Assessment Anatomic diagnosis

Etiologic diagnosis—Differential diagnoses for right facial nerve (cranial nerve VII) paralysis considered for the cat of the present report were otitis media, infectious diseases (FeLV or FIV infection, toxoplasmosis, or feline infectious peritonitis [FIP]), noninfectious inflammatory neuropathy, or neoplasia. Given the cat's signalment, neoplasia was considered unlikely, but lymphoma was a possible differential diagnosis. The cat also had no known history of trauma; thus, a trauma-related problem was also considered unlikely. Diagnostic testing included a CBC and serum biochemical analysis to evaluate general wellness. A blood sample was obtained, and an immunoassay to detect circulating FeLV antigen and anti-FIV antibody and indirect fluorescent anti-Toxoplasma gondii IgG and IgM tests were performed to evaluate for the aforementioned infectious diseases. Magnetic resonance imaging^a of the head was performed to detect potential structural abnormalities within the brain, peripheral nerves, skull, or surrounding tissues. A sample of CSF was collected via cerebellomedullary cisternal puncture following MRI for fluid analysis (to evaluate for evidence of infection, inflammation, or neoplasia) and PCR assay testing for feline coronavirus (assessment for FIP).

View Full Size

Sagittal (A) and transverse (B) T2-weighted images of the brain of a 9-month-old domestic shorthair cat that was examined because of intermittent elevation of the right third eyelid. Notice that there are no abnormalities of the cerebral hemispheres, cerebellum, or cranial nerves. The dotted reference line in the sagittal image (A) corresponds to the position of transverse image (B). In panel B, the tympanic bullae and middle ear structures (arrows) appear normal.

Citation: Journal of the American Veterinary Medical Association 253, 2; 10.2460/javma.253.2.163

• Download Figure
• Download figure as PowerPoint slide

Diagnostic test findings—The CBC revealed that the cat had mild thrombocytopenia (200,000 platelets/μL; reference interval, 300,000 to 800,000 platelets/μL) with no other abnormalities. A manual platelet count was not performed, but platelet clumping could potentially explain the low value. Serum biochemical analysis revealed no abnormalities. Neither circulating FeLV antigen nor anti-FIV antibody was detected. The cat was anesthetized, and MRI of the brain was performed. Image sequences included sagittal and transverse T2-weighted, transverse T2-weighted fluid-attenuated inversion recovery, transverse gradient echo T2*, and pre- and postcontrast 3-plane T1-weighted images. The MRI images were interpreted by a board-certified veterinary radiologist. Images obtained without contrast agent administration revealed no important abnormalities of the cerebral hemispheres, cerebellum, brainstem, retrobulbar spaces, globes, or cranial nerves. While awaiting the results of the CSF analysis, FIP PCR assay, and anti-Toxoplasma antibody titer assessments, treatment with clindamycin (13 mg/kg [5.9 mg/lb], PO, q 12 h) was initiated, and lubrication of the right eye with artificial tear ointment every 8 hours was continued. The CSF analysis revealed a WBC count of 1 WBC/μL (reference interval, 0 to 8 WBCs/μL); the RBC count was 1,000 RBCs/μL (reference limit, 0 RBCs/μL), which was suggestive of blood contamination. The CSF protein concentration was normal (26 mg/dL; reference interval, < 36 mg/dL). No evidence of infectious agents, neoplasia, or pleocytosis was present within the CSF sample. There were no genetic sequences of feline coronavirus in the CSF sample as determined by PCR assay. The indirect fluorescent anti–T gondii IgG and IgM tests revealed IgG against T gondii (maximum dilution, 1:2,048), but no IgM against T gondii was detected at the starting dilution of 1:64. On consideration of the test findings in combination, a presumptive diagnosis of protozoal neuritis (toxoplasmosis) resulting in right cranial nerve VII (facial nerve) dysfunction was made.

Comments

Toxoplasma gondii is a protozoal parasite that has the potential to infect all warm-blooded animal species, including humans.¹ Felids are the only definitive host and typically become infected by ingestion of intermediate hosts that have developed tissue cysts containing bradyzoites.¹ Cats rarely develop clinical signs after ingestion of bradyzoites; however, systemic spread of Toxoplasma organisms can be severe in kittens infected in utero or via lactation, which are often stillborn or die before weaning.¹ Adult cats rarely develop clinical disease as a result of acute exposure or reactivated chronic infection following immunosuppression.¹ Clinical signs of toxoplasmosis include anorexia, lethargy, dyspnea (secondary to pneumonia), fever, weight loss, icterus (secondary to hepatitis or cholangiohepatitis), myocarditis, gastrointestinal tract signs, abdominal effusion, musculoskeletal pain, ocular disease, neurologic deficits, cystitis, dermatitis, and death.¹ Sudden onset or slow progression of signs is possible, but toxoplasmosis can be rapidly fatal with respiratory tract and CNS involvement.¹ Neurologic disease without concurrent systemic signs is more often a result of reactivated infection than a result of acute infection.¹ Segmental myelitis and intracranial granulomas have been reported^2,3 as toxoplasmosis-associated CNS changes in cats. In cats, Toxoplasma infection may also cause peripheral nervous system signs similar to those of protozoa-induced polyradiculoneuritis in dogs, and distal polyneuropathy secondary to toxoplasmosis in a cat has been described.^3,4

Currently, the guidelines for making a tentative diagnosis of clinical toxoplasmosis include a combination of serum anti-Toxoplasma IgM titer > 1:64 or a 4-fold increase in serum anti-Toxoplasma IgG titer over a period of 2 to 5 weeks, presence of relevant clinical signs, exclusion of other possible causes of the clinical signs, and positive clinical response to appropriate medical treatment.^1,3 Interpretation of serologic test results for Toxoplasma infection in cats can be challenging because presence of antibodies can indicate current infection or previous exposure, either with or without clinical signs.⁵ In 1 study,⁵ the overall T gondii seroprevalence among clinically ill cats in the United States was 31.6%. Compared with T gondii–specific IgG, the presence of T gondii–specific IgM is thought to indicate more recent exposure and may be more useful as a marker of clinical toxoplasmosis in cats.⁵ Serum IgG concentration can peak in 2 to 3 weeks after infection, making a 4-fold increase in antibody titer difficult to detect because of the narrow time frame for monitoring dramatic changes in IgG concentration.¹ The cat of the present report did not have detectable T gondii–specific IgM at the time of the initial serologic testing, but did have detectable T gondii–specific IgG at a high dilution. In a previously described case,² a cat with T gondii meningomyelitis also had no detectable T gondii–specific IgM at the time of diagnosis, suggesting that the infection was not recent but possibly reactivated by stress.

Drugs considered for the treatment of clinical toxoplasmosis are usually associated with suppression of Toxoplasma replication rather than with parasiticidal action. Clindamycin (10 to 12.5 mg/kg [4.55 to 5.68 mg/lb], PO or IM, q 12 h for 4 weeks) is the treatment of choice for clinical toxoplasmosis. A combination of trimethoprim and a sulfonamide (15 mg/kg [6.8 mg/lb], PO, q 12 h for 4 weeks) may act synergistically with clindamycin in the treatment of systemic toxoplasmosis.¹ Relapse of clinical signs has been reported even after appropriate drug selection and strong positive response to treatment.^3,6 The cat of the present report had complete return of right facial nerve function and no other neurologic deficits when examined 1 month following initiation of treatment with clindamycin. The cat was evaluated every 60 days for 6 months. Assessment of anti-Toxoplasma antibody titers was performed at each follow-up visit during the treatment period, and the cat remained positive for Toxoplasma-specific IgG, IgM, or both, despite continued treatment with clindamycin (13 mg/kg, PO, q 12 h) and the addition of ponazuril (7.5 mg/kg [3.4 mg/lb], PO, q 12 h) and trimethoprim-sulfonamide (15 mg/kg, PO, q 12 h). The cat was considered seropositive for Toxoplasma when antibodies were detected at a dilution of ≥ 1:64. Although acquired polyneuropathy caused by infections with Toxoplasma spp in cats has previously been described,³ solitary cranial neuropathy has not, to our knowledge. As illustrated by the case described in the present report, Toxoplasma infection should be considered as a differential diagnosis for cranial mononeuropathies in cats.