is recommended to decrease cholinergic side effects. Supportive care with a blood transfusion or Oxyglobin® (10-30 ml/kg IV) may be needed in severely anemic dogs.

Dogs that are febrile and dehydrated may require intravenous fluid support. Treatment with imidocarb usually does not eliminate the parasite, but most dogs show marked clinical improvement. Recently, a new treatment has shown promise in eliminating the organism, but it is very expensive. Dogs treated with atovaquone (13.4 mg/kg PO q 8 h with a fatty meal) and azithromycin (10 mg/kg PO q 24 h) for 10 days became negative on PCR testing 60 to 90 days post-treatment. If anemia and thrombocytopenia do not improve with anti-protozoal treatment, immunosuppressive therapy with prednisone (1 mg/kg q 12 h) may be needed and tapered off gradually until anemia resolves.

The babesia microti-like organism in Spain has been associated with azotemia and protein-losing nephropathy. The cause of renal pathology is thought to be secondary to immunoproliferative glomerulonephritis, but more research is needed to better elucidate the renal lesions.