The below mentioned article provides a study-note on the intestinal protozoa.
I. Rhizopoda — Entamoeba histolytica, E. Coli, Acanthamoeba, Castellani, Naegleria fowleri.
II. Mastigophora — Giardia intestinalis, Trichomonas hominis
III. Sporozoa — Isospora belli, Cryptosporidium, Toxoplasma gondii
IV. Ciliata — Balantidiumcoli
E. histolytica is cosmopolitan, occurs in three forms Trophozoite (Fig.46a.1) precystic (Fig.46a.2) and cystic (Fig. 46a.3-5) forms and passes its life cycle in one host only, i.e., man. When the fully developed cysts containing four nuclei are swallowed by man, they pass down the intestine where the excystation of oocytes takes place at alkaline pH, hence the trophozoites (Vegetative amoebae) are formed and invade the intestinal mucosa, multiply, cause flask shaped ulceration of the intestine; few enter the blood stream, are carried to other organs (i.e., liver, lung, brain) where they give rise to amoebic abscess, some are discharged into the lumen of the gut and are transformed into small precystic forms from which the adult cysts are developed and passed in the faeces. Thus the life cycle is repeated.
Clinical features:
The incubation period is 4-5 days. E. histolytica causes amoebic dysentery or amoebiasis which is characterised by the passage of blood and mucus in the stool.
The macroscopic and microscopic differences between the stools of amoebic and bacillary dysentery are described below:
In intestinalamoebiasisa definite diagnosis can be done by 1) Stool examination in which the cysts (in formed stool), and the trophozoites (in diarrhoeal stool) are identified; 2) Sigmoidoscopy, in which scrapings from any lesions in the rectum are examined for trophozoites.
In extra-intestinal amoebiasis, the following procedures are followed:
1. Clinical diagnosis of amoebic liver abscess (ALA) by (a) hepatomegaly,pain,fever and sweating, which is later confirmed by the presence of cysts and trophozoites in the tissues, (b) X-ray or ultrasonography of the abdomen, (c) Immuno-diagnosis tests.
The haemagglutination, complement fixation, gel diffusion; recent cellulose acetate precipitin (CAP), dot immuno binding assay (DIB) and sandwich enzyme linked. Immuno sorbent Assay (ELISA) tests. Western blot of E. histolytica may become one of the very recent more accurate methods for the successful immune diagnosis of acute intestinal amoebiasis.
Treatment:
Amicline is a complete current amoebiciae used for eradication of extra intestinal and intestinal amoebiasis. Amicline plus is effective for amoebic and bacillary dysentery. Tinidazole is useful.
Prophylaxis:
Personal prophylaxis consists of:
(1) Use of boiled drinking water,
(2) Protection of food and drink from flies, cockroaches and rats,
(3) Avoiding eating unwashed raw vegetables and fruits and
(4) Personal cleanliness while taking food.
Community prophylaxis comprises:
(1) Effective sanitary disposal of faeces,
(2) Protection of water supplies from fecal pollution,
(3) Avoidance of the use of human excreta as fertiliser, and
(4) Detection and isolation of carriers.
E. coli are worldwide and live in the large intestine of man. They are similar morphologically and in their life cycle to E. histolytica and are commensal.
Trophozoites and Cysts of E. histolytica AND E. Coli:
Naegleria fowleri (Free — living amoeba), Acanthamoeba castellani, elongated, 10-22 x 7 microns, are rapidly motile. Their cytoplasm contains vacuoles and mitochondria (absent in Entamoeba), no red blood cells. They develop flagella after 2-4 hours in distilled water. They can be stained with Giemsa stain.
Though they survive transit through the gastrointestinal tract and passed in stool, they are known to cause primary amoebic meningoencephalitis (PAM). In children swimming in warm soil – contaminated pools, these amoebae enter, via the nose and cribriform plate, into the brain tissue where they cause extensive haemorrhage and damage in the cerebrum and cerebellum; even they may enter from skin ulcers.
There is report of corneal ulceration or keratitis from contaminated saline used with contact lenses.
Microscopic examination of cerebrospinal fluid (CSF) will show the trophozoites and red blood cells but no bacteria.
Treatment with amphotericin B has been successful. Sulphonamide and a hydroxystibamide have been recommended for Acanthamoebiasis.
Prophylaxisby avoiding swimming in warm soil contaminated pools. Contaminated saline should not be used with the contact lenses.
Giardia intestinalis, causal agent of giardiasis, has both trophozoite (Fig. 46d. 1, Fig. 46d.2) and cyst (Fig. 46d.3) stages.
Human infection is brought about by ingestion of food or drink contaminated with cysts. Within 30 minutes of ingestion, the cyst hatches out two trophozoites which then multiply in enormous numbers and colonies in the duodenum. When conditions in the duodenum become unfavorable, encystment occurs and the cysts are passed out along with faeces.
Their trophozoites attach themselves on the epithelial cells of the intestine and disturb the intestinal function leading to malabsorption of fat. There is mild steatorrhoea (passage of stools with excess fat), loose motions, chronic enteritis and cholecystopathy.
G. lamblia has been shown to induce an intestinal Ig A response against the parasite. This antibody blocks adherence of trophozoite to intestinal epithelium with subsequent removal of trophozoite from the intestine by peristalsis.
Diagnosis is by:
(1) Microscopic examination of trophozoites in diarrhoea stools and cysts in formed cysts; trophozoites in the duodenal aspirates;
(2) Fluoroscopy which may demonstrate the hyper-motility of the jejunum and
(3) X-ray which may reveal mucosal defects.
Treatment:
Metronidazole or Quinacrine can eliminate the infection. Only by personal hygiene, its spread can be prevented. Albendazole is a current effective antigiardial agent. TRICHOMONAS HOMINIS, found in ileo-caecal region may invade the vagina; but they are non-pathogenic (Fig.46d.5), T.tenax (Fig. 46d.6).
ISOSPORA BELLI are parasites of the small intestine of man and form oocysts and sporocysts. After ingestion by man, the mature oocysts liberate sporocysts which enter into the cells of the villi of small intestine where they multiply by schizogony (Trophozoite, schizont and merozoites) and, ultimately, the oocysts develop by sporogony and passed in the faeces. The lesion produced by I. belli is unknown in man; but in calf, there is mucous diarrhoea. In man, the symptoms are anorexia, nausea, abdominal pain and diarrhoea. The infection in man is usually self-limited. In immuno-compromised (AIDS) patients, I. belli causes severe complications (diarrhoea).
Oocysts of I, belli can be demonstrated microscopically in the faeces.
There is no specific treatment for human infection. Rest with bland diet is effective.
Prophylaxis can be done by adopting the methods recommended for amoebiasis and giardiasis.
CRYPTOSPORIDIUM are coccidia related to Isospora, have long been known as parasites of fowls, rodents, cattle and have probably been an un-recognised cause of self-limited, mild gastroenteritis and diarrhoea in man. It is distributed in many countries including India. The children are more susceptible than adults.
These parasites are minute (2-5 microns) intracellular sphere found in great number just under the mucosal epithelium of the stomach or intestine. The mature trophozoite (Schizont) divide into arc shaped merozoites which are released from the infected mucosal cell to begin a new life cycle. Oocysts (4-5 microns) containing 4 sporozoites are passed into feces and become infective agents. If stained by modified Ziehl-Neelsen staining, oocysts in the stool appear faintly blue with reddish or purple corpuscles.
Patients infected with cryptosporidim have watery diarrhoea, cramps, upper abdominal pain (exacerbated by food ingestion), weight loss and flatulence, nausea, vomiting, anorexia, myalgia, malaise, dehydration, fever not common. The disease is self-limited. They cause severe intractable diarrhoea in the immune compromised persons (e.g., those with AIDS) and immune competent individuals. Only supportive therapy is available for those with AIDS or congenital immunodeficiency. Spiramycin (Rovamycin) may temporarily be effective.
Prophylaxis:
Though initially recognised in animals, Cryptosporidial infection is increasingly recognised as important cause of diarrhoea in both immune compromised and immune competent individuals. Previously, it was thought that the source of infection was in animals but the transmission from human to human is possible.
TOXOPLASMA GONDII is distributed all over the world and is an obligatory, intracellular, coccidial parasite. It may occur in two forms: extracellular and intracellular forms.
The life cycle of T. gondii may be (a) enteric and (b) exo-enteric:
(a) Enteric cycle. After eating mouse brain containing cysts of T. gondii, cycles of schizogony and sporogony develop inside the intestinal mucosa of the cat ultimately liberating oocysts in the infected cat’s feces.
(b) Exo-enteric cycle. P The oocysts, after ingestion, liberate sporozoites which, in man, penetrate the mucosa of the intestine and are carried by blood and lymph stream to distant organs (brain, eyes, liver, lymph nodes, heart, skeletal muscles and placenta of the pregnant uterus) where they from pseudocysts which multiply causing damage to the central nervous system and musculature.
Toxoplasmosis may be congenital or acquired:
In congenital toxoplasmosis, there is encephalitis, chorioretinitis, hydrocephalus, mental retardation and convulsion.
Acquired toxoplasmosis is very rare in adults, often fatal.
In laboratory diagnosis, complement fixation test of Warren and Sabin; skin test of Sabin and Feldman are often used; ELISA (recent) test is used to assist the diagnosis.
The direct agglutination test with 2 mercaptoethanol (AD, 2ME) and Immuno fluorescent test(IFAT) are very recently used in the diagnosis of Toxoplasmosis. The former is little superior to the latter Latex agglutination test (LAT) or ELISA can detect T.gondii antibody.
Radiological diagnosis is done to show cerebral calcification.
Treatments unsatisfactory:
Sulphonamides and pyrimethamine are currently used. Balantidium Coli is the largest cosmopolitan protozoon of the large intestine of man, monkey and pig, where the trophozoites feed on bacteria and mucus and on the cells of the intestinal wall. The pig is the reservoir of infection and does not suffer from the infection.
It has two stages: trophozoite (Fig. 46c.1) and cysts (Fig. 46c.2).
Life cycle:
Man gets infected after ingestion of cysts in pig’s faeces. Excystation takes place in the large intestine liberating trophozoites which enter into the intestinal mucosa causing ulceration and encyst in the lumen and cysts are excreted in the feces.
In majority of cases, dysentery is characteristic accompanied by abdominal pain, tenesmus, nausea and vomiting. Loss of appetite, headache, insomnia, muscular weakness and loss of weight are also observed. Laboratory diagnosis depends on the demonstration of trophozoites and cysts in dysenteric and formed stools, respectively.
Treatment:
Carbarsone, Diodohydroxyquin and Tetracycline are used in treating human cases.
Prophylaxis is same as that of amoebiasis.
Microsporidia are ubiquitous obligate intracellular new protozoan parasites found commonly in laboratory animals. They are unicellular Gram-positive organisms with mature spores 0.5 – 2 x 1 – 4μ in diameter. The spores have an extrusion apparatus consisting of a coiled polar filament and anchoring disk and contain the infective agent known as sporoplasm. The potential of Microsporidia for infecting warm blooded vertebrates is only now being recognised. Significant microsporidiosis in human is increasing in association with the increase in patients with AIDS.
There are four genera of microsporidia known to infect human beings:
1. Enterocytozoan bieneusi, the most common microsporidian observed in AIDS patients, infects the intestinal mucosa and causes diarrhoea. Its estimated prevalence may be as high as 10% in AIDS patients.
2. Pleistophora species was reported in an immuno compromised HIV negative patient with myositis.
3. Encephalitozoon cuniculi was reported in AIDS patients with peritonitis, hepatitis. Very recently a new E. heliun sp. has been isolated from three AIDS patients.