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Cytauxzoonosis in Cats
What it is:
A life-threatening infectious disease of domestic cats.
Caused by infection with a protozoan parasite, Cytauxzoon felis.
An apicomplexan parasite.
Distribution:
First discovered in Missouri in the mid-1970s.
Distribution is expanding.
Reported in domestic cats in many US states, including Missouri, Arkansas, Florida, Georgia, Louisiana, Mississippi, Oklahoma, Texas, Kentucky, Kansas, Tennessee, North Carolina, South Carolina, Nebraska, Iowa, Virginia, and Illinois.
Anecdotally reported in Alabama and Ohio.
Primarily found in the southcentral and southeastern United States.
Etiology (Cause):
Cytauxzoon felis.
Hosts:
Aberrant/Dead-end Host: Domestic cat (initially considered due to acute/fatal course, but survivors exist).
Natural Host: Bobcat (Lynx rufus).
Reservoir Hosts: Bobcats and domestic cats that survive infection.
Other Wild Felids (USA & Other Countries): Cougars, panthers, tigers, lions, jaguars, pumas, ocelots, Iberian lynx, European wild cats, an Asiatic wildcat.
Other animals: Meerkats.
Susceptibility: In experimental studies (1980s), only bobcats and domestic cats were confirmed susceptible among 91 animal types tested.
Transmission:
Primarily by the lone star tick (Amblyomma americanum).
Also reported experimentally with the American dog tick (Dermacentor variabilis) (considered less effective).
Occurs after ticks are attached for >36-48 hours after infestation.
Experimental infections induced by parenteral injection of tissue homogenates (SC, IP, IV) from acutely infected cats.
Not induced by: Intragastric administration of tissues, housing noninfected with infected cats without vectors, or perinatal transmission (in one study). Suggests oral and direct "cat-to-cat" transmission does not occur.
Life Cycle and Pathogenesis:
Tick transmits sporozoites into the cat.
Sporozoites infect macrophages and undergo schizogony to form schizonts.
Schizonts increase dramatically in size (~15 mcm to ~250 mcm).
Schizonts are most commonly found in lymph node, spleen, liver, lung, and bone marrow, but can be in many organs.
Schizonts form "parasitic thrombi" occluding blood vessels.
This leads to widespread ischemia, tissue necrosis, and death.
Schizonts rupture and release piroplasms (merozoites), which infect RBCs.
Piroplasms in RBCs are innocuous.
Parasitemia (piroplasms in RBCs) is typically 1%-4%, but can be >10%.
Cats that survive the acute stage remain chronically parasitemic and clinically asymptomatic.
Risk Factors:
Seasonal tick activity: Typically diagnosed April through September. Can occur earlier or later depending on climate.
Habitat: Cats living near heavily wooded, low-density residential areas, especially close to natural or unmanaged habitats where ticks and bobcats may be present.
Clinical Findings & Lesions:
Onset of signs typically 5–14 days (average ~10 days) after tick transmission.
Most common presenting signs: Depression, lethargy, and anorexia.
Most common physical exam findings: Fever (up to 106°F / 41°C) and dehydration.
Additional findings: Icterus, lymphadenopathy, hepatosplenomegaly, dyspnea.
Less often: Splenomegaly, hepatomegaly, lymph node enlargement, pulmonary edema.
In extremis: Often hypothermic, dyspneic, and vocalize as if in pain.
Without treatment, death typically occurs within 2–3 days after peak temperature.
Necropsy findings: Splenomegaly, hepatomegaly, enlarged lymph nodes, renal edema, pulmonary edema/congestion/serosal surface petechiation, progressive venous distention, often hydropericardium with epicardial petechiation.
Laboratory Findings:
CBC: Leukopenia with toxic neutrophils and thrombocytopenia. Normocytic, normochromic anemia seen at later stages.
Biochemistry: Most common abnormalities are hyperbilirubinemia and hypoalbuminemia. May see increased liver enzymes and azotemia.
DIC: Identified in 5/5 cats in one study. Supported by prolonged PT/aPTT, thrombocytopenia, elevated D-dimers.
Diagnosis:
Based on clinical signs and history [implied].
Microscopic observation: Identification of piroplasms in RBCs or schizonts in tissues or blood smears.
Piroplasms: Found in RBCs. Variable detection, seen with increasing body temp, typically 1-3 days before death. Round to oval (~0.8-2.2 mcm), pale center, magenta nucleus (round/crescent). Can be pleomorphic. Must differentiate from Mycoplasma haemofelis, Howell-Jolly bodies, artifact.
Schizonts: Occur in tissues before piroplasms in RBCs. Can be seen in peripheral blood smears (feathered edge), potentially mistaken for platelet clumps. Best seen on cytology of fine-needle aspirates of lymph node, spleen, or liver. 15–250 mcm diameter, ovoid nucleus with prominent nucleolus, distended cytoplasm with basophilic particles.
Microscopy sensitivity can be poor (cyclic parasitemia, rapid disappearance, dissociation in EDTA), specificity poor if morphology atypical [implied by PCR description].
PCR: Greater sensitivity and specificity than microscopy. Can discriminate between Cytauxzoon species [implied]. Run on whole blood, spleen aspirates [implied]. Recommended in suspect cases when parasite isn't seen, and to confirm identification. Used to screen blood donors [implied by other parasitic diseases].
Serologic assays not mentioned [implied lack of availability].
Treatment and Recovery:
Combination therapy: Atovaquone (15 mg/kg, PO, three times daily) and azithromycin (10 mg/kg, PO, once daily) for 10 days is recommended. Start quickly.
Other drugs (parvaquone, buparvaquone, trimethoprim/sulfadiazine, etc.) have less success and more side effects.
Supportive care: IV fluids, nutritional support, heparin (100–200 U/kg, SC, three times daily).
May include oxygen, blood transfusions (recipients need monitoring).
Anti-inflammatory drugs (glucocorticoids) may be considered for severe hemolysis or possible IMHA [implied from Hemotropic Mycoplasma context], NSAIDs contraindicated with azotemia/dehydration.
Minimize stress and handling. Quiet/dark environment helpful.
Recovery (resolution of fever) is often slow, may take 5–7 days.
Survivors have complete clinical recovery within 2–3 weeks.
Treated animals may remain persistently infected with piroplasms (carriers).
No therapeutic regimen completely clears the organisms [implied].
Prevention:
Routine use of a tick preventive is recommended. Disease can still occur despite topical agents alone.
Tick-repellent collar (imidacloprid 10%/flumethrin 4.5%) prevented infection in one study.
Topical acaracide (selamectin 6mg/kg + sarolaner 1mg/kg) prevented infestation and transmission in one study, especially if applied several days before exposure.
Best method of prevention: Exclusion of cats from risky areas (i.e., indoor only).
Additional studies needed for acaracidal products.
Prognosis:
Historically, mortality was nearly 100% without treatment.
With atovaquone/azithromycin + supportive care, survival rate was 64% in a large case series.
Survival may be associated with specific parasite subtypes (e.g., cytb1).
Survival of natural infection without treatment has been reported in some cats that appeared less sick initially.
Hypotheses for survival: atypical infection route, innate immunity, carrier detection, decreased virulence/new strain, inoculum dose, treatment timing/type.
Key Points (Summary):
Life-threatening infectious disease transmitted by the lone star tick.
Common signs: depression, lethargy, anorexia, fever. Additional signs: icterus, lymphadenopathy, hepatosplenomegaly, dyspnea.
Diagnosis: Microscopy (piroplasms/schizonts) or PCR.
Treatment: Atovaquone + azithromycin, heparin, supportive care, minimal stress.
Prevention: Tick preventives, exclusion from risky areas.
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