Cryptosporidiosis in Snakes
                  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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