Cryptosporidium parvum (Morphology, Life cycle, Pathogenesis, Clinical manifestation, Lab diagnosis, Treatment and Prevention and Control)

  • Cryptosporidium is an intestinal coccidian parasite, which causes infection of the small intestine. Numerous species of Cryptosporidium are known to affect amphibians, fish, birds and mammals, but parvum is the only species known to cause infection in man.
  • Tyzzer first described the parasite in 1907, in the peptic glands of a laboratory mouse. He suggested its present name Cryptosporidium. The first infection in man was reported in a three year old healthy girl in the USA as late as 1976. Since then, the infection has been frequently diagnosed in patients with acquired immune deficiency syndrome (AIDS) and others receiving immunosuppressive therapy.


  • C. parvum inhabits the small intestine. It is found attached to the surface epithelial cells of villi or crypts of the small intestine.
  • The organisms are also found but less frequently in the stomach, appendix, colon, rectum and pulmonary tree.


  • The parasite shows six distinct morphological forms during its life cycle:
    1. Oocyst:
      • Oocyst is the diagnostic form excreted in human faeces. Cryptosporidium oocyst is the smallest coccidian known to cause infection in man. It is colorless, spherical to oval, and measures 4.5 µm to 6 µm in diameter. It doesn’t stain with iodine and is acid-fast. The cyst is surrounded by a 50 nm thin cyst wall. The latter consists of an electroluscent middle zone surrounded by two electron dense layers.
    2. Sporozoite:
      • Each oocyst contains upto four slender and fusiform sporozoites. These four slender bow-shaped sporozoites always remain parallel to each other within an oocyst and are released only after partial digestion of the oocyst.
      • The sporozoites are slender, crescent-shaped and measures 1.5 µm to 1.75 µm in diameter. The anterior end containing a prominent nucleus is rounded. These sporozites invade enterocytes in which they parasitise.
    3. Trophozoite:
      • In the enterocytes, the sporozoites subsequently differentiate into intracellular trophozoites.
      • Trophozoites are the intracellular transitional form of the parasite. They are round or oval and measure 2 µm to 2.5 µm in diameter. Each trophozoite consists of a large nucleus with or without a conspicuous nucleolus.
    4. Meronts:
      • These trophozoites multiply asexually by nuclear division (mitotically) to produce two types of meronts; type I and type II.
      • These meronts are crescent-shaped and measure 1 µm to 5 µm in diameter showing rounded anterior and posterior ends. These meronts in turn produce type I and type II merozoites that resemble sporozoites and amplify asexual infectious cycles .
    5. Microgamont:
      • Some of the type II merozoites invade new host cells and initiate sexual replication.
      • Inside the host cells, some of them differentiate into male forms (microgamont). Each microgamont produces 16 separate rod-like non-flagellated microgametes which are 1.4×0.5 µm in size.
    6. Macrogamont:
      • Some of type II merozoites differentiate into a spherical or oval structure of 4 to 6 µm in diameter having a large central nucleus called macrogamont. Microgamonts are fertilized by microgametes to form oocysts (zygote).

Life cycle:

  • Cryptosporidium completes its life cycle through the stages of asexual generation (schizogony) and sexual generation (gametogony) in a single host.
  • All the morphological stages of the parasite are truly intracellular and are being surrounded by a host cell membrane, which is extra-cytoplasmic.
  • Man acquires infection on ingestion of food or drinks contaminated with the faeces, containing sporulated thick-walled oocysts of Cryptosporidium.
  • On ingestion, the sporozoites are released from the oocysts in the small intestine. These sporozites invade enterocytes in which they parasitise.
    • Asexual generation (Schizogony):
      • In the enterocytes, the sporozoites subsequently differentiate into intracellular trophozoites.
      • These trophozoites multiply asexually by nuclear division to produce two types of meronts; type I and type II.
      • These meronts in turn produce type I and type II merozoites that resemble sporozoites and amplify asexual infectious cycles.
    • Sexual generation (Gametogony):
      • Some of the type II merozoites invade new host cells and initiate sexual replication. Inside the host cells, they differentiate either into female (macrogamont) or male (microgamont) forms. Each microgametocyte produces 16 sperm-like microgametes, which fertilize the maccrogamonts resulting in the formation of oocysts (zygote). Four sporozoites are formed inside each sporulating oocyst in situ.
      • The sporulating oocysts are of two types;
        • Thin-walled
        • Thick-walled
      • The thin-walled oocysts release the sporozoites inside the lumen of the intestine and cause auto-infection in the same host by repeating the cycle of schizogony and gametogony.
      • The thick-walled oocysts excreted in the faeces are infective to other human hosts. The cysts under favorable conditions remain viable and infectious relatively for a long time. These cysts when taken up by other susceptible human hosts, cause infection and the cycle are repeated.
                                                Life cycle of Cryptosporidium parvum                                                                                       Source:

Pathogenesis and host immunity:

  1. Mode of transmission:
  • The oocysts of Cryptosporidium excreted in the faeces are highly infectious. As low as 10 oocysts to 100 oocysts can cause disease in humans. Cryptosporidium infection can be transmitted to man in the following ways:
    • Human to human transmission:
      • It takes place by faecal-oral route by drinking water contaminated with human faeces infected with oocysts. Rarely, it is acquired by ingestion of milk or food contaminated with oocysts.
    • Animal to human (zoonoses) transmission:
      • It is transmitted from the livestock, cattle or pet animals (cat, dog) either directly by ingestion of the oocysts derived from the faeces of these animals or indirectly by close contact with these animals.
    • Cryptosporidium can also be transmitted but rarely by; aerosols, sexual contact and possibly by accidental laboratory infection.
    • Autoinfection: This is caused by sporozoites released from the thin-walled oocysts inside the lumen of the intestine. It is primarily responsible for persistence of infection in the infected host.
  1. Pathogenesis:
    • Intestinal infection by parvum has been associated with marked alteration in the structure and function of the intestine. Blunting and loss of villi, lengthening of the crypts and infiltration of lamina propria by lymphocytes, polymorphonuclear cells and plasma cell are the pathological changes of the intestinal tract, in cryptosporidiosis.
  • Infection begins with the firm attachment of Cryptosporidium to the mucosal surface of the intestine followed by invasion of epithelial cells. After invasion of the enterocytes by the parasite, the epithelial cells release cytokines. These cytokines activate phagocytes and attract new leukocytes, which, in turn, release soluble factors. These factors lead to increased intestinal secretion of chloride and water and inhibition of absorption. This is also associated with damage of the enterocytes, which is accompanied by nutrient malabsorption and osmotic diarrhea.
  • Cryptosporidium doesn’t invade beyond the mucosal layer of the intestine. The parasites are found attached to the brush border of the mucosal surface. They appear as small, basophilic round structures, staining readily with Giemsa and haematoxylin eosin stain. They are arranged in a row or clusters, along the border of the epithelial cells alone or in association with other intestinal parasites such as Giardia intestinalis.

Host immunity:

  • Increase in circulating immunoglobulin IgM and IgG antibodies have been demonstrated in cryptosporidiosis. The circulating antibodies possibly reduce severity of subsequent symptomatic infection, but don’t confer any protective immunity against reinfection.

Clinical manifestations:

  • The clinical manifestations of Cryptosporidium infection vary depending upon the immune status of the host. Incubation period varies from 7 days to 10 days (range 5 days to 30 days). parvum causes two distinct clinical entities.
    • Cryptosporidiosis in immunocompetent hosts:
      • It is a mild infection in normally healthy patients and children. The duration of symptoms is relatively short (1 week to 2 weeks) and recovery is complete with rarely fatal condition.
      • Watery diarrhea, malaise, nausea, fever, crampy abdominal pain and flu-like illness are the characteristic features of cryptosporidiosis in immunocompetent hosts. Diarrhea is foul smelling with 2 motions to 10 motions per day, beginning on the first or second day of the illness. In some other cases, it is accompanied by prostration (extreme physical weakness) and weight loss even up to 10%.
      • The oocysts may continue to be excreted in the faeces of the cases, twice as long, as they had in diarrhea.
    • Cryptosporidiosis in immunocompromised hosts:
      • Cryptosporidiosis is a serious condition in;
        • Patients with AIDS
        • Patients with congenital hypogammaglobunemia or severe combined immunodeficiency syndrome
        • Patients with renal transplantation
        • Persons with IgA deficiency and with severe malnutrition
      • In immunocompromised people, Cryptosporidium produces cholera-like watery or mucus diarrhea. Watery diarrhea can be more severe and chronic especially in those people with CD4 counts <200/µ Diarrhoea with as many as 70 stools per day and loss of body fluids even up to 17 liters/ day has been noted. Diarrhoeic stool may contain mucus but rarely blood or leucocytes. The main duration of diarrhea is 20 weeks with variability from 1 week to 48 weeks. The prolonged diarrhea may lead to significant weight loss.
      • Low grade fever (390C), nausea, vomiting and crampy abdominal pain are other but less frequent symptoms of the condition. Occasionally, non-specific symptoms such as malaise, myalgia and headache may be present.
      • In some of the immunocompromised patients, Cryptosporidium affects the entire gastro-intestinal tract including the gall bladder, bile duct and pancreas and even pharynx and bronchial tree.
      • Biliary infection in patients with AIDS is associated with nausea, vomiting and right upper quadrant pain.


  • Clinical diagnosis of cryptosporidiosis is difficult as the condition clinically mimics giardiasis, isosporiasis, cyclosporiasis and a few other infections caused by enteropathogens.
  • The absence of blood, pus cells and Charcot-Leyden crystals in the faeces may rule out amoebiasis, isosporiasis and bacillary dysentery, and suggest the possibility of cryptosporidiosis.

Laboratory diagnosis: The specific diagnosis of the condition is made by identification of oocysts in specimens.

  • Specimens: Faeces is the specimen of choice. Sputum, bronchial washings and duodenal or jejunal aspirations are less frequent specimens collected from immunocompromised patients like AIDS.
  • Method of examination:
    • Microscopy:
      • Wet mount examination: Direct wet mount of stool in iodine is used for screening of stool specimens for oocysts.
      • Stained smear examination: Kinyoun’s modified acid fast technique, hot safranine-methylene blue stain, modified Kohn’s stain, modified Koster stain, fluorescent stains etc. are used to stain Cryptosporidium oocysts in faecal smears. Red-stained acid-fast oocysts against blue background are seen after Kinyoun’s modified acid-fast staining technique.
    • Fluorescent microscopy: Direct immunofluorescence microscopy using auramineO, auramine-rhodamine, auramine-carbol fuchsin, acridine orange etc. is the method of choice to detect oocysts in stool smears.
    • Antigen detection in stool: ELISA is employed to detect Cryptosporidium copro-antigen in the faeces.
    • Serodiagnosis: The indirect fluorescent antibody (IFA), or ELISA using purified oocysts as antigens have been used to detect circulating antibodies specific to Cryptosporidium in the serum which appear in about 6 to 8 weeks after the onset of infection.
    • Molecular diagnosis: Detection of Cryptosporidium by PCR is still a research tool and is yet to be widely used in clinical diagnosis.
    • Histopathological diagnosis: This is based on the demonstration of the developmental stages of parasite in the biopsy specimen from the jejunum and occasionally from the rectum.
  • Treatment:
    • Cryptosporidium infection in the immunocompetent hosts is self-limiting and requires supportive treatment to prevent dehydration.
    • Infections in the immunocompromised hosts with severe diarrhea and symptoms of malabsorption require supportive therapy with replacement of fluid, electrolytes and nutrients. Antidiarrhoeal agents are of no value.
    • Limited and transient benefit has been reported in patients treated orally with spiramycin (a macrolide antibiotic) in a dosage of 1 gm three to four times daily. Nitazoxanide has also been reported to be effective against cryptosporidial diarrhea in AIDS patients.
  • Prevention and control:
    • The reduction or elimination of oocysts from the environment forms the mainstay of control of cryptosporidiosis but is difficult.
    • Freezing and heating at 650C of food or drinks for 30 minutes kill all the oocysts. The care to avoid contamination of food and water with faecal oocysts prevent transmission of infection to man.
    • Hand washing, use of gloves and improved personal hygiene will minimize the risk of acquiring the infection in a hospital.

Cryptosporidium parvum (Morphology, Life cycle, Pathogenesis, Clinical manifestation, Lab diagnosis, Treatment and Prevention and Control)


  1. II: Protozoology :  2.4   Opportunistic protozoan parasites of man: Pnemocystis carinii & Cryptosporidium parvum
  2. Gordon J Leitch and Qing He , Cryptosporidiosis-An overview, The journal of biomedical research,