Wednesday, March 29, 2017

Amoebiasis

DEFINITION

Amoebiasis is an infection of the large intestine produced by Entamoeba histolytica.

There are 7 species of amoeba that naturally parasitize the human mouth and intestine, but of these only E. histolytica causes disease. The organism may behave as a parasite (by harming the host) or as a commensal (when it does no harm to the host).

EPIDEMIOLOGY

Worldwide distribution

It is estimated that 10% of the world’s population is infected with amoebae. More prevalent in tropical areas where invasive amoebic infection is common. The presence of pathological zymodemes in tropics and poor sanitation is responsible for this state of affairs.


Note : Worldwide, amoebiasis is the 3rd most common parasitic cause of death (i.e. after malaria and schistosomiasis).

E. HISTOLYTICA

Type : Protozoa
2 forms : Trophozoite & cyst.
Best environment for growth : Anaerobic
Division : Binary

Incubation period : As short as a few days or as long as several months or even a year.

TRANSMISSION

  • MOT : Faecal-oral route. (Direct person-to-person transmission or contamination of food)
  • Water-borne transmission (unusual)
  • Homosexual transmission (strong association with oro-anal sex)

Note : Trophozoites are short-lived outside the body and do not survive in the upper GIT. Thus they are not important in the transmission of the disease. In contrast, cysts remain viable and infective for several days in feces and water.

LIFE CYCLE

The trophozoites is the parasitic form and dwells in the lumen and/or wall of the colon (esp the caecum and ascending colon). They feed on bacteria and other food residues and probably live in symbiosis with the intestinal bacteria. As they pass down the colon and the faecal material becomes drier the conditions are less favourable and the trophozoites protect themselves by encysting .

Young cysts have :
  • A single nucleus
  • A glycogen vacuole
  • Chromatoid bodies - sausage-shaped collections of ribosomes
  • As it matures, it becomes quadrinucleate

Infection is by swallowing quadrinucleated cysts in contaminated food (and not by swallowing trophozoites!). The cysts pass through the stomach to the small intestine. In the small intestine, the cyst wall disintegrates, and trophozoites are released. The immature amebas are carried to the caecum, where they live in the lumen of the gut and mature there.

The adult amoeba (trophozoite) is highly motile by means of its pseudopodia and characteristic ‘flowing’ motion. When in an aggressive stage, it usually contains ingested RBCs.
After ingestion, cysts undergo further nuclear division.

VIRULENCE

E. histolytica infection :

Commonly without producing any lesions in the bowel --> non-invasive @ non pathogenic amoebae.
In other cases - invade the bowel and produce lesions --> invasive @ pathogenic amoebae.

Enzyme electrophoresis has shown that there are 22 zymodemes of E. histolytica distributed on a geographical basis of which only 9 are invasive. By using enzyme electrophoresis, pathogenic strains can be distinguished from non-pathogenic strains with a high degree of confidence.

Other factors affecting the ability of E. histolytica to invade the bowel and produce disease may be diet high in cholesterol and carbohydrate.

Factors that render the host more susceptible to invasion are :

  • State of the Host
  • Virulence of the Infecting Organism
  • High Carbohydrate Intake
  • Corticosteroids
  • Protein Malnutrition
  • Pregnancy
  • HIV infection and; other immunosuppressed states

PATHOGENESIS AND PATHOLOGY

When E. histolytica invades the tissues of the intestine the lesions are most often found in the caecum and ascending colon or the sigmoid. The early lesions are minute ulcers in the mucous membrane. Amebic ulceration is characteristic. A small mucosal defect overlies a larger, burrowing area of necrosis in the submucosa and muscularis --> bottle-shaped lesion @ flask-shaped lesion. The process is essentially one of necrosis with lysis of cells rather than inflammatory response. Trophozoites can be found in the depths of these ulcers. Intestinal hemorrhage and perforation can occur.

There is little acute inflammatory response (provided that 2o bacterial infection does not take place), and in contrast to the picture in bacillary dysentery, the mucosa between ulcers is normal. Most of the swelling is due to edema.

Involvement of the colonic musculature may lead to the formation of large masses of granulation tissue or amoebomas (amoebic granulomas). It is a chronic inflammatory mass. Most commonly in the caecum or rectosigmoid region. It seems highly likely that 2o infection plays an important role, because amoebae by themselves do not excite an inflammatory response. The mass often develops as a diffuse thickening of the bowel wall, closely resembling a carcinoma. 

Amoebas can enter the portal circulation and lodge in venules; liquefaction necrosis of liver tissue leads to the formation of an abscess cavity. Rarely, embolization results in lung, brain, or splenic abscess. Cysts are never found in metastatic lesions. Only hematophagous trophozoites are found in such lesions (especially in the wall ?).

Note : If a patient is excreting E. histolytica cysts or trophozoites, he has amoebiasis. Meaning to say that patient may be asymptomatic but still has amoebiasis

NATURAL HISTORY

Varied Course

The course of intestinal amoebiasis is usually self-limiting, but amoebic liver abscess is potentially fatal, unless it is diagnosed promptly and treated appropriately.

The results of infection are varied :

1. Symptomless cyst passer
2. Cyst passer with intestinal disturbance
3. Amoebic dysentery (@Frank amoebic colitis)
4. Mild chronic amoebiasis with or without disturbance in the function of the colon.

Presentation of amoebic colitis :

Systemic manifestations - headache, nausea & anorexia
Gradual onset with mild intermittent diarrhea and abdominal discomfort, usually progressing to bloody diarrhea with mucus.

Tenderness over cecum (stimulating appendicitis) or over transverse colon (stimulating peptic ulcer) or more commonly the sigmoid colon. High fever, tenesmus and colic are rare.

Amoebic liver abscess + hepatitis :

  • High-swinging fever + sweats
  • Right hypochondrial pain
  • Tender hepatomegaly
  • Leucocytosis

The stretching of the liver capsule produced by the abscess is presumably the main source of pain.

IMMUNITY

There is no evidence that one attack of amoebic dysentery protects against subsequent attacks.

Normal commensal E. histolytica does not make parenteral contact with the host and therefore does not provoke the formation of antibodies. But invasive E. histolytica can provoke the formation of persisting antibodies, though these are not obviously protective.


COMPLICATIONS

Death may result from

1. Exhaustion
2. Hemorrhage
3. Perforation (commonest cause of death)
4. Liver abscess

Others

1. Amoeboma - Occurs in 10% of pts. and may bleed, cause obstruction or intussusception. There is abdominal pain and constipation. Sometimes fever.
2. Intussusception - usually caecocolic. Pain is severe with a sausage-shaped mass in the course of the colon and an empty right iliac fossa
3. Stricture - of the colon. Rectal stricture, though rare, can follow acute amoebic dysentery or even chronic infection in which dysentery is not prominent.
4. Post-dysenteric ulcerative colitis - may follow a severe attack of amoebic colitis which has been treated and although the colon remains damaged amoeba are absent. The mucosa appears red and edematous with superficial erosions but no ulceration.

Entamoeba Histolytica

A - Amoeboma, Abscess (liver)
H - Hemorrhage and perforation
I - Intussuception
S - Stricture

DIAGNOSIS


1. Stool FEME @ sigmoidoscopy

Direct examination for amoebic trophozoites and cyst. If the stools are formed, the search is for cysts, not for amoebae. 3 -ve samples can safely exclude the diagnosis.


2. Serology

Fluorescent antibody titre (FAT)
+ve in 75% of pts. with active colitis
+ve in ≈90% of pts. with liver abscess
Seropositive is low in asymptomatic cyst passers.

If liver abscess

LFT - Increasing ALP serum
Hepatic Ultrasound - Confirm Abscess

TREATMENT

1. Drug

Metronidazole@ Tinidazole
Diloxanide furoate

Acute Amoebic Dysentery

Give metronidazole 800mg/8h PO for 5 days followed by diloxanide furoate 500mg/8h PO for 10 days to destroy any gut cysts.


AMOEBIC INFECTION OF THE LIVER (AMOEBIC HEPATITIS, AMOEBIC LIVER ABSCESS)

Age : 20-60
Sex : Male and Female

It is surprising that whereas the incidence of amoebic dysentery is qually distributed between the sexes, liver abscesses are far more common in men. The commonest metastatic complication of amoebiasis is hepatic amoebiasis or liver abscess.

PATHOGENESIS

The trophozoites reach the portal system via the portal veins from the bowel. They enter the liver, usually in the upper and posterior portion of the right lobe. The pathological process is one of necrosis by lysis at the centre of the lobules. These necrotic patches liquefy and coalesce, forming the characteristic ragged abscess cavities full of viscid, chocolate-brown (anchovy sauce) thick pus (Pus + broken-down liver cells, leukocytes & RBCs). Trophozoites of E. histolytica can often be found in the pus after drainage of the abscess. Cysts are never found. In about half the cases the pus contains staphylococci, streptococci and E.coli. In the remainder the pus is sterile.

As the abscess develops the liver enlarges.

Single (65-75%) and multiple (25-35%)
Right lobe and left lobe (4:1)

CLINICAL FEATURES
 
The condition usually develops soon after an attack of amoebic dysentery. Less frequently its appearance is delayed, sometimes for many months. Occasionally, an amoebic abscess develops in a carrier who has not had overt dysentery.

  • Early symptoms - Anemia, loss of weight, an earthy complexion
  • Pyrexia - rising to 38o C or more at night, with profuse sweating. Rigors especially in the early stages.
  • Pain - constantly present in the liver area, and is occasionally referred to the right shoulder.
  • Tenderness and rigidity - in acute cases are comparable to that of acute cholecystitis. In chronic cases tenderness may be absent.
  • Hepatomegaly
  • Basal lung signs - on the corresponding side and dullness to percussion

COURSE

Liver abscess may :

1. Heal following adequate chemotherapy
In the early stages, resolution may occur under metronidazole treatment
2. Increase in size
3. Become encapsulated and remain dormant for long periods
4. Rupture
Unrecognized and untreated abscess may burst into the peritoneal cavity. Exceptionally, the abscess bursts through the diaphragm or points subcutaneously. Erosion into the lung and the expectoration of a quantity of chocolate-coloured sputum sometimes results in a natural cure.
5. Disseminate

Note: Bacterial infection is a rather frequent and serious complication of amoebic abscess.

INVESTIGATION

U/S and CT scan - will localize the abscess
LFT - Increasing ALP
Serological test - +ve in ≈ 90% of patients with liver abscess

TREATMENT

Metronidazole 800mg tds for 7-10 days
Needle aspiration
Not necessary unless:
Patient very toxic
Very large abscess
Lack of response to metronidazole treatment after 5 days
Small abscesses usually respond to drugs.
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