Clinical, pathological, and molecular characterization of feline leprosy syndrome in the western USA
Authors: Foley J. E. , Gross T. L. , Drazenovich N. , Ramiro‐Ibanez F. , Anacleto E. 
Published: August 2004

Feline leprosy syndrome is caused by multiple species of mycobacteria; at least two histomorphologic subtypes have been reported from Australia and Canada, and PCR/DNA sequencing studies suggest that several species of mycobacteria may be implicated. To the authors’ knowledge, similar studies from the United States have not been performed. Ten cats with skin lesions characteristic of feline leprosy syndrome and acid‐fast confirmation of organisms were included in the study. The cats were evaluated by clinical follow‐up, histopathology, and molecular characterization (PCR with DNA sequencing). Eight of 10 cats were from coastal cities of Hawaii, Washington or California; two cats were from the coastal mountain range in California, approximately 30 miles inland. Additional environmental risk factors included access to the outdoors in nine cats, four of which were observed hunting. Skin lesions ranged from mildly alopecic and swollen to nodular and ulcerated. Lesions were evaluated histopathologically, using both H&E and Fites acid‐fast stains for necrosis, number and distribution of acid‐fast bacteria, and visibility of organisms on H&E examination. PCR and DNA sequencing of a fragment of the 16S rRNA gene was performed in all cases. Lesions from four cats yielded Mycobacterium visibilis/IWGMT 90242 species, as previously identified in Canadian but not Australian cases; in each of these, large numbers of acid‐fast bacteria were seen diffusely within non‐necrotic lesions. These organisms also were visible with H&E examination. Lesions from four cats were associated with M. lepraemurium: three had necrosis with few (three cases) to moderate (one case) numbers of acid‐fast bacteria that were not visible upon H&E examination. Organisms tended to cluster in necrotic foci. The remaining lesions from two cats included one each of Rhodococcus erythropolis and M. kansasii;both of these had M. lepraemurium‐type histomorphology. Clinically, cats with M. visibilis/IWGMTinfection tended to be older (mean age 10.3 years, P = 0.008) and have larger numbers of lesions (range four to too numerous to count) with recurrence (three cats), unexplained mortality(one cat), or concurrent disease (one cat coinfected with T. gondii). Cats with M. lepraemurium, or histomorphologically similar Rhodococcus erythropolis and M. kansasii infections,were younger (mean age 2.2 years) and tended to have few lesions (range 1–5; mean 2.2). These cases responded completely to excision and treatment with miscellaneous broad‐spectrum antibiotics. The presence of two clinically and histomorphologically distinct syndromes supports previous reports from Canada and Australia. Clinical differences from Australian cases were identified, specifically the benign course of M. lepraemurium‐typeinfections. The significance of the Rhodococcus erythropolis and M. kansasii is not clear; however, multiple species of mycobacteria have been recently identified by PCR in Canadian cases of feline leprosy syndrome. Geographic differences in specific organisms associated with feline leprosy syndrome may reflect local differences in risk factors, possibly due to differing ecologies of M. lepraemurium and M. visibilis in Australia, Hawaii and the continental United States.

Funding: Self‐funded.