Was disease involved in the decimation of Guam's avifauna?

Between 1982 and 1986, 402 (290 live, 112 dead) exotic, migrant or native resident birds on Guam were surveyed for disease-causing agents to determine the role of disease in the decline of native forest bird populations on Guam. Traumatic injury, primarily from collisions with motor vehicles and predation, was the most prevalent (46%) cause of death. Thirty-eight percent of the carcasses examined were in poor body condition largely as a result of inadequate nutrition in captive native birds and poultry and adipose exhaustion in errant migrants. A variety of commensal or opportunistic bacteria, including Salmonella spp., were cultured from 220 birds, and nothing remarkable was found in 15 fecal samples. Lastly, no haematozoans, the suspected cause for the decline of the Hawaiian avifauna, were observed in blood slides examined from 260 birds. Based on the results of the survey and other lines of evidence presented in the discussion, we concluded there were no data implicating disease in the decline of Guam's avifauna.

Intestinal multiplication of Mycobacterium paratuberculosis in athymic nude gnotobiotic mice.

In this study gnotobiotic mice were inoculated with a human isolate of Mycobacterium paratuberculosis (strain Linda; ATCC 43015) in an attempt to investigate the pathogenesis of intestinal paratuberculosis. Mycobacterium paratuberculosis-monoassociated nu/+ mice developed a persistent low-level intestinal infection but did not support progressive bacillary multiplication. In contrast, monoassociated nu/nu mice eventually harbored approximately 10(7) M. paratuberculosis per g of intestinal tissue. Acid-fast bacilli and granulomas were observed in the intestinal mucosa and livers of nu/nu but not nu/+ mice. Similar results were obtained after intragastric inoculation of M. paratuberculosis into nu/+ and nu/nu flora-defined mice. These observations suggest that the presence of an intact cellular immune system is important for limiting intestinal multiplication of M. paratuberculosis. The results of this study may be relevant to our understanding of the pathogenesis of Johne's disease in ruminants and of human inflammatory bowel diseases that have a mycobacterial etiology (e.g., some cases of Crohn's disease and Mycobacterium avium-Mycobacterium intracellulare enteritis in patients with acquired immunodeficiency syndrome).

Inclusion body disease of cranes: comparison of pathologic findings in cranes with acquired versus experimentally induced disease.

Inclusion body disease of cranes was the cause of death in 17 immature and mature cranes of 5 different species in Wisconsin. A herpesvirus of unknown origin was the apparent cause. An isolate of this herpesvirus was used to experimentally infect 3 species of cranes. Macroscopic and microscopic lesions associated with naturally acquired and experimentally induced disease were essentially identical. Multifocal hepatic and splenic necrosis was found in all cranes evaluated. Necrosis of the gastrointestinal tract, thymus, and bursa of Fabricius also was seen in some of the cranes. Eosinophilic intranuclear inclusion bodies often were commonly associated with hepatic lesions, sometimes with the splenic lesions, and rarely with the thymic or gastrointestinal tract lesions. The lesions of this inclusion body disease were similar to those reported for cranes in Austria from which a crane herpesvirus was isolated.

Neoplasms identified in free-flying birds.

Nine neoplasms were identified in carcasses of free-flying wild birds received at the National Wildlife Health Laboratory; gross and microscopic descriptions are reported herein. The prevalence of neoplasia in captive and free-flying birds is discussed, and lesions in the present cases are compared with those previously described in mammals and birds.