AETIOLOGY
Micro-organisms of the genus Cryptosporidium are considered important zoonotic agents that often induce asymptomatic infections. They represent important pathogens especially in very young or immunocompromised hosts.
The life cycle requires only one host with an endogenous and exogenous stage. The exogenous stage is represented by a sporulated oocyst, which is excreted in the environment with the faeces of infected hosts.
The endogenous phase begins with the ingestion of an oocyst by a suitable host. Sporozoites encyst from the oocyst and infect epithelial cells of the gastrointestinal or respiratory tract, according to the species.
At the end of the endogenous cycle, sporulated oocysts are formed which, once shed in the environment with faeces, are ready to infect a new suitable host.
The prepatent period, which is the time between the ingestion of infecting oocysts and the excretion of a new generation of oocysts, varies with the host and species of Cryptosporidium. Usually, it ranges from 4 to 22 days. The patent period, which is the duration of oocyst excretion, ranges from 1 to 20 days.
The susceptibility of different hosts to Cryptosporidium is a complex feature that is not yet completely understood. On a regular basis, isolates from one class of vertebrates are not infectious to animals of another class (Fayer, Speer and Dubey, 1997). According to this scenario cryptosporidiosis has long been considered a classical zoonosis in which the aetiological agent is spread between different mammals and humans.
Nevertheless, new light was recently shed on the epidemiological patterns of cryptosporidiosis. Indeed, another species named Cryptosporidium hominis, has been described (Morgan-Ryan et al., 2002). Cryptosporidium hominis was isolated in human faeces and was able to infect neonatal gnotobiotic piglets, but not Wistar rat pups, puppies, kittens or calves.
The existence of this new species suggests that there are at least two different scenarios in human cryptosporidiosis. One is due to C. parvum and involves mammals, mainly calves; the other is due to the newly described C. hominis and probably can also involve piglets.
EPIDEMIOLOGY
When samples from diarrhoeic patients were analysed, prevalence of C. parvum (O’Donoghue, 1995) ranged from 0.1 to 27.1 percent in developed industrialized countries compared with 0.1 to 31.5 percent in developing countries. In contrast, when samples from asymptomatic individuals were examined, prevalence ranged from 0 to 2 percent in developed countries compared with 0 to 9.8 percent in developing countries.
In addition to coprological data, several immunoserological surveys have been conducted. Seroprevalence ranged from 25 to 91 percent. These data strongly suggest that Cryptosporidium is highly prevalent in humans, both in developed and developing countries.
The infection often seems to be subclinical and according to clinical findings, it seems that Cryptosporidium has a minor pathogenic effect in healthy individuals.
CLINICAL FEATURES
Young children are much more susceptible to Cryptosporidium infections than other age groups, probably due to their immunological immaturity. The most common clinical signs of Cryptosporidium infection are profuse and watery diarrhoea. Other general signs include crampy abdominal pain, fever, nausea and vomiting. A plethora of such signs is often associated with a marked weight loss.
The duration and severity of clinical signs reflect the immune status of the patients. Most immunocompetent persons are able to respond rapidly and resolve the disease within 1-2 weeks.
Due to their immunological deficiency, HIV infected and AIDS affected patients are at a high risk of contracting cryptosporidiosis. In such patients, infection produces persistent diarrhoea that worsens with time and eventually contributes to death. Infections are not always confined to the small intestine and parasites have been found in the oesophagus, stomach, appendix, colon and rectum.
Histology performed on the site of infection reveals enteritis with mild to severe villous atrophy, increased crypt size and cellular infiltrates in the lamina propria.
According to epidemiological animal health data, cryptosporidiosis is a major problem in cattle, where the majority of infections occur in fattening units, in multiple suckler beef herds and in dairy farms with multiple-cow maternity facilities (Reynolds et al., 1986; Garber et al., 1994). Natural infections have been reported in calves as young as four days old but they are most common at around two weeks of age and are rare in calves under one and over four weeks old (Pohlenz et al., 1978; Snodgrass et al., 1980). The most prominent symptoms in neonatal calves include watery diarrhoea, dehydration and weight loss; death may occur in the most severe cases even in the absence of other enteropathogens. It has been shown that a prepatent and a patent period ranging from 3-6 days and 4-13 days respectively, occur following an experimental C. parvum infection in neonatal calves (Fayer et al., 1998). This scenario suggests an age-related susceptibility to infection that is not completely understood. There is in fact evidence to suggest that the basis of susceptibility of neonatal animals to cryptosporidiosis, relies on the immunological immaturity of the host (Pasquali et al., 1997; Canals et al., 1998).
PREVENTION OF INFECTION
In order to develop a control strategy to reduce the incidence of infection, the following features of cryptosporidiosis have to be taken into account:
Cryptosporidium infections are spread through the ingestion or inhalation of oocysts;
avoid direct contact with faeces;
wash hands after changing nappies or touching objects that may be contaminated with faeces of human or animal origin;
wash hands before preparing food;
use filtered drinking water.
