Objectives of this study were to determine prevalence of infection in feral cats in Northern Florida with a select group of infectious organisms and to determine risk factors for infection. Blood samples or sera from 553 cats were tested with a panel of antibody, antigen or PCR assays. Male cats were at higher risk for FIV, Mycoplasma haemofelis, and M. haemominutum. Infection with either FeLV or FIV was associated with increased risk for coinfection with the other retrovirus, M. haemofelis, or M. haemominutum. Bartonella henselae had the highest prevalence and was the only organism that did not have any associated risk for coinfection with other organisms. Feral cats in this study had similar or lower prevalence rates of infections than those published for pet cats in the United States. Thus, feral cats assessed in this study appear to be of no greater risk to human beings or other cats than pet cats.

Canine histiocytic ulcerative colitis (HUC) is characterized by colonic inflammation with predominantly periodic acid-Schiff (PAS)-positive macrophages. The inflammation results in colonic thickening, ulcerations, and distortion of normal glandular architecture. Resultant clinical signs consist of chronic large bowel diarrhea, tenesmus, and marked weight loss, and the disease frequently results in euthanasia. Conventional therapy consists of some combination of prednisone, azathioprine, sulfasalazine, and metronidazole. Nine dogs (8 Boxers and 1 English Bulldog) with histologic confirmation of HUC were treated with antibiotic therapy (either with enrofloxacin alone or in combination with metronidazole and amoxicillin). Clinical signs, physical examination findings, laboratory abnormalities, and the histologic severity of the disease were evaluated. Four of the 9 dogs had been treated previously with conventional therapy and had failed to respond favorably; then, these dogs were placed on antibiotic therapy (enrofloxacin, n ϭ 1; enrofloxacin, metronidazole, and amoxicillin, n ϭ 3) and had resolution of clinical signs within 3-12 days. Five dogs were treated solely with antibiotic therapy (enrofloxacin, n ϭ 1; enrofloxacin and metronidazole, n ϭ 1; enrofloxacin, metronidazole, and amoxicillin, n ϭ 3), and clinical signs resolved in 2-7 days. Repeated biopsy specimens were obtained from 5 dogs after treatment, and all showed marked histologic improvement. The increase in body weight after treatment was statistically significant (P ϭ .01). Three dogs currently are not on any treatment and have had resolution of clinical signs for up to 14 months. These observations suggest that an infectious agent responsive to antibiotics plays an integral role in the clinical manifestation of canine HUC, and they support the use of antibiotics in its treatment.

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These findings support the development of genetic heterogeneity of H. pylori during long-term colonization either by genetic drift or by in vivo recombination. Such genomic modification in vivo could explain the naturally occurring heterogeneity of H. pylori.