Cryptosporidiosis is an increasingly diagnosed parasitic infection in reptile collections, particularly in snakes. The course of the disease is unusual since it tends to be self-limiting in immunocompetent bovines, canines, felines, and other species, but can be fatal in its reptilian host. The infection is often insidious in onset, causing irreversible pathological changes before physical signs develop. Clinically healthy, intermittent shedders may become symptomatic years after the parasite is first diagnosed in the animal. Additionally, the affected animal may die acutely, or the clinical disease may take up to two years before killing its host.
The life cycle of Cryptosporidium serpentis is thought to be similar to that of Cryptosporidium parvum,muris, and other species in mammals. Two types of infective stages are produced. The first is a thick-walled oocyst which contains four sporozoites. The oocysts are passed in the feces and remain infective in the environment for months, where they are extremely resistant to temperature extremes and disinfectants. These oocysts are responsible for both infections in new hosts as well as reinfection of the original host. The oocysts are ingested, and the four sporozoites are released. The second stage involves four sporozoites encased not in a thick wall, but rather in a single, thin membrane. This membrane ruptures after breaking out of a host cell, releasing the sporozoites and immediately reinfecting the host animal. In both stages, the sporozoites infect the microvillus border of the gastric glands, and in snakes, lesions are usually localized to the stomach.
The classic presentation of Cryptosporidium serpentis infection in the snake is an animal which regurgitates its meal within four days or less of ingestion. This regurgitation occurs because of decreased gastric lumen size and mucosal irritation. Since the diameter of the stomach has often increased, a noticeable swelling can be visualized and palpated in the mid-body region. The snake may
or may not be anorexic, depending^n how far the disease has progressed. Often, a mucoid diarrhea is noticed.
It is important to differentiate Cryptosporidiosis from other causes of regurgitation and gastritis. Suboptimal temperatures, inappropriate prey size, stress, and foreign body obstructions are other potential causes of regurgitation. Hibernation associated necrotizing gastroenteritis, parasitism from other protozoa and nematodes, viruses, Salmonella and other bacteria can all cause similar signs, but the gastric swelling is pathognomonic for Cryptosporidiosis.
In the living animal, Cryptosporidiosis can be diagnosed by gastric lavage,endoscopic gastric biopsy, fecal smears, and smears of mucous adhered to regurgitated prey items. Since oocysts are intermittently shed, it is recommended that multiple samples be taken. It is important to note that a negative result does not imply that the animal is not infected, only that oocysts may not be present in the particular sample. Acid fast staining is the preferred technique for cytology and fecal preparations, and is easily performed.
Gross lesions include gastric hyperplasia and fibrosis, a decreased diameter of the gastric lumen, and an increased overall diameter of the stomach. Often, the gastric mucosa will be edematous and the rugal folds thickened longitudinally. Additionally, petechial hemorrhage and focal areas of necrosis may be observed.
Histopathologically, the microvillus brush border becomes disrupted as new oocysts burst out of their host cells. The acid secreting cells that line the gastric pits become reduced in number. Mucous secreting cells are hyperplastic, and the mucosa atrophies while the submucosa and musculature becomes fibrotic.Leukocytes may be present in response to the inflammatory process, and the lamina propria may become edematous. The organisms are microscopically visible attached to the epithelial cells of the brush border microvilli. It is recommended that multiple samples of gastric tissue, taken at necropsy, be submitted for histopathology in order to improve the chances of recognizing the organism.
Currently, there is no evidence that Cryptosporidium serpentis is transmissible to humans or other mammals.
References available upon request.
-by David Kolins, Class of 1996
-Edited by M. Randy White, DVM,PhD
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