Amoebiasis is an intestinal infection caused by the parasite Entamoeba histolytica. While it can affect individuals of all ages, including pediatric populations, it is more common in areas with poor sanitation and hygiene practices. In pediatrics, amoebiasis can present with a range of symptoms, which can vary from mild to severe. Some children may be asymptomatic carriers, meaning they carry the parasite without showing any signs of illness. However, when symptoms do occur, they typically include diarrhea, abdominal pain, bloating, and sometimes blood or mucus in the stool. In severe cases, the infection can lead to dysentery, with frequent, watery, and bloody stools, along with fever and dehydration. Amoebiasis is transmitted through the ingestion of food or water contaminated with fecal matter containing the parasite. This can occur through improper handwashing, consumption of contaminated food or water, or contact with contaminated surfaces. The parasite can also spread from person to person in areas with poor sanitation. Diagnosing amoebiasis in pediatric patients involves laboratory testing of stool samples to identify the presence of Entamoeba histolytica. Treatment typically involves medications to eliminate the parasite, such as metronidazole or tinidazole. In some cases, additional medications may be prescribed to alleviate symptoms and manage complications. Prevention of amoebiasis in pediatrics focuses on practicing good hygiene and ensuring the consumption of clean and safe food and water. Measures include regular handwashing, especially before eating or handling food, drinking purified or boiled water, avoiding raw or undercooked foods, and maintaining hygienic conditions in food preparation and storage. Early recognition and appropriate treatment of amoebiasis in pediatrics are important to alleviate symptoms, prevent complications, and minimize the risk of transmission to others. Parents and caregivers should seek medical attention if they suspect their child has amoebiasis or if the child develops persistent diarrhea or other concerning symptoms.

1. ENTAMOEBA HISTOLYTICA

2. ETIOLOGY
Four morphologically identical but genetically distinct species of Entamoeba
are known to infect humans.
1. Entamoeba dispar, the most prevalent species, does not cause symptomatic
disease.
2. E. moshkovskii, previously thought to be nonpathogenic, has increasingly
been shown to cause diarrhea in infants and children.
3. E. histolytica, the main pathogenic species, causes a spectrum of disease.
4. E. bangladeshi, was discovered in 2012, but more studies are needed to
ascertain its human pathogenicity.
Four other species of nonpathogenic Entamoeba are known to colonize the
human gastrointestinal tract: E. coli, E. hartmanni, E. gingivalis, and E. polecki.

4. • Cysts are resistant to harsh environmental conditions, including
chlorine concentrations commonly used in water purification, but
can be killed by heating to 55°C (131°F).
• Cysts are resistant to gastric acidity and digestive enzymes and
germinate in the small intestine to form trophozoites.

5. EPIDEMIOLOGY
• Infection with E. histolytica causes 100 million cases of symptomatic disease
and 2,000 to 17,000 deaths annually.
• Prospective studies have shown that 4–10% of individuals develop amebic
colitis and that < 1% of infected individuals develop disseminated disease,
including amebic liver abscess.
• Food or drink contaminated with Entamoeba cysts is the most common
means of infection.
• Untreated water and night soil (human feces used as fertilizer) are important
sources of infection in resourcelimited settings.
• Food handlers shedding amebic cysts play a role in spreading infection.

6. • Trophozoites, actively motile organisms colonize the lumen of the
large intestine and invade the mucosal lining.
• Host: Humans only
• Habitat: Caecum and Colon
• Reservoir: No animal reservoir.
• Infective form: Quadrinucleate cyst
• Mode of infection: Feco-oral

7. LIFE CYCLE
• Ingestion of Quadrinucleate cysts in contaminated food/water
• Excystation in small intestine.
• Trophozoites multiply by binary fission
• Invade colonic mucosa. Some tranform to Precysts.
• Then, to uninucleate cysts, to binucleate cysts, to quadrinucleate.
• These are then shed in feces.

11. PATHOGENESIS
• Trophozoites are responsible for tissue invasion and destruction.
• Amebic cysteine protease leads to degradation of the mucus layer, exposing
colonic epithelial cells.
• Amebae then attach using a galactose and N-acetyl-D-galactosamine–specific
lectin.
• This lectin also provides resistance to complement-mediated lysis and have
hemagglutinating, hemolytic, and cytolytic activity.
• Once attached to the colonic mucosa, trophozoites penetrate the epithelial
layer, destroying host cells by cytolysis and induction of apoptosis.

12. • Cytolysis is mediated by trophozoite release of amebapores (pore-forming
proteins), phospholipases, and hemolysins.
• Trogocytosis, where amebae ingest pieces of living cells and induce
intracellular calcium elevation leading to apoptosis.
• Once host cells are partially digested by amebic proteases, the degraded
material is internalized through phagocytosis.
• Early invasive amebiasis produces significant inflammation by parasite-
mediated activation of nuclear factor-κB.

13. • Once E. histolytica trophozoites invade the intestinal mucosa, the organisms
multiply and spread laterally underneath the intestinal epithelium to produce
the characteristic flask-shaped ulcers.
• E. histolytica–induced epithelial cell damage releases neutrophil
chemoattractants, and E. histolytica is able to kill neutrophils, which then
release mediators that further damage epithelial cells.

14. • The disparity between the extent of tissue destruction and the absence of a
local host inflammatory response in the presence of systemic humoral
(antibody) and cell-mediated responses may reflect both parasite mediated
apoptosis and the abilies of the trophozoite to kill not only epithelial cells but
neutrophils, monocytes, and macrophages.

15. CLINICAL MANIFESTATIONS
• Clinical presentations range from asymptomatic cyst passage to amebic
colitis, amebic dysentery, ameboma, and extraintestinal disease.
• Up to 10% of infected persons develop invasive disease within a year, and
asymptomatic carriers should be treated.
• Severe disease is more common in young children, pregnant women,
malnourished individuals, and persons taking corticosteroids, and invasive
disease is more common in men.
• Extraintestinal disease usually involves the liver, but less common
extraintestinal manifestations include amebic brain abscess,
pleuropulmonary disease, ulcerative skin, and genitourinary lesions.

16. Amebic Colitis
• Amebic colitis may occur within 2 wk of infection or may be delayed for
months. Incidence is common in children 1-5 yr of age.
• The onset is usually gradual, with colicky abdominal pains and frequent
bowel movements (6-8/day).
• Diarrhea is frequently associated with tenesmus. Generalized constitutional
symptoms and signs are characteristically absent, with fever documented in
only one third of patients.
• In dysentery, stool is heme-positive and associated with fever and result in
dehydration and electrolyte disturbances.
• Severe amebic colitis in infants and young children tends to be rapidly
progressive, with more frequent extraintestinal involvement and high
mortality rates, particularly in tropical countries.

17. Amebic Liver Abscess
• Liver abscesses occur in < 1% of infected individuals and may appear in
patients with no clear history of intestinal disease.
• May occur months to years after exposure, so obtaining a careful history is
critical.
• In children, fever with chills is the hallmark of amebic liver abscess and is
frequently associated with abdominal pain, distention, and enlargement and
tenderness of the liver.
• Changes at the base of the right lung, such as elevation of the diaphragm and
atelectasis or effusion, may also occur.

18. • Central Anchovy sause pus surrounded by degenerating hepatocytes, WBCs
and trophozoites of entamoeba.
• Most common site is Right lobe of liver.
• Slight leukocytosis, moderate anemia, high erythrocyte sedimentation rate,
and elevations of hepatic enzyme (particularly alkaline phosphatase) levels.
• Stool examination for amebae is negative in more than half of patients with
documented amebic liver abscess.
• Ultrasonography, CT, or MRI can localize and delineate the size of the abscess
cavity.

19. DIAGNOSIS
• Microscopic examination of stool samples for ova and parasite has a
sensitivity of 60%. Sensitivity can be increased to 85–95% by examining
three stools.
• formal ether stool concentration test shows charcot leyden crystals from
degenerated eosinophils.
• Phagocytosed erythrocytes (specific for E. histolytica) are seen is
pathagnomic.
• Endoscopy and biopsies of suspicious areas should be performed when stool
sample results are negative and suspicion remains high.
• Antigen detection i.e. Gal/Gal NAC Lectin specific by ELISA.

22. • Conventional and real-time multiplex PCR performed on stool is the most
sensitive and preferred method for distinguishing E. histolytica from
nonpathogenic E. dispar and E. moshkovskii.
• Serology for detecting antibodies against lectin antigen by ELISA/IHA.
• USG shows cystiv hypoechoic lesion.
• CT/MRI shows abscess with non-enhancing centre surrounded by rim of
inflammation.

23. COMPLICATIONS
• Acute necrotizing colitis,
• Amebomas, are nodular foci of proliferative inflammation that sometimes develop in
the wall of the colon.
• Toxic megacolon,
• Extraintestinal extension, or
• Local perforation and peritonitis.
• Chronic form of amebic colitis develops, often recurring over several years.
• Amebiasis should be excluded before initiating corticosteroid treatment for
inflammatory bowel disease, because this is associated with high mortality rates.
• An amebic liver abscess may rupture into the peritoneum, pleural cavity, skin, and
pericardium.

24. TREATMENT
• Invasive amebiasis is treated with a nitroimidazole such as metronidazole for
10 days or tinidazole for 5 days and then a luminal amebicide such as
paromomycin for 20 days (which is preferred) or iodoquinol. Diloxanide
furoate for 5 days can also be used in children > 2 yr of age,.
• Tinidazole has similar efficacy to metronidazole, with shorter and simpler
dosing, and is better tolerated. Adverse effects include nausea, abdominal
discomfort, and a metallic taste that disappears after completion of therapy.
• Paromomycin should not be given concurrently with metronidazole or
tinidazole, because diarrhea is a common side effect of paromomycin and
may confuse the clinical picture.

25. • Asymptomatic intestinal infection with E. histolytica should be treated,
preferably with paromomycin for 5-10 days or alternatively with either
iodoquinol or diloxanide furoate.

27. • Intestinal perforation and toxic megacolon are indications for surgery.
• In amebic liver abscess, image guided aspiration of large lesions or left lobe
abscesses may be necessary if rupture is imminent (cavity >5-10 cm) or if
the patient shows a poor clinical response 5-7 days after administration of
amebicidal drugs.

28. • Chloroquine, which concentrates in the liver, may also be a useful adjunct to
nitroimidazoles in the treatment or in cases of treatment failure or
intolerance.
• To confirm cure, stool examination should be repeated every 2 wk following
completion of therapy until clear.
• Auranofin, a gold-containing antirheumatologic drug that inhibits E.
histolytica thioredoxin reductase, has been shown to be active against amebic
trophozoites and shows promise as a broad-spectrum antiparasitic agent.
Phase one clinical trials were recently completed.

29. PROGNOSIS & PREVENTION
• Most infections evolve to either an asymptomatic carrier state or eradication.
• Extraintestinal infection carries about a 5% mortality rate.
• Proper sanitation and hygiene.
• Regular examination of food handlers and thorough investigation of diarrheal
episodes may help identify the source of infection.
• No prophylactic drug or vaccine is available.

30. THANK YOU.