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AMOEBIASIS. HISTORY. 2yr 10mo girl Main Complaint: 7 days of loose, bloody diarrhoea and vomiting Lethargic and doesn’t feed well Previous history: Uneventful perinatal history No previous admissions to hospital Numerous clinic visits in preceding months for diarrhoea RVD status unknown

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Presentation Transcript

History
HISTORY

  • 2yr 10mo girl

  • Main Complaint:

    • 7 days of loose, bloody diarrhoea and vomiting

    • Lethargic and doesn’t feed well

  • Previous history:

    • Uneventful perinatal history

    • No previous admissions to hospital

    • Numerous clinic visits in preceding months for diarrhoea

    • RVD status unknown

    • No TB or other infectious contacts

    • No recent travel history / No significant family history

    • DIET: Never breastfed , Feeds on a family diet that includes mainly veg protein and carbohydrates. Denies traditional medicine ingestion.


Examination
EXAMINATION

  • Growth paramoeters:

    • Weight: 11kg - 73% of expected for age

    • Length: 86cm – Below 3rd centile

    • Head Circ: 48cm – On 50th centile

    • Weight for height: Just below 3rd centile

    • Temp: 37.1 HR:135bpm RR:42/m BP:70mmHg syst

    • Distressed, ill-looking, pale, 7.5% dehydrated

    • Chest, CVS & CNS: Normal


Examination1
EXAMINATION

  • Abdomen:

    • Soft, distended abdomen with decreased bowel sounds

    • 3cm hepatomegaly – Firm, sharp edge, smooth surface non-displaced and not tender.

    • Fullness possibly a mass lesion extending from R flank across midline & tender to touch.

    • Normal hernial orifices and female genitalia

    • PR: No exterior abnormalities noted

      Irregular rectal mucosa

      Bloody, foul-smelling diarrhoea mixed with pus noted


Special investigations

FBC:

WCC: 3.12

Hb: 9.5

MCV: 80.1

Platelets: 127

Diff: Neut: 42.7%

Mono: 17.8%

Lymph: 35.7%

Eosino: 1.8%

Smear: Left shift + toxic granulation.

CRP: 337

U&E:

129 / 2.6 / 91 / 24 / 3.4 / 38

LFT:

Tbili: 13 Cbili: 1

TP: 46 Alb: 17 Glob: 29

ALP: 54 GGT: 32

ALT: 68 AST:81

Urine culture: Negative

Stool culture: Negative

Blood culture: Negative

RVD Elisa: Positive

CD4: 188 (4.62%)

TB W/Up: Negative

SPECIAL INVESTIGATIONS


Special investigations1

AXR:

Distended loops of large bowel with air fluid levels

No free air noted

Abd. Sonar:

Aperistaltic thickened loops of bowel in RFI

No mass seen

CT Abdomen:

Fluid-filled large & small bowel loops

Closely related bowel loops in RFI – bowel wall thickening

No definite mass seen

Sigmoidoscopy:

Mass seen at recto-sigmoid junction – biopsy taken

Histology:

Rectal biopsy with extensive mucosal ulceration.

Marked inflammatory cell infiltrate composed predominantly of chronic inflamm. cells and fibrin deposition

Amoebae noted and confirmed with PAS stain.

SPECIAL INVESTIGATIONS


Summary management
SUMMARY & MANAGEMENT

  • 2yr 10mo girl with

    • Immunosuppression

    • Amoebic proctitis and a chronic inflammatory mass at the recto-sigmoid junction consistent with an amoeboma.

  • Treated with oral Metronidazole

  • Optimized general condition in terms of nutrition

  • Referred for initiation of HAART



The organism
The Organism

  • 4 species of Entamoeba:

    • Nonpathogenic: E. dispar, E. coli, E. hartmanni

    • Pathogenic: E. histolytica

  • amoebiasis = A Parasitic infection caused by the protozoon Entamoeba histolytica

    • 2nd to Malaria as protozoan cause of death worldwide

  • 10% of world’s population infected – Increased prevalence in developing countries (up to 25%)

    • In SA – More common in KZN

  • Factors contributing to faecal-oral spread:

    • Poor education

    • Poverty and overcrowding

    • Unsanitary conditions

    • HIV infection


The life cycle

1. Cyst Stage

Infective stage

Survive from –4 to 40 Celcius

Size – 12mm

Quadrinucleated

Ingested by contact with fecally contaminated food

Passes through stomach, excysts in lower small bowel.

Metacystic amoeba with four cystic nuclei from each cyst

8 Small trophozoites from each metacystic amoeba

Trophozoites carried to cecum

The Life Cycle


The life cycle1

The Trophozoite Stage:

10-40 qm, fragile

Uninucleate

Erythrophagocytosis

Reside, feed and multiply by binary fission in lumen of colon

May invade – Lytic & physical mechanisms and metastasize to liver and other extra-intestinal sites

Galactose-containing molecules & receptors regulate cyst formation

Precyst – Cyst – Uninucleate to Quadrinucleate and passed in stool

The Life Cycle


The pathogenesis
The Pathogenesis

  • 10% of infected individuals develop invasive disease

  • Factors contributing to developing invasive disease:

    • Pathogenicity of infecting Entamoeba species

    • Dose of inoculum

    • Host factors: Impaired cell-mediated immunity, on steroids

    • Virulence of infecting species:

      • Presence of surface adhesion factors

      • Release of proteolytic enzymes

      • Release of cytotoxins and inflicting of cytolysis


The pathogenesis1
The Pathogenesis

  • Trophozoites adhere to colonic mucosal glycoproteins via a galactose and N-acetyl-D-galactosamine-specific lectin.

    • (Gal/GalNac) – Lectin is 260kD-surface protein consisting of a 225kD subunit and a 35kD subunit.

  • Adherence results in cell lysis (apoptosis) and PMN invasion

  • PMN’s are then lysed releasing lytic enzymes, causing more tissue destruction

  • Small foci of necrosis in the intestinal wall coalesce to form ulcers (Flask-shaped ulcers)

  • Parasites resist destruction by complement arm of immune system via Gal/GalNac mediated inhibition of the membrane attack complex

  • Cell-mediated immunity is important in clearing infection through generating Ұ-INF and TNF-α to activate macrophages and neutrophils to kill the trophozoite


The pathogenesis2

Area most commonly involved = Cecum, then Recto-sigmoid area

May invade blood vessels causing thrombosis, infarction and dissemination via portal circulation to liver and extra-intestinal sites eg. brain, pleura, pericardium and genito-urinary system.

Flask-shaped ulcers

The Pathogenesis


The clinical features
The Clinical Features

  • Many infections = Asymptomatic ‘cyst passers’

  • Symptomatic infections may have a gradual, acute or rapid, fulminant course.

  • Clinical incubation period = 4 days to several months

  • Oftengradual development of symptoms = Irregular bouts of diarrhoea, abdominal pain, weight loss, nausea, loss of appetite

    (amoebic proctocolitis)

  • Less often sudden onset of copious diarrhoea containing mucus and blood.

  • Findings may include low-grade fever, tenderness on palpation of the abdominal wall overlying involved large bowel.


The complications
The Complications

  • Complications of Intestinal amoebiasis:

    • Fulminant Amoebic Colitis with Perforation

      • May have a mortality rate of up to 50%

      • Children less than 2 yrs at increased risk of perforation

    • Massive Haemorrhage

      • Due to vasculitis of large arteries or multiple ulcers leading to small arterial leaks

    • amoebomas

      • A granulomatous thickening of the colon resulting from lytic necrosis followed by secondary pyogenic inflammation, leading to fibrosis and proliferative granulation tissue. Lesions are firm, hard, may resemble a carcinoma.

    • amoebic Stricture

      • Resulting from fibrosis of intestinal wall. Can involve rectum, anus or sigmoid.


The complications1
The Complications

  • Complications of Extra-Intestinal Amoebiasis:

    • Amoebic Liver Abcess

      • Most frequent complication of amoebiasis

      • Male:Female Ratio = 1 in Children and infants

      • In adulthood = More common in young males

      • Third to Half may have no history of diarrhoea

      • Commonly found in Right Lobe of liver

      • Presents acutely with high fever, RUQ tenderness

      • Jaundice an unusual finding

      • Have marked leucocytosis and may have XR abnormalities in 25 to 90% of patients


The complications2
The Complications

  • Complications of Extra-Intestinal amoebiasis:

    • amoebic Peritonitis

      • As a complication of a ruptured hepatic abcess

    • Pleuropulmonary amoebiasis

      • Caused by rupture of Rt. Lobe Liver abcess in 10% of patients

      • Has cough, pleuritic chest pain & dyspnoea

    • amoebic Pericarditis

      • Rare, but most serious complication in 3% of pts. with liver involvement

      • Rupture of Left Lobe liver abcess

    • Cerebral amoebiasis

      • Rare, has altered consciousness and focal neuro signs

      • CT – Irregular lesions without surrounding capsule or enhancement

    • Genito-Urinary Involvement

      • Painful genital ulcers – Punched out appearance & profuse discharge


The diagnosis
The Diagnosis

  • Light Microscopy of Stool

    • Identification of trophozoites / cysts in fresh stool

    • Disadvantages:

      • Not sensitive (miss up to two thirds of infections)

      • Cannot distinguish between E.histolytica and E. dispar

  • Serology:

    • Anti-amoebic antibodies (IgM) 70% sensitive for amoebiccolitis and 90% sensitive for amoebic liver abcess

  • Stool antigen-detection test or PCR

    • Sensitive and Specific

    • Disadvantages:

      • Antigen detection test (EIA) only available from Blacksburg VA


The diagnosis1
The Diagnosis

  • Colonoscopy / Sigmoidoscopy

    • Colonoscopy preferable

    • Wet preps of material from ulcer-base can show trophozoites

    • Biopsies should be taken from edge of ulcers

    • Recommended to evaluate for amoebic colitis even when Ulcerative Colitis considered


The diagnosis2
The Diagnosis

  • amoebic Liver Abcess:

    • Diagnosis relies on:

      • Detection of risk factors for E.histolytica infection

      • Positive Serology

      • Lesion in Liver :

        • Abdominal USS

        • Abdominal CT: Well-rounded, wall enhances

      • Aspiration may yield “anchovy-paste” material

        • More often yellow / gray-green

        • Often odourless and sterile – Highly suggestive of amoebicabcess


The management
The Management

  • Asymptomatic infections

    • Luminal agent only recommended but ?not available in SA

    • In general, not treated in endemic areas

  • Symptomatic infections

    • Oral Metronidazole for 10 days

    • Effective in eradicating amoebae in bowel lumen and wall

    • Effective in eradicating extra-intestinal disease

    • Additional luminal agent not necessary

  • E. dispar infection doesn’t require treatment


Prevention
Prevention

  • Improved sanitationandclean water supplyreducefecal-oral transmission

  • Boiling water, Washing veg with vinegar

  • Vaccination:

    • None available currently

    • Prototype subunit vaccines based on the Gal/GalNAc-lectin under study


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