Gastrointestinal parasites are insidious causes of disease in cats. Protozoan parasitic infections in particular can be difficult
to detect because there are often no signs of disease, or the signs, such as diarrhea, are nonspecific. But these infections
must be uncovered and cured before they cause serious disease or spread to housemates or even owners.
Three important protozoan parasites in cats are Cryptosporidium species, Giardia species, and Tritrichomonas foetus. Cryptosporidium species are coccidians; Giardia species and T. foetus are flagellates. Our understanding of infections with these organisms has changed dramatically in the last several years
as the ability to genetically characterize the organisms has advanced. For example, it was previously thought that Giardia and Cryptosporidium species in dogs and cats were identical to those that infect people; it is now known that there are species-specific strains
of both organisms. In addition, T. foetus in cats is not zoonotic but was previously thought to be Pentatrichomonas hominis, an agent that also is occasionally detected in the feces of people. There have also been many advances in the diagnosis
and treatment of these infections.
In this article, we provide an update on the clinical management of Cryptosporidium species, Giardia species, and T. foetus infections in cats. We emphasize recently published articles and experiences we have had in our research laboratory and clinic.
THE ORGANISMS AND THEIR LIFE STYLES
In the past, most cases of mammalian cryptosporidiosis were attributed to Cryptosporidium
parvum. However, molecular studies have demonstrated that cats are usually infected with the host-specific Cryptosporidium
felis.1-5 In one study in our laboratory, all Cryptosporidium species isolated from North American cats were C. felis.5
The life cycle of all Cryptosporidium species begins with a host ingesting sporulated oocysts.6 The 4-x-6-Ám oocysts (Figure 1) excyst in the gastrointestinal tract, releasing infective sporozoites, which become enclosed as trophozoites within parasitophorous
vacuoles of the microvillus surface of enterocytes. The organisms are covered by the plasma membrane of the host cell, but
they do not lie in the cytoplasm. This association with the cytoplasm of the host cell allows it to obtain nutrients.
Figure 1. Cryptosporidium species oocysts stained with modified Ziehl-Neelsen acid-fast stain. The oocysts are about 4 x 6 Ám.
The trophozoites produce two types of meronts. Within 24 hours, type I meronts leave the parasitophorous vacuoles to invade
other epithelial cells where they develop into more type I meronts or type II meronts. Type I meronts can recycle indefinitely,
so new type I meronts can arise continuously. The type II meronts produce sexual reproductive stages (gamonts). The zygotes
form either thick-walled or thin-walled oocysts, each containing four sporozoites. About 20% of the oocysts produced in the
gut are thin-walled oocysts that fail to form an oocyst wall. Thus, Cryptosporidium species appear to have two autoinfective cycles: the first through continuous recycling of type I meronts and the second through sporozoites
released from ruptured thin-walled oocysts.7
The thick-walled oocysts are passed in the feces and into the environment. Oocysts are infective on excretion and are extremely
environmentally resistant, which permits direct fecal-oral transmission. In one of our studies, after inoculation of cats
with C. parvum, C. parvum DNA was detected in the feces on Day 3 after infection, and oocysts were detected on Day 7 after infection.8 In cats, only small numbers of oocysts per gram of feces are passed, making diagnosis difficult.