Lifecycle of Entamoeba

7/31/2019 Lifecycle of Entamoeba

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Introduction

History

Life cycle of Entamoeba Histolytica

Intestinal amoebiasis

Surgical complications of IntestinalAmoebiasis


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Introduction

Amebiasis is a parasitic infestationcaused by the protozoon Entamoebahistolytica.

Amebiasis is the third leading parasiticcause of death worldwide, after malariaand schistosomiasis.

On a global basis, amebiasis affectsapproximately 50 million persons each


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Amebiasis is a Global disease, with highestincidence

in tropical and subtropical climates.

Incidence is increased in areas with higherpoverty

levels, presumably a direct reflection ofpoor


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History

1869 -the parasite was first identified infaecal specimens by Lewis.

1875 - Fedor Aleksandrovich Losch, firstdescribed amebiasis.

1886 - Kartulis proved amoebae to be thecause of intestinal and hepatic lesions inpatients with diarrhea.


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1890 William Osler reported case ofyoung man with dysentery who later diedof liver abscess.

1891- Councilman and Lafleur,distinguished between bacillary and

amebic dysentery.

1913 - Walker and Sellards described the

pathogenic role of amebae in extensive


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LIFE CYCLE

Entamoeba Histolytca occurs in threeforms :

TROPHOZOITE Stage Growing orFeeding stage

PRE CYSTIC Stage Intermediate stage

CYSTIC Stage Infective stage


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Stable Cysticform:

Ranges from

10-20 m. It has 1-4

nuclei

Containiodine-

stainableglycogenmass andchromatoid

bodies withsmooth


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Infection by Entamoeba histolyticaoccurs by

ingestion of mature cysts in fecallycontaminated

food, water, or hands.

Transmission can also occur through

fecal exposure


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INTESTINALAMOEBIASIS


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Amoebiasis is generally defined asinfestation with

Entamoeba histolytica with or without overt

clinical

symptoms.

The intestinal form affects the caecum,recto sigmoid

junction , ascending colon and transverse

colon.


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PATHOGENESIS

Trophozoites pass to the large intestineand using lectin-carbohydrate interaction,adhere to the colonic mucosa.

Invasion is mediated by direct cell killingof host epithelial cells and other immune

cells.

There is a direct amebic-cell interaction


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E. histolytica also has been found tosecrete a protein that may also contributeto host cell lysis and amebic invasion

through colonic tissue.

The cellular invasion extends to thesubmucosa, then extends laterally,

creating the classic flask-shaped


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CLINICAL FEATURES :

Asymptomatic -cyst passers 90% .

Symptomatic - 10 %.

Gradual

Acute

Fulminant


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Gradual course

Irregular bouts ofdiarrhoea,

Abdominal pain,

Weight loss,

Nausea ,Loss of appetite (amoebic

proctocolitis)


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Fulminant form

Several blood-stained,mucous stools

Severe tenesmus,High fever,

Abdominal pain,

Distended abdomen withtenderness,

Toxaemia, rapid pulse,


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DIAGNOSIS

Definitive diagnosis of amoebic infectionrests on finding amoebae in the stools orspecific antibodies in the serum.

Mucus and blood are found on digitalrectal examination. Palpation reveals

oedema and ulceration of the rectalmucosa.


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Light Microscopy of Stool

Identification of trophozoites / cysts infresh stool

Disadvantages:

Not sensitive (miss up to two thirds ofinfections)

Cannot distinguish betweenE.histolytica and E. dispar

Serology:

Anti-amoebic antibodies (IgM) 70%

sensitive for amoebiccolitis and 90%


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Colonoscopy / Sigmoidoscopy

Colonoscopypreferable

Wet preparations of material from ulcer-base can show trophozoites.

Biopsies should be taken from edge ofulcers.


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Stool antigen-detection test or PCR

Sensitive and Specific

Disadvantages:

Antigen detection test (EIA) only

available from some centers.

ELISA for detection of the galactose-

inhibitable adherence protein in serum andfeces and

Indirect hemagglutination (IHA) testsappear to be the most reliable and

sensitive serologic tests, both with


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Plain radiographs of the abdomen are

important when acute fulminatingamoebic colitis is suspected.

At an early stage there is generalizedgaseous distension of the bowel.

Later, when colonic necrosis is imminent,there is marked dilatation of the largebowel from caecum to sigmoid colon (toxicmegacolon).


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Surgical complications ofIntestinal amoebiasis:

ACUTE :

Fulminant Amoebic Colitis with Perforation Massive Haemorrhage

Toxic megacolon

CHRONIC :

Amoebomas


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Fulminant Amoebic Colitis withPerforation

Acute intestinal perforation occurs inpatients with severe enteropathy.

May have a mortality rate of up to50%.

Children less than 2 yrs at increasedrisk of perforation.


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Toxic mega colon

- Due to transmural extension of

the

inflammatory process to all coats of thecolonic wall.

- Use of loperamide in amoebiccolitis may precipitate toxic megacolon.

Massive Haemorrhage

incidence of less than1%, generally occurred in patients with

amoebic dysentery or granuloma, due to


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Amoebomas

A granulomatous thickening of thecolon resulting from lytic necrosisfollowed by secondary pyogenicinflammation, leading to fibrosis and

proliferative granulation tissue.

Lesions are firm, hard, may resemble

a carcinoma.

Increasing size can cause intestinal

obstruction.


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Amoebic Stricture

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

Perianal ulceration- Miliary rash , the edge of

confusion, and finally the formation ofulcers or abscesses, rupture and pus

discharge.

- Easily be mistaken for anorectal

cancer, basal cell carcinoma or skin


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Amoebic Appendicitis :

Clinical features are those of Acuteappendicitis,

although chronic right iliac fossa pain

may occur.

Some patients recover on anti amoebic

therapy.

Most cases undergo surgery.

A endix is inflamed , ma su urate or


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Results of surgery are poorer than usual

cases of appendicitis.

Complications are

Caecal blowout,

Fistula formation,

Amoebiasis cutis.

In endemic areas it is prudent to givemetronidazole


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TREATMENT

Metronidazole 750mg + Diloxanide furoate500mg

TID

for 10 days.

Metronidazole + Iodoquinol 650mg TID

for 21 days.

Metronidazole + Paromomycin 30 mg/kg

TID for 5 to 7 days.


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SURGERY

- indicated for toxicmegacolon, peritonitis from colonicperforation, or severe bleeding.

The optimal management for acutefulminating amoebic colitis remainscontroversial.

Most authorities agree that operation is

indicated only for patients who fail torespond after 48 h of intensive

management, unless peritonitis develops


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It is best to avoid aggressive surgery and

use minimal procedures to deal with theproblem.

If there is no obvious necrosis of thebowel, simple suture, faecal diversion, anddrainage should suffice in severely illpatients.

If necrosis is present, segmental resectionof the affected segment of bowel is

essential, followed by a double-barrelled


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EXTRA INTESTINALAMOEBIASIS

Extraintestinal disease


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Extraintestinal disease

Liver abscess

Pleuropulmonary disease

Peritonitis

Pericarditis

Brain abscess

Genitourinary


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AMOEBIC LIVER ABSCESS


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Amebic liver abscesses are the most

common

extraintestinal manifestation ofamebiasis.

The reasons for great male preponderanceare

Heavy alcohol consumption in men,

Hormonal effects in premenopausal

women,


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Liver abscess can develop within days ofan attack of amoebic dysentery or mayfollow after months or even years.

Up to 50 per cent of patients have noprevious symptoms suggestive of

intestinal amoebiasis.


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Average size of an amebic abscess is 5 to15 cm in

diameter and most occur in the right lobe.

The right-sided preponderance has beenexplained

by the right lobe receiving a majority ofsuperior


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The liver abscess is a well-circumscribedarea where the parenchyma has beenreplaced by necrotic tissue.

The abscess contains acellular fluid thatis usually dark reddish brown, classicallydescribed as anchovy sauce.


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Gross pathology of amoebicliver abscess and anchovy

sauce us


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Trophozoites are conspicuosly absent fromthe fluid of the abscess, which iscomposed of the products of necrosis of

the hepatocytes and cellular debris.

Trophozoites reside in the necrotic tissuesurrounding the abscess along withconnective tissue and inflammatory cells.


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Risk factors for amebic liver abscessinclude:

Alcoholism

Cancer

Immunosuppression

Malnutrition

Old age

Pregnancy

Recent travel to a tropical region

Steroid use


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Clinical manifestations

The clinical presentation may be 3 types :

GRADUAL

ACUTE

WITHCOMPLICATION


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Gradual, with

Abdominal pain (79 per cent),

Fever (53 per cent),

Malaise,Weight loss, and

Occasionally jaundice.

The pain is often a vague discomfort inthe

right upper quadrant, and there is point


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Acute with

Fever

Pain

Chills

Painful and tender abdominal mass.

Pain may be referred to the right shoulderand

aggravated by deep inspiration.


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Symptoms and signs of a complication:

Cardiac tamponade

Shock

Dyspnoea or

Cough result from a

complicated liver

PYOGENIC


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CLINICAL FEATURES AMEBIC ABSCESSPYOGENICABSCESS

Age (yr) 20-40 >50

Male-to-female ratio 10:1 1.5:1

Solitary vs. multiple Solitary 80%[*] Solitary 50%

Location Usually right liver Usually right liver

Travel in endemicarea

Yes No

Diabetes Uncommon ( 2%) More common( 27%)

AMEBIC PYOGENIC


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CLINICAL FEATURES ABSCESS ABSCESS

Alcohol use Common Common

aundice Uncommon Common

Elevated bilirubin Uncommon Common

Elevated alkaline

phosphatase

Common Common

Positive blood culture No Common

Positive amebic serology Yes No


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DIAGNOSIS :

Laboratory abnormalities are common in

amebic abscess.

Patients typically have a mild to moderate

leukocytosis without eosinophilia.

Anemia is common.

Mild abnormalities of LFTs, includingalbumin,


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Pl i X


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Plain X-raychest

Elevatedright dome of

thediaphragm,i.e. morethan 2.5 cm

or more thanoneintercostalspace higher

than the left


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Ultrasound

Appears as aRound,

Subcapsular,Hypoechoicareacontaining

fine echoeswhich maylayer in thedependant

portions.

CT


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CT scan

Appearancesare in theform of a

well-definedhomogeneous, hypodensearea, whose

Hounsfieldunits aregreater thana benign cyst

and less than

TREATMENT


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TREATMENT Metronidazole 750mg + Diloxanide

furoate 500mg

TID for 10 days.

Metronidazole + Iodoquinol 650mg

TID for 21 days.

Metronidazole + Paromomycin 30

mg/kg TID for 5 to 7 days.

i


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Percutaneous Drainage :

- Conservative medicalmanagement of

uncomplicated liverabscesses is safe.

- Thick viscous materialcharacteristic of

amebic abscesses isdifficult to drain

through standard

I di ti f P t


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Indications for Percutaneousdrainage are :

- Persistence of symptoms orclinical

deterioration with medicalmanagement,

- Concern of impending rupturebased on size

or location,


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S i l D i


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Surgical Drainage: Indications :

- Patients failing less invasivemanagement,

-Patients with complications ofamebic hepatic

abscess,

-Patients with large left-sidedabscesses not


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PROGNOSIS :

Factors


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The mortality rate for all patients with

amebic liverabscess is about 5%.

When an abscess ruptures, the mortalityrate is

reported to be from 6% to as high as

50%.

The average time to radiologic resolution

is


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Pulmonary Amoebiasis

-Direct primary infection (bloodcirculation)

-Secondary infection: after liveramoebiasis

On the superior surface, when the abscessextends

upward, the process reaches thedia hra m and the


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A large right amoebicempyema with raised

right diaphragm and rightlower lobe consolidation, all

due to an amoebic abscess inthe liver.

Symptoms


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Symptoms

Difficulty breathing

Rapid breathing

Chest pain:

Chest pain when taking a breath Chest pain when coughing

Pain often described as sharp


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Chest congestion

Persistent cough

Coughing up thick mucus:

Mucus may be green, brown, yellow ortan

Mucus may contain blood

Amoebic Peritonitis :


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Amoebic Peritonitis :

Amoebic peritonitis is considered to be thesecond most common complication ofamoebic liver abscess afterpleuropulmonary amoebiasis.

When an abscess ruptures suddenly thenatural restrictive factors like adhesionsand paralytic ileus do not come into playearly enough to restrict the spread of the

pus. Thus, acute generalised peritonitis


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The initial picture is similar to that of anyperitonitis

caused by perforation of a hollow viscus,

and acute

pancreatitis.

'Shock' is often considerable and theclassical signs of

' '

Pl i X f bd


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Plain X-ray of abdomen

- Elevation of right dome of

diaphragm.- Does not show air under the

diaphragm.

Diagnostic tapping in all the fourquadrants of the abdomen with a deVerres spring loaded needle should betried.

Detection of brownish pus would indicate


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Amoebic


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pericarditis:

The extension ofthe hepaticamebiasis to thepericardium

through contiguity.

Responsible for

serious syndromesthat range frommild pericarditis tocatastrophic

purulent

G it i bi i


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Genito urinary amoebiasis :

Renal Amoebiasis Rupture of liver

abscess

Haematogenousspread.

Genital amoebiasis Occur inrectovaginal fistula

Direct inoculationfrom

intestinal amoebiasis.

Cutaneousbi i


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amoebiasis : Rare complication.

Differentialdiagnosis ofperineo vulvar orpenile ulcers.

Cutaneousamebiasis mayalso occur on theabdominal wallsurrounding adraining hepaticabscess, colostomy

site, or laparotomy

Treatment:


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Treatment:

Spreading peritonitis: drugs,laparotomy, Careful peritoneal toilette,drainage of the peritoneal cavity, drainageof the abscess cavity , careful aspiration ofthe subdiaphragmatic spaces andexclusion of multiple abscesses.

Pericarditis : drugs, aspiration anddrainage.


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On head computed tomography (CT)scanning the lesion appears irregularwithout a capsule or surrounding

enhancement.

Diagnosis is made directly by examiningtissue for amebic trophozoites.

Medical therapy


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Medical therapywith

metronidazoleand surgicaldecompressionfor increased

intracranialpressure haveimproved the

outcome ofcerebral

amebiasis.

BIBILIOGRAPHY


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BIBILIOGRAPHY Text book of Medical Parasitology Jayaram

Paniker 6 th Edition.

Shackelford's Surgery of the AlimentaryTract - 6th Edition.

Maingot's Abdominal Operations 11 thEdition.

Surgical diseases in Tropical countries-suneet sood.


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Documents

Lifecycle of Entamoeba