Entamoeba Histolytica Overview

Entamoeba Histolytica

• Entamoeba histolytica is a protozoan parasite that causes amoebic dysentery and amoebic liver abscess.
• The parasite is found worldwide but is more common in tropical regions.
• It's estimated that 10% of the global population and 50% of people in developing countries are infected with the parasite.
• E. histolytica is a leading cause of parasitic mortality, ranking third after malaria and schistosomiasis.

Morphology

• E. histolytica exists in three forms: trophozoite, precystic stage, and cyst.
• The trophozoite is the vegetative or active form of the parasite.
• It's the only form present in tissues, ranging in size from 12-60 µm with an average of 20 µm.
• Trophozoites are characterized by their irregular shape and amoeboid movement.
• They have a clear outer ectoplasm and a finely granular inner endoplasm.
• Trophozoites in acute dysenteric stool often contain ingested red blood cells (RBCs), which is a diagnostic feature.
• Trophozoites divide by binary fission (splitting into two) every 8 hours.
• They can survive for up to 5 hours at 37°C and are killed by drying, heat, and chemical sterilization.
• Infection is not transmitted by trophozoites because they cannot survive outside the body to initiate infection.
• The precystic stage is a transition phase where the trophozoite prepares for encystment.
• The cyst is the spherical, dormant form of the parasite.
• It's 10-20 µm in size and can contain one to four nuclei.

Life Cycle

• E. histolytica completes its life cycle solely in humans.
• The mature cyst with four nuclei is the infective stage.
• Infection occurs when humans ingest food or water contaminated with cysts.
• Cysts survive passage through the stomach and reach the small intestine, where excystation occurs.
• During excystation, the cyst wall breaks down due to trypsin.
• The liberated quadrinucleate amoeba then divides into eight smaller metacystic trophozoites.
• These trophozoites are found in the submucosal tissue of the caecum and colon.
• Some metacystic trophozoites develop into precystic forms and cysts.
• Cysts are passed in feces, completing the cycle.

Pathogenesis

• E. histolytica can cause both intestinal and extraintestinal amoebiasis.
• The incubation period is highly variable, typically ranging from four days to four months.
• Symptoms and severity depend on the organ affected and the extent of damage.

Intestinal Amoebiasis

• Metacystic trophozoites penetrate the colon's epithelial lining.
• Penetration is aided by the amoeba's motility and the enzyme "histolysin," which damages the mucosal cells.
• Amoeba penetration creates distinctive ulcers with a pinhead center and raised edges.
• Amoebic ulcers are the characteristic lesion of intestinal amoebiasis.
• Ulcers are often multiple and concentrated in the caecum and sigmoidorectal region.
• The ulcers can undermine and spread laterally, causing extensive mucosal loss.
• Occasionally, ulcers penetrate deeper into the colon wall, leading to perforation and peritonitis.
• Deep ulcers can form scars that constrict the colon, leading to obstruction.
• These amoebic granulomas can be mistaken for malignant tumors.

Clinical Features

• Amoebic dysentery is the typical manifestation of intestinal amoebiasis.
• Patients experience large, foul-smelling, bloody stools with mucus.
• The stools contain clumped, reddish-brown RBCs.
• Trophozoites with ingested RBCs can be observed in the stool.
• Patients are usually afebrile (not feverish) and nontoxic.
• Fulminant colitis (acute inflammation of the colon) causes confluent ulceration and necrosis.
• Other intestinal symptoms like diarrhea or vague abdominal discomfort can occur.
• Chronic involvement of the caecum can mimic appendicitis.

Extraintestinal Amoebiasis

• E. histolytica can spread beyond the intestines and cause complications in other organs.
• The most common extraintestinal complication is hepatic amoebiasis, which can lead to liver abscesses.
• Pulmonary amoebiasis can occur due to the spread of liver abscesses to the lungs.
• Metastatic amoebiasis can involve other organs like the brain, skin, and genitourinary tract.

Hepatic Amoebiasis

• Liver damage might not be directly caused by amoeba but by enzymes and inflammatory mediators released by surrounding cells.
• Liver abscesses are present in about 5%-10% of patients with intestinal amoebiasis.
• Abscesses typically occur in the upper right lobe of the liver and contain thick, chocolate-brown pus.
• Abscesses can rupture into surrounding tissues, causing complications depending on the location.
• Liver abscesses are less common in women and rare in children under 10 years old.

Pulmonary Amoebiasis

• Pulmonary amoebiasis often results from a hepatobronchial fistula and can lead to amoebic empyema.
• Patients present with chest pain, dyspnea (difficulty breathing), and non-productive coughs.

Treatment

• Luminal amoebicides like diloxanide furoate, iodoquinol, paromomycin, and tetracycline target the intestinal lumen but have limited effect on tissue amoebae.
• Tissue amoebicides such as emetine and chloroquine are effective against systemic infection but less potent against intestinal amoebae.
• Metronidazole and its related compounds (tinidazole, ornidazole) are the drugs of choice for treating both intestinal and liver involvement.
• Metronidazole dosage for liver abscess is 1 g for two days, followed by 5 g daily for three weeks.

Prophylaxis

• General prophylaxis measures for fecal-oral infections are crucial.
• Food and water must be protected from contamination with human excreta.
• Detection and treatment of carriers and their exclusion from food handling jobs help limit infection spread.
• Healthy personal hygiene practices and education contribute to control efforts.

Entamoeba Histolytica: A Brief Overview

• Entamoeba histolytica is responsible for amoebic dysentery and amoebic liver abscess.
• Its prevalence is widespread, particularly in tropical regions.
• Around 10% of the global population and 50% of inhabitants in developing countries are estimated to be infected.

Morphology of Entamoeba Histolytica

• Entamoeba histolytica exists in three forms: trophozoite, precystic stage, and cyst.
• Trophozoite: The vegetative or growing stage, present only in tissues.
  • Size: 12–60 μm, averaging 20 μm
  • Active in fresh dysenteric stool, smaller in convalescents and carriers.
  • Cytoplasm: Consists of clear, transparent outer ectoplasm and finely granular inner endoplasm.
  • Motility: Exhibits amoeboid movement, crawling or gliding, driven by pseudopodia.
  • Nucleus: Spherical, 4–6 μm, containing a central karyosome.
  • Important diagnostic feature: Contains phagocytosed erythrocytes, not found in other intestinal amoebae.
  • Divides via binary fission every 8 hours.
  • Survival: Survives for up to 5 hours at 37°C. Killed by drying, heat, and chemical sterilization.
• Precystic Stage:
  • Forms in the intestinal lumen during encystment.
  • Trophozoites round or oval, extruding food vacuoles.
  • Contains a large glycogen vacuole and two chromatid bars.
  • Secretes a cyst wall, transforming into a cyst.
• Cystic Stage:
  • Spherical shape, 10–20 μm.
  • Early cyst: Contains a single nucleus and two chromatid bars.
  • Mature cyst: Contains four nuclei, known as a quadrinucleate cyst.
  • Staining:
    • Hematoxylin: Nuclear chromatin and chromatoid bodies appear blue or black.
    • Iodine: Nuclear chromatin and karyosome bright yellow, chromatoid bodies appear clear (unstained).

The Life Cycle of Entamoeba Histolytica

• Involves only one host: Humans.
• Infective form: Mature quadrinucleate cyst.
• Transmission: Ingestion of contaminated food and water containing cysts.
• Cysts pass through the stomach unharmed, reaching the small intestine.
• Excystation: In the lower ileum, trypsin damages the cyst wall, leading to excystation.
• Metacyst stage: The cytoplasm detaches from the cyst wall, freeing the quadrinucleate amoeba.
• Metacystic trophozoites: The nuclei divide, forming 8 nuclei, each surrounded by cytoplasm, resulting in 8 small metacystic trophozoites.
• Optimal habitat: Submucosal tissue of the caecum and colon.
• Some metacystic trophozoites develop into precystic forms and cysts, which are eliminated in feces, continuing the cycle.

Pathogenesis of Entamoeba Histolytica

• Causes intestinal and extraintestinal amoebiasis.
• Incubation period: Variable, ranging from 4 days to 4 months.
• Forms and severity of amoebiasis depend on the affected organ and extent of damage.

Intestinal Amoebiasis

• Metacystic trophozoites invade the columnar epithelial cells of the colon.
• Penetration facilitated by trophozoite motility and the tissue lytic enzyme, histolysin, which breaks down the mucosal epithelium.
• Results in ulcers with pinhead centers and raised edges.
• May heal spontaneously if invasion remains superficial.
• More often, amoebae penetrate the submucosal layer, multiplying rapidly and causing lytic necrosis, leading to abscess formation.
• Abscesses break down, forming ulcers.
• Ulcers are multiple, mainly located in the caecum and the sigmoidorectal region.
• Initially appear as raised nodules with pouting edges, later breaking down, releasing brownish necrotic material containing numerous trophozoites.
• Typical amoebic ulcer is flask-shaped with a narrow mouth and neck, and a large, rounded base.
• Ulcers generally don't extend beyond the submucosal layer but spread laterally in the submucosa, causing undermining and patchy mucosal loss.
• Amoebae are found at the periphery of the lesions and extend into surrounding healthy tissues.
• In rare instances, ulcers may affect the muscular and serous coats of the colon, causing perforation and peritonitis.
• Deep ulcers form scars, leading to strictures, partial obstruction, and thickening of the gut wall.
  • This amoebic granuloma or amoeboma may be mistaken for a malignant tumor.

Clinical Features of Intestinal Amoebiasis

• Incubation period: Variable, ranging from 1 to 4 months.
• Clinical course: Characterized by prolonged latency, relapses, and intermissions.
• Amoebic dysentery:
  • Large, foul-smelling, brownish-black stools with blood-streaked mucus and feces.
  • Erythrocytes in stools appear clumped and reddish-brown.
  • Presence of E.histolytica trophozoites with ingested erythrocytes is a key diagnostic feature.
• Patient is usually afebrile and non-toxic.
• Fulminant colitis: Confluent ulceration and necrosis of the colon, accompanied by fever and toxicity.
• Not all intestinal amoebiasis manifests as dysentery.
  • It can present as diarrhea or vague abdominal symptoms.
• Chronic involvement of the caecum can mimic appendicitis.

Extraintestinal Amoebiasis

• Entamoeba histolytica can affect organs beyond the intestines.
• Major sites of extraintestinal amoebiasis:
  • Hepatic amoebiasis (including liver abscesses)
  • Pulmonary amoebiasis
  • Metastatic amoebiasis
  • Cutaneous amoebiasis
  • Genitourinary amoebiasis

Hepatic Amoebiasis

• Liver enlargement and tenderness are common, without significant liver function impairment or fever.
• Damage may not be directly caused by amoebae but by lysosomal enzymes and cytokines from inflammatory cells surrounding the trophozoites.
• Liver abscesses occur in 5–10% of individuals with intestinal amoebiasis.
• Liver abscesses usually solitary, located in the upper right lobe of the liver, contain thick chocolate brown pus.
• Multiple abscesses and abscesses pressing on the biliary tract can lead to jaundice.
• Uncontrolled abscesses can rupture into surrounding tissues, including the lung, pleural cavity, pericardium, peritoneal cavity, stomach, intestine, inferior vena cava, or externally through the abdominal wall and skin.
• Lower incidence in women and rare in children younger than 10 years.

Pulmonary Amoebiasis

• Often results from a hepatobronchial fistula, characterized by expectoration of chocolate brown sputum.
• Less commonly, amoebic empyema can develop.
• Clinical presentation: Severe pleuritic chest pain, dyspnea (difficulty breathing), and non-productive cough.

Treatment of Amoebiasis

• Luminal amoebicides:
  • Diloxanide furoate, iodoquinol, paromomycin, and tetracycline act within the intestinal lumen but not in tissues.
• Tissue amoebicides:
  • Emetine, chloroquine, etc., effective in systemic infections, but less so in the intestine.
  • Dosage of chloroquine for amoebic liver abscess: 1 g for 2 days followed by 500 mg daily for 3 weeks.
• Both luminal and tissue amoebicides:
  • Metronidazole and related compounds (tinidazole and ornidazole) are effective in both the intestine and tissues, and are preferred for treating amoebic colitis and amoebic liver abscess.

Prophylaxis

• General measures:
  • Similar to other fecal-oral infections.
  • Food and water must be protected from contamination with human excreta.
• Additional approaches:
  • Detection and treatment of carriers.
  • Exclusion of carriers from food-handling professions.
  • Health education and promotion of healthy personal hygiene habits.

Entamoeba histolytica

• A parasitic protozoan responsible for amoebic dysentery and amoebic liver abscess.
• Found globally, with higher prevalence in tropical regions.
• Estimated to infect 10% of the world's population and 50% of those in developing countries.
• Third leading parasitic cause of death worldwide, after malaria and schistosomiasis.

Morphology

• Entamoeba histolytica exists in three forms:
  • Trophozoite: The vegetative or growing stage. Present in tissues. Irregular shape, 12-60 μm in size. Actively motile in dysenteric stool.
  • Precyst: Transition stage between trophozoite and cyst.
  • Cyst: The infective stage, passed in feces. Spherical, 10-20 μm in size.

Life Cycle

• Entamoeba histolytica has a single-host life cycle (human).
• Infective form: Mature quadrinucleate cyst
• Transmission: Ingestion of contaminated food and water containing cysts.
• Excystation occurs in the ileum, releasing metacystic trophozoites.
• Metacystic trophozoites multiply in the colon.
• Some trophozoites transform into precystic stages and cysts, completing the cycle.

Pathogenesis

• Causes intestinal and extraintestinal amoebiasis.
• Incubation period varies from 4 days to 4 months.
• Intestinal amoebiasis:
  • Metacystic trophozoites penetrate the colonic epithelium, causing ulcers.
  • Amoeba utilize histolysin to penetrate the mucosal barrier.
  • Ulcers may be superficial or deep.
  • Deep ulcers may lead to scarring, strictures, and amoebomas.

Clinical Features

• Intestinal amoebiasis presents as:
  • Amoebic dysentery: Characterized by bloody, foul-smelling stools.
  • Diarrhea: Often asymptomatic or with vague abdominal complaints.
  • Chronic caecal involvement: Mimicking appendicitis.

Extraintestinal Amoebiasis

• Hepatic Amoebiasis:
  • Liver abscesses: Usually solitary, located in the right lobe.
  • Characterized by chocolate-brown pus (anchovy sauce pus).
  • May lead to complications such as rupture into surrounding organs.
• Pulmonary Amoebiasis:
  • Often secondary to liver abscesses.
  • Results in hepatobronchial fistula with expectoration of chocolate brown sputum.
• Other forms:
  • Metastatic amoebiasis: Affecting various organs.
  • Cutaneous amoebiasis: Skin infections.
  • Genitourinary amoebiasis: Affecting reproductive organs.

Treatment

• Luminal amoebicides: Act in the intestinal lumen (Diloxanide furoate, iodoquinol, paromomycin, Tetracycline)
• Tissue amoebicides: Act systemically (Emetine, chloroquine)
• Both luminal and tissue amoebicides: Preferred treatment (Metronidazole, tinidazole, ornidazole)

Prophylaxis

• General measures for fecal-oral infections.
• Food and water protection from contamination with human excreta.
• Detection and treatment of carriers, exclusion from food handling.
• Health education and promotion of healthy personal habits.

Entamoeba histolytica

• Entamoeba histolytica causes amoebic dysentery and amoebic liver abscess
• It is a common parasite, particularly in tropical regions
• It is the third leading parasitic cause of death worldwide

Morphology

• Entamoeba histolytica exists in three forms: trophozoite, precystic, and cyst
• The trophozoite is the active, feeding stage, found in tissues
• It is irregular in shape, ranging from 12-60 µm in size
• The trophozoite displays amoeboid movement with finger-like projections
• It contains a single nucleus with a central karyosome
• Trophozoites from acute dysenteric stools often contain phagocytosed red blood cells, a distinguishing feature
• The trophozoite divides by binary fission
• The precystic stage is a transition form, losing food vacuoles and becoming rounder
• It contains a glycogen vacuole and two chromatid bars
• The cyst is the infective stage, spherical and 10-20 µm in size
• Mature cysts contain four nuclei (quadrinucleate)
• Cysts are resistant to environmental conditions and can survive for extended periods

Life Cycle

• The life cycle of Entamoeba histolytica occurs solely in humans
• Infection occurs through ingestion of mature cysts
• Cysts reach the small intestine unharmed and undergo excystation
• The metacyst stage releases quadrinucleate amoebae which then divide to form 8 metacystic trophozoites
• Optimal habitat for metacystic trophozoites is the submucosal tissue of the caecum and colon

Pathogenesis

• E. histolytica causes both intestinal and extraintestinal amoebiasis
• Incubation period ranges from 4 days to 4 months
• The severity and manifestation of amoebiasis depend on the affected organ and extent of damage

Intestinal Amoebiasis

• Metacystic trophozoites penetrate the colon's epithelium
• Penetration is facilitated by the amoebae's motility and histolysin, a tissue lytic enzyme
• Amoebic penetration creates discrete ulcers with a central pinhead and raised edges
• Deeper penetration leads to submucosal abscess formation
• Amoebic ulcers are flask-shaped, forming scar tissue that may lead to strictures and thickening of the gut wall

Clinical Features

• Intestinal amoebiasis presents with diverse symptoms, from mild diarrhea to severe dysentery
• Patients with amoebic dysentery experience bloody, foul-smelling stools and can exhibit fever and toxicity in more severe cases
• In chronic cases, involvement of the caecum can mimic appendicitis

Extraintestinal Amoebiasis

• Liver abscess is the most common extraintestinal manifestation
• Other forms include pulmonary, metastatic, cutaneous, and genitourinary amoebiasis

Hepatic Amoebiasis

• Liver abscesses are often solitary and located in the upper right lobe
• Jaundice occurs with multiple abscesses or blockage of the biliary tract
• Untreated abscesses can rupture into surrounding tissues, including the lung, pleura, pericardium, and peritoneum

Pulmonary Amoebiasis

• Often arises from a hepatobronchial fistula, resulting in brown sputum
• Symptoms include pleuritic chest pain, dyspnea, and non-productive cough

Treatment

• Luminal amoebicides (diloxanide furoate, iodoquinol, paromomycin, and tetracycline) act in the intestinal lumen but not tissues
• Tissue amoebicides (emetine, chloroquine) target systemic infection and are less effective in the intestine
• Metronidazole and related compounds (tinidazole, ornidazole) are the drugs of choice for both intestinal and systemic amoebiasis

Prophylaxis

• Prevention measures focus on avoiding fecal-oral contamination of food and water
• Detection and treatment of carriers are essential
• Promoting healthy personal habits and sanitation practices is vital for control

Entamoeba Histolytica

• A parasitic protozoan that causes amoebic dysentery and amoebic liver abscess.
• Globally prevalent, with higher rates in tropical regions.
• Estimated to infect 10% of the world population and 50% of those in developing countries.
• Third leading parasitic cause of death, after malaria and schistosomiasis.

Morphology

• Exists in three forms: trophozoite, precyst, and cyst.
• Trophozoite:
  • Active, growing stage.
  • Found in tissues, irregularly shaped, 12-60 μm in size (average 20 μm).
  • Larger and more active in dysenteric stool, smaller in convalescent and carrier stages.
  • Cytoplasm: clear outer ectoplasm and finely granular inner endoplasm.
  • Possesses finger-like pseudopodia for movement.
  • Contains a spherical nucleus (4-6 μm) with a central karyosome.
  • Often contain phagocytosed red blood cells, a diagnostic feature.
  • Divides via binary fission every 8 hours.
  • Survives for up to 5 hours at 37°C, but is killed by drying, heat, and chemical sterilization.
• Precystic Stage:
  • Formed when trophozoites undergo encystment in the intestinal lumen.
  • Round or oval shape with a large glycogen vacuole and two chromatid bars.
  • Secretes a cyst wall around itself.
• Cystic Stage:
  • Spherical, 10-20 μm in diameter.
  • Early cyst has one nucleus and two chromatid bars.
  • Mature cyst has four nuclei.
  • Nuclear chromatin and chromatoid bodies stain dark blue or black with hematoxylin.
  • With iodine stain, nuclear chromatin and karyosome appear bright yellow, while chromatoid bodies remain clear.

Life Cycle

• Only occurs in humans.
• Infective form: Mature quadrinucleate cyst.
• Mode of transmission: Ingestion of cysts through contaminated food and water.
• Excystation: Cyst wall breaks down in the ileum by trypsin, releasing the amoeba.
• Metacystic stage: The amoeba (now quadrinucleate) detaches from the cyst wall.
• Metacystic trophozoites: The amoeba undergoes division to form 8 nuclei, each surrounded by cytoplasm, resulting in smaller metacystic trophozoites.
• Ideal habitat: Submucosal tissue of the caecum and colon.
• Some trophozoites develop into precystic forms and cysts, which are excreted in feces, completing the cycle.

Pathogenesis

• Causes intestinal and extraintestinal amoebiasis.
• Incubation period: Highly variable, typically 4 days to 4 months.
• Amoebiasis severity depends on the affected organ and extent of damage.

Intestinal Amoebiasis

• Metacystic trophozoites penetrate the colon's epithelial cells, facilitated by their motility and the enzyme histolysin.
• Penetration creates small ulcers with raised edges.
• Some invasions are superficial and heal spontaneously.
• Deeper penetration results in submucosal abscesses due to amoeba multiplication and tissue lysis.
• Abscess rupture leads to ulcers, which are often multiple and primarily localized in the caecum and sigmoidorectal region.
• Amoebic ulcers appear as raised nodules with pouting edges and later discharge necrotic material with trophozoites.
• Typically flask-shaped in cross-section, with a narrow mouth and a wide, rounded base.
• Amoebae spread laterally in the submucosa, causing undermining and mucosal loss.
• Ulceration may involve the muscular and serous coats, leading to perforation, peritonitis, and scarring.
• Scarring can result in strictures, obstruction, and thickening of the gut wall.
• Amoebic granulomas (amoebomas) may mimic malignant tumors.

Clinical Features

• Incubation period: 1-4 months.
• Symptoms:
  • Prolonged latency, relapses, and intermissions.
  • Amoebic dysentery: characterized by large, foul-smelling stools with bloodstreaked mucus.
  • Erythrocytes in stools are clumped and reddish-brown.
  • Fever and toxicity are usually absent.
  • Fulminant colitis: Extensive ulceration and necrosis of the colon are present.
  • Diarrhea or vague abdominal discomfort (uncomfortable belly or growling abdomen).
  • Chronic caecal involvement mimicking appendicitis.

Extraintestinal Amoebiasis

• Occurs when the amoeba spreads beyond the intestines.
• Common forms:
  • Hepatic amoebiasis (liver abscess)
  • Pulmonary amoebiasis
  • Metastatic amoebiasis
  • Cutaneous amoebiasis
  • Genitourinary amoebiasis

Hepatic Amoebiasis

• Enlarged, tender liver without significant liver dysfunction or fever.
• Liver damage may be caused indirectly by enzymes and cytokines from inflammatory cells surrounding the amoeba.
• Amoebic liver abscesses develop in 5-10% of cases.
• Abscesses contain thick, chocolate-brown pus (anchovy sauce pus) composed of liquefied necrotic liver tissue.
• Usually solitary and located in the upper right lobe of the liver.
• Multiple abscesses can cause jaundice by pressing on the biliary tract.
• Untreated abscesses can rupture into adjacent tissues, such as the lung, pleural cavity, pericardium, peritoneal cavity, stomach, intestine, inferior vena cava, or externally through the abdomen and skin.
• Less common in women and rare in children under 10 years old.

Pulmonary Amoebiasis

• Results from a hepatobronchial fistula, leading to expectoration of chocolate-brown sputum.
• Less commonly, amoebic empyema develops.
• Symptoms: Severe pleuritic chest pain, dyspnea, and non-productive cough.

Treatment

• Luminal amoebicides:
  • Target amoebae in the intestinal lumen.
  • Include diloxanide furoate, iodoquinol, paromomycin, and tetracycline.
• Tissue amoebicides:
  • Effective for systemic infections but less effective in the intestine.
  • Examples include emetine and chloroquine.
  • Chloroquine dosage for amoebic liver abscess: 1 g for 2 days followed by 5 g daily for 3 weeks.
• Both luminal and tissue amoebicides:
  • Preferred for treating amoebic colitis and liver abscess.
  • Examples include metronidazole, tinidazole, and ornidazole.

Prophylaxis

• Similar to other fecal-oral infections.
• Prevention includes protecting food and water from contamination with human excreta.
• Detecting and treating carriers and excluding them from food handling helps control spread.
• Promoting healthy personal habits and education are essential.

This quiz covers the essential aspects of Entamoeba histolytica, a protozoan parasite responsible for amoebic dysentery. Explore its morphology, lifecycle stages, and global impact on human health. Understanding this parasite is crucial for studying infectious diseases.