No matter what species is involved, Cryptosporidiumfelis or Cryptosporidiumparvum, cats do present with severe disease due to infection with this pathogen. A typical presentation of a cat with disease is one that has an underlying immunosuppressive disorder such as a feline leukemia virus infection (Monticello et al., 1987). However, there are cases where cats develop severe disease and persistent cryptosporidiosis where there is no apparent underlying condition (Lappin et al., 1997). Also, the recent development of serological tests that detect antibody in the blood of cats that have been infected would suggest that somewhere around 15% of cats throughout the United States have been or are currently infected with Cryptosporidium (Lappin et al, 1997; McReynolds et al., 1999).
The cat that presents with cryptosporidiosis will be having recurring bouts of diarrhea. The disease caused by Cryptosporidium infection is a water-losing diarrhea caused by the development of the parasites within the epithelial cells of the mucosa. Histologically, infection causes a blunting of the intestinal villus and crypt hyperplasia that is accompanied by an intense neutrophilic response (Tzipori et al., 1983). In AIDS patients with cryptosporidiosis, it has been found that net water, sodium, and chloride movement was the same as that in healthy controls (Kelly et al., 1996). From this work, these authors concluded that the diarrhea may be due to the secretion of electrolytes and water efflux distally to the site of infection or as to some yet undefined feature or the infection. Using monolayers of polarized colonic epithelial cells and the experimental infection of these cells with Cryptosporidiumparvum, it has been shown that there is an increased macromolecular permeability of the monolayer, and it was felt that disruption of the epithelial cell barrier play a role in the observed diarrhea (Adams et al., 1994). Additional work using the cell monolayer system has shown rather conclusively that the infection of the epithelial cells will ultimately result in significant changes in the host cell permeability and the permeability of the entire monolayer (Griffiths et al., 1994). Also, the infection will result in the death of the infected cells.
Treatment of cats that are undergoing infection is a difficult as treatment is in humans. The basic therapy is the relief of symptoms and increased fluids. Paromomycin has been used to treat cats with some success (Barr et al., 1994); but this therapy is not without potential complications that can include renal failure (Gookin et al., 1999).
Cats have on occasion been experimentally infected with Cryptosporidium isolated from calves and considered to be Cryptosporidiumparvum (Current et al., 1983; Pavleski, 1983), but cats seem rather refractory to such infections. In a trial we performed at Cornell where two virus-free kittens were each fed 10 million oocysts, only a very few oocysts were shed in the feces of these cats, and they never developed signs of infection. Dogs have until very recently been considered to be infected with the same species, Cryptosporidiumparvum, that occurs in calves and humans. Dogs can be experimentally infected with oocysts from calves, but the number of oocysts shed by these dogs appears to remain relatively low (Lloyd and Smith, 1997). Also, recent evidence tends to indicate that dogs may have their own phenotype as determined by DNA sequencing methods (Pieniazek et al., 1999).
The potential transmission of Cryptosporidium between cats and people is currently pretty much undefined. There have been reports linking feline cryptosporidiosis to human infection (Egger et al., 1990; Pieniazek et al., 1999). At the same time it would seem that many of the human isolates are neither from cats nor cattle, rather the infections are acquired from other humans. There have also been studies that have shown that pet ownership is not a risk factor for HIV-infected individuals (Glaser et al., 1998).
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