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Cryptosporidium parvum: Transmission and Infection
Cryptosporidium parvum is a protozoan intestinal parasite causing a short-term enteric illness in individuals with functioning immune systems, and can cause a potentially fatal infection in immunosuppressed individuals. Because of C. parvum's resistance to many of the procedures used to process drinking water and food, and the parasite's extremely high fecundity, the potential for a large scale outbreak is very high. In fact, C. parvum was responsible for an outbreak in Milwaukee in 1993 when an estimated 403,000 people became ill. This was the largest waterborne outbreak of disease in United States history. This paper will cover some aspects of C. parvum's life cycle, human sickness caused by the parasite, routes of transmission, and practices of control. There are six different species of Cryptosporidium, C. parvum being the only species which infects mammals (Gutierrez, 1990). Oocysts, which are ingested by the mammal host, each contain four sporozoites. Upon excystment in the small intestine, the sporozoites infect an intestinal epithelial cell by becoming attached to the base of the microvilli. The sexual stages follow, where zygotes and eventually oocysts are formed. But C. parvum also has an "auto-infecting" asexual stage in which thin walled oocysts are produced to cause infection farther along in the intestine (Donnelly & Stentiford,1997). Approximately 20% of the oocysts produced will have these thin walls, leaving 80% of the oocysts to be excreted out of the host and into the environment, where they will be infective immediately. Thirty oocysts are enough to cause infection, and one infected person can excrete over a billion oocysts in one day (Graczyk et al., 2000).
Symptoms of Cryptosporidiosis in immunocompetent individuals include watery diarrhea (up to 3 liters a day), cramps, weight and appetite loss, nausea, vomiting and malaise (Gutierrez, 1990). Symptoms begin 3 to 5 days after the initial infection, and can last up to 2 weeks. Several relapses may occur due to the auto infecting mechanism of the parasite, but an otherwise healthy individual will rarely experience any more than 21 days of symptoms. Oocysts, however, may continue to be shed in the host's feces for up to 2 months (Gutierrez, 1990).
Because there is no known treatment for cryptosporidiosis, symptoms in immunocompromised individuals may be much more severe. The infective dose may be as little as one oocyst, and severe diarrhea can occur, causing the individual to pass up to 20 liters of fluid in one 24 hour period (Donnelly & Stentiford, 1997). This inevitably leads to death.
Transmission of the parasite can occur in several different ways. Direct transmission can occur by handling infected animal or human feces. One quarter of reported direct transmission infections occurred by direct contact with feces, while the rest were reported to have happened by person to person contact (Donnelly & Stentiford, 1997).
Person to person transmission can occur through poor hygiene habits or by handling human waste. Daycares and nursing homes are at a high risk for person to person transmission because of the high risk of handling infected feces. Family outbreaks are common, as are outbreaks among children at nurseries (Donnelly & Stentiford, 1997).
Indirect transmission by the water or foodborne route is one of the most common ways C. parvum is spread. Because of the oocyst's resistance to chlorination, several outbreaks have been caused by waterborne transmission. In one study (Carpenter et al.), oocysts were removed from the feces of an experimentally infected calf, cleaned of fecal matter, and placed into different amounts of chlorinated water at different temperatures. Although this experiment had been performed before, this was the first time that simulated recreational water was...
References: Donnelly, J.K., Stentiford, E.I. (1997) "The Cryptosporidium Problem in Water
Food Supplies" Lebensm.-Wiss.U.-Technol., 30, 111-120
Gutierrez, Yezid (1990) "Diagnostic Pathology of Parasitic Infections with
Clinical Correlations" 94-107
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