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Intestinal and Luminal Protozoa



 
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PostPosted : Thu Sep 08, 2005    Post subject:

Intestinal and Luminal Protozoa

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A parasite is an organism that obtains food and shelter from another organism and derives all benefits from this association. The parasite is termed obligate when it can live only in a host; it is classified as facultative when it can live both in a host as well as in free form. Parasites that live inside the body are termed endoparasites whereas those that exist on the body surface are called ecto-parasites. Parasites that cause harm to the host are pathogenic parasites while those that benefit from the host without causing it any harm are known as commensals.

The organism that harbors the parasite and suffers a loss caused by the parasite is a host. The host in which the parasite lives its adult and sexual stage is the definitive host whereas the host in which a parasite lives as the larval and asexual stage is the intermediate host. Other hosts that harbor the parasite and thus ensure continuity of the parasite's life cycle and act as additional sources of human infection are known as reservoir hosts. An organism (usually an insect) that is responsible for transmitting the parasitic infection is known as the vector.

INTESTINAL AND UROGENITAL PROTOZOA

Intestinal and luminal protozoa significant to human health include

Entamoeba histolytica (Amebae)

Balantidium coli (Ciliates)

Giardia lamblia and Trichomonas vaginalis (Flagellates)

Cryptosporidium parvum and Isospora belli (Sporozoa)

AMEBIASIS (amebic dysentery, amebic hepatitis)

Etiology

E. histolytica is the major cause of amebic dysentery.

Epidemiology

0.5 to 50% of the population world wide harbors E. histolytica parasites with the higher rates of infection being in underdeveloped countries. 1 to 3% of the population of the britain are infected. Infection is associated with poor hygiene. Humans are the principal host, although dogs, cats and rodents may be infected.

Morphology

Trophozoite: This form has an ameboid appearance and is usually 15-30 micrometers in diameter, although more invasive strains tend to be larger. The organism has a single nucleus with a distinctive small central karyosome. The fine granular endoplasm may contain ingested erythrocytes. The nuclear chromatin is evenly distributed along the periphery of the nucleus.

Cyst: Entameba histolytica cysts are spherical, with a refractile wall; the cytoplasm contains dark staining chromatoidal bodies and 1 to 4 nuclei with a central karyosome and evenly distributed peripheral chromatin.

Life cycle

Infection occurs by ingestion of cysts on fecally contaminated food or hands. The cyst is resistant to the gastric environment and passes into small intestine where it decysts. The metacyst divides into four and then eight amoebae which move to the large intestine. The majority of the organisms are passed out of the body with the feces but, with larger bolus of infection, some amebae attach to and invade the mucosal tissue forming "flask-shaped" lesions (bomb craters). The organisms encyst for mitosis and are passed through with feces. There are no intermediate or reservoir hosts.

Symptoms

Acute: Frequent dysentery with necrotic mucosa and abdominal pain.

Chronic: Recurrent episodes of dysentery with blood and mucus in the feces. There are intervening gastrointestinal disturbances and constipation. Cysts are found in the stool. The organism may invade the liver, lung and brain where it produces abscesses that result in liver dysfunction, pneumonitis, and encephalitis.

Pathology

Intestinal ulcers (craters/flasks) are due to enzymatic degradation of tissue. The infection may result in appendicitis, perforation, stricture granuloma, pseudo-polyps, liver abscess; sometimes brain, lung and spleen abscesses can also occur. Strictures and pseudo-polyps result from the host inflammatory response.

Immunology

There is an antibody response after invasive infection (liver abscess or colitis) but it is of questionable significance in immunity, as there is recurrence of enteric episodes in these patients.

Diagnosis

Symptoms, history and epidemiology are the keys to diagnosis. In the laboratory, the infection is confirmed by finding cysts in the stool. E. histolytica infection is distinguished from bacillary dysentery by the lack of high fever and absence PMN leukocytosis.

Distinction must be made from other non-pathogenic intestinal protozoa (e.g., Entamoeba coli, Entamoeba hartmanni, Dientamoeba fragilis, Endolimax nana, Iodamoeba buetschlii, etc.).

Treatment

Iodoquinol is used to treat asymptomatic infections and metronidazole is used for symptomatic and chronic amebiasis, including extra-intestinal disease.

GIARDIASIS (lambliasis)

Giardia lamblia (a flagellate)

Epidemiology

Giardia has worldwide distribution and is not uncommon in South Carolina. It is the most frequent protozoan intestinal disease in the US and the most common identified cause of water-borne disease associated with breakdown of water purification systems, drinking from contaminated streams, travel to endemic areas (Russia, India, Rocky Mountains, etc.) and day care centers.

Morphology

Trophozoite: Giardia is a 12 to 15 micrometer, half pear-shaped organism with 8 flagella and 2 axostyles arranged in a bilateral symmetry. There are two anteriorly located large suction discs. The cytoplasm contains two nuclei and two parabasal bodies.

Cyst: Giardia cysts are 9 to 12 micrometer ellipsoidal cells with a smooth well-defined wall. The cytoplasm contains four nuclei and many of the structures seen in the trophozoite.

Life cycle

Infection occurs by ingestion of cysts, usually in contaminated water. Decystation occurs in the duodenum and trophozoites (trophs) colonize the upper small intestine where they may swim freely or attach to the sub-mucosal epithelium via the ventral suction disc. The free trophozoites encyst as they move down stream and mitosis takes place during the encystment. The cysts are passed in the stool. Man is the primary host although beavers, pigs and monkeys are also infected and serve as reservoirs.

Symptoms

Early symptoms include flatulence, abdominal distension, nausea and foul-smelling bulky, explosive, often watery, diarrhea. The stool contains excessive lipids but very rarely any blood or necrotic tissue. The more chronic stage is associated with vitamin B12 malabsorption, disaccharidase deficiency and lactose intolerance.

Pathology

Covering of the intestinal epithelium by the trophozoite and flattening of the mucosal surface results in malabsorption of nutrients.

Immunology

There is some role for IgA and IgM and there is increased incidence of infection in immunodeficient patients (e.g. AIDS).

Diagnosis

Symptoms, history, epidemiology are used in diagnosis. Giardia caused dysentery is distinct from other dysenteries due to lack of mucus and blood in the stool, lack of increased PMN leukocytes in the stool and lack of high fever. Cysts in the stool and trophs in the duodenum can be identified microscopically after content has been obtained using a string device (Enterotest®). Trophs must be distinguished from the non-pathogenic flagellate Trichomona hominis, which is an asymmetrical flagellate with an undulating membrane.

Treatment

Metronidazole is the drug of choice.

OTHER INTESTINAL PROTOZOA

Balantidium coli and Cryptosporidium (parvum) are both zoonotic protozoan intestinal infections with some health significance. Isospora belli is an opportunistic human parasite.

Balantidium coli

This is a parasite primarily of cows, pigs and horses. The organism is a large (100 x 60 micrometer) ciliate with a macro- and a micro-nucleus (Figure Cool. The infection occurs mostly in farm workers and other rural dwellers by ingestion of cysts in fecal material of farm animals. Man-to-man transmission is rare but possible. Symptoms and pathogenesis of balantidiasis are similar to those seen in entamebiasis, including intestinal epithelial erosion. However, liver, lung and brain abscesses are not seen. Metronidazole and iodoquinol are effective.

Cryptosporidium parvum

C. parvum is a small round parasite measuring 3 to 5 micrometers which is found in the gastrointestinal tract of many animals and causes epidemics of diarrhea in humans via contaminated food and water. Humans are infected by ingestion of C. parvum oocysts containing many sporozoites. The sporozoites are released in the upper GI tract and attach to the gut mucosal cells where they divide to produce merozoites. The merozoites invade other mucosal cells and further multiply asexually. Some of the merozoites differentiate into male and female gametocytes and form an oocyst in which they multiply and differentiate into sporozoites. The mature oocyst is excreted with fecal material and infects other individuals.

When a large number of humans in a community have diarrhea, the most likely cause is C. parvum. A small bolus of infection may cause mild diarrhea, whereas a larger intake of organisms may cause more pronounced symptoms including copious watery diarrhea, cramping abdominal pain, flatulence and weight loss. Severity and duration of symptoms are related to immuno-competence. In AIDS patients, the organism may cause prolonged, severe diarrhea and the organisms may invade the gallbladder, biliary tract and the lung epithelium. There is no approved effective treatment for cryptosporidiasis, although paromycin is used as an investigational drug.

There are a variety of antibody tests for detection but many of these detect other species of Cryptosporidium than C. parvum. Sensitive polymerase chain reaction tests are available for C. parvum detection in environmental and animal samples.

Isospora belli

I. belli is a rare infection of normal humans, although it is being seen in increasing numbers in AIDS patients. The infection occurs via the oro-fecal route. The infective stage of the organism is an oval oocyst (Figure 11) which, upon ingestion, follows the same course as C. parvum. The disease produces symptoms similar to those of giardiasis. In normal individuals, mild infections resolve themselves with rest and mild diet and heavier infections can be treated with sulpha drugs. The treatment may have to be carried on for a prolonged period in AIDS patients.

LUMINAL PROTOZOA

TRICHOMONIASIS

Trichomonas vaginalis (a flagellate)

Epidemiology

Trichomonas vaginalis has a world-wide distribution; incidence is as low as 5% in normal females and as high as 70% among prostitutes and prison inmates.

Morphology

The trophozoite form is 15 to 18 micrometers in diameter and is half pear shaped with a single nucleus, four anterior flagella and a lateral flagellum attached by an undulating membrane. Two axostyles are arranged asymmetrically. The organism does not encyst.

Life cycle

T. vaginalis colonizes the vagina of women and the urethra (sometimes prostate) of men. Infection occurs primarily via sexual contact, although non-venereal infections are possible. The organism does not encyst and divides by binary fission which is favored by low acidity (pH > 5.9; the normal pH is 3.5 to 4.5). There is no non-human reservoir.

Symptoms

T. vaginalis infection is rarely symptomatic in men, although it may cause mild urethritis or occasionally prostatitis. In women, it is often asymptomatic, but heavy infections in a high pH environment may cause mild to severe vaginitis with copious foul-smelling yellowish, sometimes frothy discharge.

Pathology

The organism causes contact-dependent damage to the epithelium of the infected organ.

Diagnosis

Clinical suspicion may be confirmed by finding the organism in Giemsa-stained smears of vaginal discharge or, in difficult cases, by cultivation of a swab sample in Diamond's medium. Trophozoites must be distinguished from the non-pathogenic flagellate Trichomona hominis.

Treatment

Metronidazole (although teratogenic) is effective in both males and females. Vinegar douche may be useful. Personal hygiene and the use of condoms are helpful.
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