Subacute and Fulminating Pulmonary Cryptococcosis with Dissemination in an Atlantic Bottlenosed Dolphin (Tursiops truncatus)
IAAAM 1998
Robert D. Murnane1, DVM, PhD; Michael J. Kinsel1, DVM; Michael B. Briggs2, DVM, MS
1University of Illinois Zoological Pathology Program, Loyola University Medical Center, Maywood, IL, USA; 2Brookfield Zoo, Brookfield, IL, USA

Abstract

An 18+ year old, approximately 180 kg, male Atlantic bottlenosed dolphin (Tursiops truncatus) presented dead in fair postmortem condition and poor nutritional condition with greatly reduced muscling and scant adipose stores. There was a solitary, moderate-sized, healing cutaneous ulceration on the ventrum of the peduncle. The lungs were diffusely firm and dark red with black mottling, and contained multiple, discrete nodules. The left, cranial lobe was most severely affected. Histologically the lungs contained massive numbers of Cryptococcus sp organisms effacing the majority of alveoli. The organisms were 4-8 µm diameter not including the capsule, with abundant, thick and clear, mucicarmine and periodic acid Schiffs positive capsule, and were often budding. Organisms were associated with extensive edema and hemorrhage and also with moderate to large regions of necrosis. There was generally mild to moderate, though regionally severe, pyogranulomatous infiltrate associated with the organisms. Organisms and inflammation extended multifocally into arteries, arterioles, veins and venules. Bronchioles often contained organisms though the lumen of larger airways were mostly clear. The trachea had moderate numbers of organisms in the submucosa associated with moderate inflammation.

Dissemination of the Cryptococcus sp organism had occurred in virtually all tissues examined except for the brain, urinary bladder, testis and skeletal muscle. Renal cortices had numerous, moderate-sized to coalescing and large aggregates of organisms obliterating parenchyma, and associated with mild to moderate pyogranulomatous inflammation. Numerous glomeruli had few to large numbers of organisms in capillary loops which partially to completely obliterated tufts. Spleen had large numbers of often coalescing aggregates of organisms, some with necrotic centers, and associated with moderate, primarily granulomatous infiltrate. One of three lymph nodes examined had a small aggregate of organisms. Liver had multifocal though usually periportal aggregates of organisms with minimal to moderate inflammation. Stomach, small intestine and colon had scattered organisms in mucosa or submucosa, and one colonic submucosal arteriole was occluded by a group of Cryptococcus sp organisms; there was no inflammation associated with these organisms. Pancreas and heart also had scattered organisms interstitially not associated with inflammation. The ulcerated region of skin had a deep, limiting bed of fibrosis and granulation tissue, beneath which was a small focus of organisms. Sections of skin from other areas were normal. The only other lesion of note was extensive hepatic hemosiderosis with lobular collapse; this lesion was felt to be of geriatric etiology and not currently of clinical significance.

Death was from cryptococcosis, and the causative agent likely was Cryptococcus neoformans, though culture would have been necessary for specific identification; tissue for culture was not available. The infection almost certainly was primary pulmonary considering the massive numbers of organisms present in the lungs. Skin and GI tract as portals of entry are unlikely in this case: the organisms in the ulcerated region of skin were below the limiting bed of granulation tissue and fibrosis, and organisms in the GI tract were few, they were not associated with inflammation, and ulceration of the mucosa was not seen. Further, the infection was subacute and fulminating, with sepsis and widespread dissemination during the fulminating stage; this interpretation is supported by the relative paucity of inflammation associated with the organism in most organs other than lung. No predisposing factor was identified, and therefore Cryptococcus sp was a presumptive primary pathogen. However, immunosuppression secondary to poor body condition or advanced age may have predisposed the animal to cryptococcosis.

To the knowledge of the authors, this is the first report of death from cryptococcosis in a marine mammal.

Acknowledgments

The authors wish to thank Jane Chladny and the University of Illinois College of Veterinary Medicine Histopathology Laboratory for excellent technical assistance.

Speaker Information
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Robert D. Murnane, DVM, PhD
University of Illinois Zoological Pathology Program, Loyola University Medical Center
Maywood, IL, USA


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