Intestinal cryptosporidiosis is one of the most significant diarrheal diseases affecting people around the world. The condition is caused by the oocyst-forming protozoan parasite from the genus Cryptosporidium that has the propensity to survive in and transmit through source waters, making it a grave public health threat.
Although the intestine is the primary target in all cases of intestinal cryptosporidiosis, there may be significant differences in the clinical presentation, depending on the host and parasite population. The major groups at risk include immunocompetent individuals in developed countries, children in developing countries, as well as immunocompromised hosts (most notably patients with acquired immunodeficiency disorder or AIDS).
Pathogenesis and Host Immune Response
Cryptosporidium is not well-known for penetrating deep tissues and causing a systemic infection. Conversely, this parasite finds its niche in a membrane-bound compartment located on the apical side of the intestinal epithelium. Still, it can cause substantial abnormalities in the secretory and absorptive functions of the gut. The mechanism may be due to direct injury to the epithelial cells, or indirectly by recruiting inflammatory cells and cytokines to the site of infection.
A pivotal initial step is the attachment of the parasite to the host cells through two classes of proteins: thrombospondin-related adhesive proteins and mucin-like glycoproteins. Ensuing cell damage arises due to the multiple sequelae, such as:
- the interruption of tight cell junctions
- the release of lactate dehydrogenase
- a loss of barrier function
- amplified cell death
The mechanisms required for the clearance of intestinal cryptosporidiosis involve a prominent role for gamma-interferon, but the exact mode of action by which this cytokine imparts resistance is ambiguous. It is also known that the CD4 T lymphocytes are indispensable for the resolution of acute and chronic cryptosporidiosis.
Symptoms of cryptosporidiosis develop after a period of time called the prepatent period, lasting on average one week. During this time the parasites invade the epithelial cells of the intestine and proliferate. As a result of this invasion, immunocompetent adults usually present with watery diarrhea that may in certain cases be profuse, prolonged and mucoid.
Accompanying symptoms are analogous to those in other diarrheal illnesses, including but not limited to nausea, vomiting, abdominal cramps and low-grade fever. Sometimes nonspecific symptoms occur as well, such as weakness, muscle aches, headache, malaise and anorexia.
Although supportive therapy leads to a resolution of the disease, in as many as 40% of cases symptoms may become chronic, akin to irritable bowel syndrome. Relapses may follow a period without diarrhea that can last between several days and several weeks. Other chronic sequelae may include fatigue, arthralgia and eye pain.
Childhood diarrhea is the most common clinical presentation of cryptosporidiosis in developing nations. Less common features seen in children may include low-grade fever, cough, shortness of breath and cough. It must be noted that abdominal pain is less frequent in children with intestinal cryptosporidiosis when compared to other diarrheal diseases.
There is also a plethora of evidence that suggests the frequent occurrence of milder or even asymptomatic intestinal cryptosporidiosis. For example, the prevalence of seroconversion, which means the presence of detectable antibodies in the blood, is higher than that of clinically diagnosed disease, both in developed and developing countries.