Disseminated protothecosis in a dog.

A dog with forelimb lameness, bilateral retinal detachment, and hemorrhagic diarrhea, died. Necropsy demonstrated multifocal lesions in the skeletal musculature, myocardium, liver, thyroid glands, kidneys, eyes, and brain. Microscopically, the lesions contained numerous organisms and minimal cellular infiltrates. The morphologic and cultural characteristics of the organisms were similar to prototheca. The organisms in tissue sections reacted positively for Prototheca zopfii, using an indirect fluorescent antibody technique.

Lymphocyte transformation suppression caused by pyoderma--failure to demonstrate it in uncomplicated demodectic mange.

Three dogs with demodectic mange uncomplicated by a bacterial infection and 9 dogs with demodectic mange and pyoderma were tested for their lymphocyte response to phytomitogens in vitro and for the presence of the serum's lymphocyte immunoregulatory factors (SLIF) suppressing blastogenesis. None of the 3 dogs with uncomplicated demodectic mange showed any detectable dysfunction of their lymphocytes or presence of the blastogenesis suppressing SLIF. Their lymphocytes generally responded to the mitogens with more blastogenesis than lymphocytes from healthy controls. On the other hand, in the group of 9 dogs with demodicosis complicated by a bacterial infection, high levels of the blastogenesis suppressing SLIF for concanavalin A-sensitive cells were detected in 4 dogs, for phytohemagglutinin-sensitive cells in 2 dogs, and for pokeweed mitogen-sensitive cells in 1 (of only 3 tested) dog. Dysfunction of lymphocytes per se (detected by a decreased blastogenesis in nonsuppressive normal canine and bovine sera) was detected in 3 dogs with demodicosis with pyoderma. The success of the treatment of demodectic mange or the bacterial skin infection did not correlate with the previous presence or absence of the blastogenesis suppressing SLIF. The treatment of pyoderma was less successful in dogs with an increase in blastogenesis of unstimulated cells in fresh normal canine serum over that in autologous serum. All 3 dogs with a detected dysfunction of their lymphocytes either died or were euthanatized as untreatable cases. It is concluded that the development of demodectic mange per se did not cause the appearance of the blastogenesis suppressing SLIF, which was primarily related to the appearance and extent of the secondary bacterial skin infection.

Feline respiratory tract disease in Louisiana.

An investigation of feline respiratory tract disease (FRD) was made involving 65 affected cats (group 1) and 65 control cats (group 2) matched for age, sex, and residence. Feline calicivirus strains (FCV), feline herpesvirus-1 (FHV-1), or both, were isolated from 59% of group 1 cats and from 7% of group 2 cats. Isolation of these viruses showed a significantly greater (P < 0.05) relative risk for group 1 cats. Virus isolations were three times more frequent from males than from females older than 1 year (both groups), but were equally distributed between males and females younger than 1 year. Bacteria and fungi had a secondary role in both FCV- and FHV-1 associated FRD. Intestinal infections of Ancylostoma spp, Dipylidium caninum, and Toxocara cati were diagnosed more frequently in group 1 cats than in control (group 2). Paragonimus kellicotti was diagnosed in 3 group 1 cats, Taenia taeniaeformis in 1 group 1 cat, Isospora rivolta in 1 group 1 cat, and Giardia cati in 1 control cat. The present study supports the current concept of a primary viral cause for development of FRD.

Naturally occurring trypanosomiasis (Chagas' disease) in dogs.

Nine fatal cases of canine American trypanosomiasis (Chagas' disease) were encountered from November, 1972, through November, 1975. Of the 9 cases, 7 occurred in dogs from 5 central Texas counties, and all but one case was diagnosed during the months of September, October, or November. The source of infection was discovered in only one case--that being a doghouse heavily infested with Triatoma lectularius occulta. Each of 6 bugs collected had infective forms of the protozoan, Trypanosoma cruzi. Trypanosomiasis usually is not considered in the differential clinical diagnosis of cardiac dysfunction in man or other mammals in the United States. An antemortem diagnosis was made in only 1 of the 9 dogs, with diagnosis in the remaining dogs being made at necropsy. The predominant microscopic lesion in all dogs was necrotizing granulomatous myocarditis associated with the amastigotes of T cruzi.