Parasitic Infection in GI Tract

Taniawati SupaliDepartment of Parasitology

Faculty of MedicineUniversity of Indonesia

PARASITIC INFECTIONS IN GASTROINTESTINAL

TRACT

Intestinal protozoa found in the gastrointestinal tract

Intestinal helminths found in the gastrointestinal tract

Ascaris lumbricoides(roundworm)

Disease: Ascariasis

Mature eggAdult worms

Epidemiology

z Affecting about 1.3 billion people.z Distribution:

Asia, Africa, and Latin America. Occurring in slum & shanty towns (poor socio-

economic conditions)z Most severe consequences of infection occur in

children who usually suffer from heavier worm burdens than adults living under similar conditions.

Pathogenesisz Antigen released during molting process cause

inflammation associated with eosinophilic infiltration of the tissues, peripheral eosinophilia, & an increase IgElevels.

z Heavy infections may lead to the formation of a large bolus of adult worms that obstructs the lumen.

z Adult worms secrete an anti-trypsin factor that enables it to ingest a portion of any meal before its absorbed.

Life cycleInfection occurs when host ingests the mature eggs. The eggs hatch in the small intestine of host.

The immature parasite penetrates the intestinal wall, enters the lamina propria, penetrates a capillary, and is carried by the portal circulation to the liver.

It then migrates via the blood stream to the heart and into the pulmonary circulation. The larva migrates up the bronchi into the trachea and across the epiglottis.

It is swallowed, finally reaching the lumen of the small intestine again, then molts to be adult worm.

Clinical Symptoms

z Symptoms due to adult worms: Diarrhea Intestinal obstruction due to numerous of adult

worms

The worms can perforate the intestine and migrate to the appendix or bile duct (ectopic infection)

Diagnosis:

Stool examination for eggs. Recovery of adult or juvenile worms in stool

or vomit from infected human.

Egg

Treatment:

Albendazole Mebendazole Pyrantel pamoat Piperazine citrate - used for intestinal

obstruction because it paralyzes the worms

Hookworms

AncylostomaAncylostoma duodenaleduodenale NecatorNecator americanusamericanus

Epidemiology

z The distribution of those worms are not overlapping but both species can be found in the same regions in Africa, South America, and Asia.

z It is estimated that 2150 million persons are iron deficient and about half of them suffer from iron deficiency anemia.

Route of infection

z Necator americanus: percutaneousz Ancylostoma duodenale: percutaneous

and oral larvae infect orally may undergo two molts to adulthood without leaving the gastrointestinal tract.

Life cycle

The filariform larvae penetrate the cutaneous tissues, usually through a hair follicle. Then the larvae enter capillaries and are carried passively through the bloodstream to the capillaries of the lungs.

The 3th stage larvae break out of the alveolus capillaries and then crawl up the bronchi and trachea, over the epiglottis, and into the pharynx.

They are then swallowed, and proceed into the stomach. Two molts take place in the small intestine resulting in the development of adult worms.

Pathogenesisz The adult worms move several times a day to different

attachment sites in the intestinal mucosa.

z The worms eat villous tissue and also suck blood directly from their site of attachment to the intestinal mucosa and submucosa.

z The worms secrete an anticoagulant that blocks the action of host factor Xa and VII a/tissue factors. Blood loss continues after the worms move to a new location.

Pathogenesis

z The combination of constant blood loss due to hookworm infection and poor iron intake in the diet results in iron deficiency anaemia.

z The severity of iron-deficiency anemia depends upon the species of hookworms in the intestine (A. duodenale ingests 4-5 times more blood each day than N. americanus)

Clinical symptoms

Rarely itch at skin entry site of larvae Most infections are asymptomatic Minor abdominal pain Iron deficiency anemia pregnant women,

menorrhagia women, children Malnutrition

z In a child, the continued daily loss of 10ml of blood can lead to severe anaemia.

z Heavy hookworm infection results in chronic haemorrhage from the intestinal mucosa.

Head of N. americanusHead of A. duodenale

Diagnosis:

Finding eggs in stool by microscopic examination.

Treatment:- Albendazole- Mebendazole

Trichuris trichiura(Whipworm)

Disease: Trichuriasis

Adult worm Egg

Epidemiology

It has a worldwide distribution.

The prevalence is estimated to be over 1 billion.

It is coincident with infections caused by Ascarislumbricoides and hookworms.

The whipworm is especially prevalent in areas of high rainfall and high humidity.

It is a fecal oral transmission

Life cycleThe first stage of larva hatches in the small intestine, penetrates the columnar epithelium, and lie just above the lamina propia.

The immature adult emerges and is passively carried to the large intestine, where it re-embeds itself in the columnar cells and induces its essential niche.

Adult worms live in the transverse and descending colon.

Pathogenesisz Adult worms in the large intestine induces structural

defects in the epithelium.

z To invade the colonic mucosa, the adult wormreleases protein which induces pores.

z It may facilitate invasion and enable the parasite to maintain its syncytial environment in the caecalepithelium.

Diagnosis

z Finding eggs by microscopic examination.

Clinical symptoms

Most cases are asymptomatic In heavily infected patients, the symptoms include:

Dysentery ( diarrhea containing blood and mucus) Tenesmus which can lead to rectal prolapse Abdominal pain

Treatment

Albendazole Mebendazole

PreventionProper disposal of feces

Oxyuris vermicularis(Pinworm)

Disease: trichuriasis

Adult wormEgg

Epidemiology

z It affects children < 12 years oldz The transmission of enterobiasis is

especially frequent in elementary school and daycare center.

Life cycle

The embryonated eggs are swallowed & hatch into the 2nd stage larvae once they reach the small intestine. Development to the 3th & 4th stages also occurs here.

The adult worms take up residence in the large intestine.

Eggs can hatch on the skin at the site of deposition, and the 2nd stage larvae can crawl back through the anus into the rectum, and the colon where they develop into reproducing adults

Retro infection

Clinical symptomsz Most of infected individuals are asymptomatic.

Common symptoms found in children are loss of appetite, insomnia and restlessness.

z The most common symptom is itching in the perianal region due to worms migrating to the area around the rectum to lay their eggs.

z Ectopic enterobiases have been described at the vagina and the genital area.

Diagnosis

Finding eggs by microscopic examination of a sticky tape

Anal swab

Treatment

Albendazole Mebendazole Pyrantel pamoat.

Prevention Finger nail cleaning Stop finger nail chewing Wash bed sheet & cloths

Strongyloides stercoralisDisease: Strongyloidiasis

It is distributed in tropical and subtropical countries

Fecal oral transmission

Epidemiology

Life cycle

Free-living cycle: The rhabditiform larvae passed in the stool becoming infective filariform larvae or free living adult males & females that mate & produce eggs from which rhabditiform larvae hatch. The filariform larvae penetrate the human host skin to initiate the parasitic cycle.

Parasitic cycle: Filariform larvae in soil penetrate the human skin, & are transported to the lungs where they penetrate the alveolar spaces; are carried through the bronchial tree to the pharynx, are swallowed & then reach the small intestine. In the small intestine they molt twice and become adult female worms. The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs, which yield rhabditiform larvae.

The rhabditiform larvae can either be passed in the stool (Free-living cycle), or can cause autoinfection. In autoinfection, the larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection).

z Most of the pathology is associated with larval stages that moved through the tissue.

Pathogenesis

Itchy at the skin entry site of the infective larvae. Most infections are asymptomatic. Acute strongyloidiasis is characterized by a

marked IgE & blood eosinophil response with the symptoms: abdominal pain, diarrhea.

In hyperinfection (Chronic form), the symptoms are severe & bloody diarrhea.

Clinical symptomsCross-sections of female S. stercoralis(blue arrows) in small intestine tissue

Diagnosis

Stool culture for larvae Serology test (ELISA)

z Treatment Albendazole Ivermectin not registered for

human use in Indonesia

Larva

Taenia sp(Tapeworm)

Disease: taeniasis

Adult worm EggProglotide

Taenia spz There are two species infecting human:

Taenia saginata

Taenia solium (pork tape worm)

z Epidemiology: cosmopolitan

Taenia spz Taenia solium has a complex two host life cycle.

Human is the only definitive host and habour the adult worm, whereas both people and pigs can act an intermediate hosts and harbour the larvae or cysticerci.

z For Taenia saginata, human is the only definitive host and animals (cow, buffalo) are the intermediate hosts.

z Infective stage for human: T. saginata : bovine cysticercus T. solium : pig cysticercus (cysticercus cellulosae)

z

Life cycleEggs or gravid proglottids are passed with feces.

Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . In the animal's intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci.

Humans become infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into an adult tapeworm which attach to the small intestine by their scolex and reside in the small intestine. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool

Pathogenesis

z The worm which is flexible and fragile live in a large part of the lumen of the small intestine therefore the bowel obstruction does not occur.

z The worm attaches strongly to the mucosa of the upper small intestine by means of its suckers and hooks.

z The adult causes only mild inflammation at the implantation site, without substantial damage to the intestine.

Scolex of T. saginata with 4 large suckersScolex of T. solium with 4 large suckers & rostellum containing 2 rows of hooks

z Most taeniasis are asymptomatic. z Infected people become aware of

infection until discovering the proglotidsin stool.

z Rarely nausea, vomiting, abdominal pain.z Unpleasant sensation due to active

moving proglottids discharge from anus.

Taenia solium taeniasis is less frequently symptomatic than Taenia saginatataeniasis.

Head of Taenia sp

Proglottide

Clinical symptoms

Adult worm Cercaria

Schistosoma japonicum(blood fluke)

Disease: schistosomiasis

Diagnosisz Stool microscopy for eggs but can

not be used to differentiate between T. saginata & T. solium.

z Proglottid in feces used to differentiate between T. saginata & T. solium

zTreatment Praziquantel

Egg

Proglottid

Epidemiology

z Distribution: China, Japan, Taiwan, The Philippines, Vietnam, Malaysia, Indonesia.

Indonesia: It is found only in Central of Sulawesi (Lindu lake and

Napu valley) limited by the distribution of their snail intermediate host - Oncomelania hupensis lindoensis (keong air)

Life cycleEggs hatch & release miracidia , which swim and penetrate specific snail intermediate hosts.

The stages in the snail include 2 generations of sporocysts & the production of cercariae .

Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host becoming schistosomulae which migrate through several tissues and stages to their residence in the veins. Adult worms in humans reside in the superior mesenteric veins of the small intestine. The eggs are moved progressively toward the lumen of the intestine.

Pathogenesis

z Adult worms living in the venous circulation usually do not cause significant pathological damage.

z The attached bacteria on the surface of adult worms can result in the introduction of enteric bacteria in the blood stream enteric fever from non-thypoidal salmonellosis.

Pathogenesis

z Deposition of eggs in the intestine and liver result in intestinal and hepatic fibrosis due to granuloma formation around eggs.

z Eggs secrete proteolytic enzymes which cause erosion of the submucosa and villous tissue.

z In heavy infection, gastrointestinal hemorrhage results from damage to the submucosa.

Clinical symptoms

z Acute manifestation commonly occur in new immigrants frequently febrile and flu-like symptoms.

z Chronic manifestation: Intestinal & hepatic dysfunctionAbdominal painBloody diarrhea

Diagnosis:

Finding eggs by microscopic examination of stool Serological test

Treatment: Praziquantel administered in an oral form in one or two

doses from 40-60 mg/kg body weight

Control: Sanitary disposal of sewage and destruction of snails

Egg

Fasciolopsis buski(Intestinal fluke)

Disease: Fasciolopsiasis

Adult wormEgg

Epidemiology

z Distribution: China, Vietnam, Thailand, India, Indonesia

z Indonesia: Kalimantan Selatan

Life cycleUnembryonated eggs pass in feces becoming embryonated in water & release miracidia , which invade a suitable snail intermediate host.

In the snail the parasites undergo several developmental stages (sporocysts, rediae, & cercariae ). The cercariae are released from the snail and encyst as metacercariae on aquatic plants .

The mammalian hosts become infected by ingesting metacercariae on the aquatic plants. After ingestion, the metacercariae excyst in the duodenum and attach to the intestinal wall.

Pathogenesis

z The worms attach the luminal surface.z They feed on columnar epithelial cells and

injure cells.

Clinical symptoms

z Light infection does not cause any clinical disease (asymptomatic)

z Heavy infection causes continuous diarrhea, abdominal pain, intestinal hemorrhage

Diagnosis

z Finding eggs by microscopic examination of stool.

Treatment Praziquantel

Egg

Entamoeba histolytica(Subphylum: sarcodina)

Disease : Amoebiasis

Trophozoite

Morphology

Epidemiology

z The infection is distributed world wide.z The higher rates of infection is in

underdeveloped countries. z Infection is associated with poor hygiene.

Humans are the principal host, although dogs, cats and rodents may be infected.

Infection occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine & trophozoites are released, which migrate to the large intestine.

The trophozoites multiply by binary fission & produce cysts. Both stages are passed in the feces. Because of the protection conferred by their walls, the cysts can survive in the external environment & are responsible for transmission. Trophozoitespassed in the stool are rapidly destroyed once outside the body. In some patients the trophozoites invade the intestinal mucosa (intestinal disease), or, through the bloodstream, extraintestinalsites such as the liver, brain, and lungs ( extraintestinal disease), with resultant pathologic manifestations.Cysts & trophozoites are passed in feces. Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrhealstool.

Life cycle

Pathogenesis

z Trophozoites penetrate the perimucosal space and attach to epithelial cells using lectin-carbohydrate interactions.

z Causing lysis of cells, then parasites grow and divide by binary fusion develop flask-shaped ulcer .

Amebapore (a channelforming protein)Cysteine proteinases (tissue invasion)

Amoebiasis

z Clinical disease: Intestinal amoebiasis Extra-intestinal amoebiasis

Parasite erode the wall of the large intestine, enter the blood circulation of the submucosa

The parasites spread to extra-intestinal through portal system (liver, brain) or percontinuitatum (lung, rectum).

AmoebiasisClinical symptoms:1. Most of the infected individuals are

asymptomatic and some of them go on becoming carrier.

2. Symptomatic amoebiasis consists of acute amoebic dysentry, amoebic liver abscess and amoeboma.

Amoebic dysentryz Clinical symptoms

Bloody, mucous diarrhea Fever Abdominal pain

z Diagnosis Finding amoebic (hematophagous trophozoites) in stool Detecting parasite by PCR or antigen capture from stool

sample.

AMOEBIC LIVER ABSCESS

z Clinical symptoms: persisting fever epigastric pain rarely diarrhea

z Diagnosis1. serology2. aspirate microscopy to find trophozoites

Treatment

z Tissue: Metronidazole Chloroquine Emetin hidrochloride

z Bowel lumen: Paromomycin Diloxanidefuroate

Giardia lamblia(Subphylum mastigophora)Disease: Giardiasis

Cyst Trophozoite

Epidemiology

z Fecal oral transmission z increased in travellers, backpackers. z found in most mammals (beaver,cattle,

cats, dogs,etc) -- Zoonotic

Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites).In the small intestine, excystationreleases trophozoites (each cyst produces two trophozoites). Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystationoccurs as the parasites transit toward the colon.The cyst is the stage found most commonly in nondiarrheal feces. Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible.

Life cycle

Pathogenesis

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

trophozoite

Symptomsz Early symptoms include flatulence, abdominal

distension, nausea and foul-smelling bulky, often watery, diarrhea.

z The stool contains excessive lipids but very rarely any blood or necrotic tissue.

z The chronic stage is associated with vitamin B12 malabsorption, disaccharidase deficiency and lactose intolerance.

Diagnosis

z Finding either cysts or trophozoites in fresh stool by microscopic examination.

z ELISA test to detect G.lamblia antigen.

Treatment

z Metronidazolez Tinidazole

Balantidium coli(ciliate protozoa)

Disease : Balantidiosis

Vegetative Cyst

Life cycleInfection occurs when host ingests cysts (parasite stage responsible for transmission of balantidiasis) from contaminated food or water. Following ingestion, excystation occurs in the small intestine, & the trophozoites colonize the large intestine. The trophozoites reside in the lumen of the large intestine of humans and animals, where they replicate by binary fission, during which conjugation may occur. Trophozoitesundergo encystation to produce infective cysts. Some trophozoites invade the wall of the colon and multiply. Some return to the lumen & disintegrated.Mature cysts are passed with feces

Habitat

z mucosa layer of large intestine (cecum)z lumen of large intestine

Pathogenesis

z Balantidium coli usually resides in the lumen of its host, trophozoites can invade the mucosa of the large intestine (cecum and colon) and cause ulcerations.

z The parasite secretes a substance called hyaluronidase enzyme, which helps degrade intestinal tissue and facilitates penetration of the mucosa.

Clinical symptoms

z Asymptomaticz Symptomatic:

Chronic diarrhea, occasional dysentery (diarrhea with blood or mucus), nausea, colitis (inflammation of the colon), abdominal pain, weight loss, deep intestinal ulcerations, and possibly perforation of the intestine (peritonitis)

Diagnosis

z Finding either cysts in formed stool or trophozoites in watery stool by microscopic examination

Treatment

z Tetracycline

Blastocystis hominisDisease: blastocystosis

Vacuolar form

z The epidemiology of B. hominisremains almost totally unkonwnbecause the status of the organism

z is still unclear.

z B.hominis is a pathogenic or non-pathogenic organism ?

Blastocystis hominis

Life cycle is still unclear yet

Transmission: fecal-oral route through ingestion of contaminated water or food

Blastocystis hominisz B. hominis exists in 4 forms (vacuolar, granular, ameboid,

cyst)

z B. hominis can be considered as the agent of infection after all organisms causing diarrhea are negative in the stool examination.

z It should be > 5 parasites/LPF (large per field) in microscopic examination.

Clinical Symptoms

z Asymptomatic (commensal parasite)z Symptomatic :

Watery diarrhea Abdominal pain Perianal pruritis (itch) Excessive flatulence

Treatment

z The disease is self-limiting and therefore should not be treated. However, upon diagnosis with the disease, patients are usually treated with Metronidazole, which has been effective.

Cryptosporidium parvum(Phylum apicomplexa)

Disease: cryptosporidiosis

Epidemiology

z Infection can occur from animal reservoirs sheep, cattle, birds) to human Zoonotic.

z Transmission occurs mainly through contact with contaminated water

Life cycleInfection begins when the host ingests sporulated oocysts containing four sporozoites. The sporozoites excyst when the oocystreaches the small intestine. Sporozoitesparasitize epithelial cells of the gastrointestinal tract. In these cells, the parasites undergo asexual multiplication (schizogony or merogony) and then sexual multiplication (gametogony) producing microgamonts (male) and macrogamonts (female). Upon fertilization of the macrogamonts by the microgametes, oocysts, develop that sporulate in the infected host. Two different types of oocysts are produced, the thick-walled, which is commonly excreted from the host , and the thin-walled oocyst , which is primarily involved in autoinfection. Oocysts are infective upon excretion, thus permitting direct and immediate fecal-oral transmission.

Pathogenesisz Diarrhea associated with Cryptosporidium appears to be

primarily osmotic in nature. Associated with this disruption of enterocyte (i.e. intestinal epithelial cells) function is a blunting of the villi and crypt cell hyperplasia.

z A possible mechanism of pathogenesis is that the infection of intestinal epithelial cells with Cryptosporidium damages the enterocytes and eventually leads to their death.

z This triggers cell division in the crypt region (i.e., hyperplasia) to replace the damaged cells. The combination of destruction of absorbtive cells at the tips of the villi and the increase in the Cl--secreting crypt leads to an overall enhanced secretion.

Clinical symptoms

z In immunocompetent patients: Self limiting disease In acute stage: abdominal pain, nausea, vomiting,

transient episode of diarrhea.

z In immunocompromised patients: Diarrhea (chronic- lasting months & even years)

z Cholecystitis extraintestinal infection in bile duct

Diagnosis

z Finding oocysts in stool by microscopic examination/ serological test/ PCR

Treatment

z Nitazoxanide

z The effectiveness of nitazoxanide in immunosuppressed persons is unclear. For persons with AIDS, anti-retroviral therapy, which improves immune status, will also reduce oocyst excretion and decrease diarrhea associated with cryptosporidiosis.

Cyclospora cayetanensis(Phylum apicomplexa) Disease: cyclosporiasis

Cyst

Epidemiologyz The epidemiology of Cyclosporiasis is still unclear.

Cyclosporiasis has been reported in many countries, in tropical and subtropical areas.

z The unsporulated oocysts passed in the stool are not infectvestage of C. cayetanensis Fecal-oral transmission can not occur

z An infective stage is a sporulated oocyst. z Contamination of food and water can serve as vehicles for

transmission. However, the potential mechanisms of contamination of food and water are still unclear.

Life cycle

Infection starts when the sporulated oocysts are ingested. The oocysts excyst in the gastrointestinal tract, freeing the sporozoites which invade the epithelial cells of the small intestine.Inside the cells they undergo asexual multiplication and sexual development to mature into oocysts, which will be shed in stools.

Clinical symptoms

z The disease is usually self-limiting.z Watery diarrhea z The loss of appetite, weight loss,

bloating, flatulence, stomach cramps, nausea, vomiting.

Diagnosis

z Finding oocysts in stool specimens by light microscopy.

Oocyst

Treatment

z Trimethoprim-sulfamethoxazole.

z Patients with AIDS may need higher doses and long-term maintenance treatment.

Isospora belli(Disease: Isosporiasis)

Epidemiology

z It is distributed worldwide, especially in tropical and subtropical areas.

z Infection occurs in immunocompromised individuals.

Life cycleInfection occurs by ingestion of sporocysts-containing oocysts: the sporocysts excyst in the small intestine and release their sporozoites, which invade the epithelial cells and initiate schizogony . Upon rupture of the schizonts, the merozoites are released, invade new epithelial cells, and continue the cycle of asexual multiplication.

Trophozoites develop into schizontswhich contain multiple merozoites. After a minimum of one week, the sexual stage begins with the development of male and female gametocytes . Fertilization results in the development of oocysts that are excreted in the stool .

Clinical Symptoms

z Asymptomaticz Symptomatic : gastrointestinal complaints

(self limiting) Diarrhea Abdominal pain Weight loss Slight fever Malabsorption of fat

Isospora belii

Diagnosis

z Finding oocysts in stool using acid-fast stain.

Oocyst

Treatment

z Sulfamethoxazole-trimethoprim.

z In immunocompetent individuals, the symptoms disappear in 2-3 days with treatment and longer without treatment.

Coccidian Parasites Found in Human Feces

Species Excreted Form Size (m) Oocyst Structure

Cryptosporidium parvum

sporulatedoocysts 4-5

4 sporozoites, no sporocysts

Cyclosporacayetanenis

unsporulatedoocysts 8-10

2 sporocysts with2 sporozoites each

Isospora belli unsporulatedoocysts 30 x 122 sporocysts with 4 sporozoites each

MicrosporidiumDisease: Microsporidiasis

The infective form of microsporidia is the resistant spore. The spore infects the host cell The spore injects the infective sporoplasminto the eukaryotic host cell through the polar tubule. Then the sporoplasm undergoes multiplication either by merogony (binary fission) or schizogony (multiple fission). This development can occur either in direct contact with the host cell cytoplasm (E. bieneusi) or inside a vacuole termed parasitophorousvacuole (E. intestinalis). Either free in the cytoplasm or inside a parasitophorousvacuole, microsporidia develop by sporogonyto mature spores. During sporogony, a thick wall is formed around the spore, which provides resistance to adverse environmental conditions. When the spores increase in number and completely fill the host cell cytoplasm, the cell membrane is disrupted & releases the spores to the surroundings. These free mature spores can infect new cells thus continuing the cycle.

Life cycle

Organism(s) Clinical presentation

Immunocompromised host

Immunocompetent host

Enterocytozoonbieneusi

Encephalitozoonintestinalis

Encephalitozooncuniculi

Chronic diarrhea, wasting, cholangitis, acalculouscholecystitis

Chronic diarrhea; cholangiopathy

hepatitis; peritonitis; symptomatic and asymptomatic intestinal infection

Self-limiting diarrhea and traveler's diarrhea; asymptomatic carriers

Self-limiting diarrhea; asymptomatic carriers

Not identified

E. bieneusi and E. intestinalis are the most common microsporidia causing diarrhea.

Clinical presentations in immunocompromised and immunocompetent hosts are the same, however the diarrhea in immunocompromised host is more severe and prolonged

Organism Main sites of infection

Enterocytozoon bieneusi

Encephalitozoon intestinalis

Encephalititozoon cuniculi

Small intestinal epithelium, bile duct epithelium

Epithelia of the gut from small intestine to colon, gall bladder

Liver, peritoneum, intestine

The clinical symptoms resulting from the infection among 3 species are different based on the location of infection

Diagnosis

z Finding spores in the fecal sample by microscopic examination / PCR/ serological test

Treatment

z Albendazole is the drug of choice.

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