Pathology of Experimental Mycoplasmosis in American Alligators

Abstract

Mycoplasma alligatoris was the suspected etiology of an epidemic of acute multisystemic inflammatory disease which emerged in captive American alligators (Alligator mississippiensis) in Florida (USA) in 1995. In an experimental inoculation study conducted from April through October 1999, 18 alligators were inoculated with 10 2 , 10 4 , or 10 6 colony forming units (CFU) of M. alligatoris by instillation into the glottis. As early as 1 wk post-inoculation (PI), mycoplasma were cultured from blood of three of six alligators inoculated with 10 6 CFU. Two of those died and the third was euthanatized within 4 wk PI. Necropsy gross findings included fibrinous polyserositis and polyarthritis. Histopathologic changes in affected individuals included pulmonary edema, interstitial pneumonia, pericarditis, myocarditis, meningitis, and synovitis. Mycoplasma were cultured quantitatively in high numbers from trachea, lung, coelomic cavity, liver, spleen, interior of pericardial sac, heart, blood, brain, and limb joints. In alligators inoculated with 10 6 CFU, heterophilia and moderate hyperglycemia peaked about 4 wk PI, and seroconversion occurred by 6 to 8 wk PI. Necropsy gross and histologic findings were generally unremarkable for the surviving alligators inoculated with 10 6 CFU, alligators inoculated with 10 2 or 10 4 CFU, and four uninoculated control alligators. Mycoplasma were not cultured at any time point from those alligators. The findings confirm that M. alligatoris can cause fulminant inflammatory disease and rapid death of alligators.

Annual and seasonal survival of adult female Mottled Ducks in southern Florida, USA

“…Crocodilians have been known to live with opportunistic pathogenic bacterial infections but exhibit no physiological effects (Manolis et al, 1991, Madsen, 1993, Madsen et al, 1998. While crocodilians are not completely immune to microbial infections (Gorden et al, 1979, Novak and Siegel, 1986, Brown et al, 2001), these species do exhibit remarkable resistance to microbial colonization. The results from this study provide the first evidence that the American alligator has an active serum complement system.…”

Sialidase Activity in Mycoplasma Synoviae

“…The hypervirulent Mycoplasma alligatoris A21JP2 T is the only extant isolate in which sialidase activity has been demonstrated (4). The activity is congruous with the invasiveness of M. alligatoris which is rapidly fatal to susceptible hosts, in contrast to the chronic epithelial lesions observed during typical mycoplasmal infections (3). Therefore the discovery of a putative sialidase gene in an isolate of M. synoviae was remarkable for at least three reasons: M. synoviae is phylogenetically distant from M. gallisepticum within the class Mollicutes (16); it is in the same phylogenetic cluster as M. alligatoris, although M. synoviae is less virulent; and sialic acid degradation pathways are absent from the other annotated Mycoplasma spp.…”

Role of sialidase in Mycoplasma alligatoris-induced pulmonary fibroblast apoptosis

“…The lung is a target organ of M. alligatoris in vivo, and acute interstitial or fibronecrotic pneumonia is the likely proximate cause of death of individuals that succumb to M. alligatoris infection (Brown et al, 2001b;Pye et al, 2001). Alveolar fibroblasts are the major cell type comprising the gas-exchanging structures of the lung.…”

“…M. alligatoris can be cultured in high numbers from the lower respiratory tract of infected individuals, where pathologic changes include fibrinous pleuritis, pulmonary edema and congestion, and diffuse interstitial to fibronecrotic pneumonia as early as 1 wk after exposure (Brown et al, 2001b;Brown et al, 2001c;Pye et al, 2001). A genome survey revealed that M. alligatoris strain A21JP2 T notably possesses the "spreading factors" sialidase and hyaluronidase, a combination unprecedented among mycoplasmas but common among other invasive pathogens, which could degrade host extracellular matrix (ECM) glycans during nutrient scavenging to contribute to disease (Brown et al, 2004).…”