Life cycle and pathogenesis The cycle of E histolytica is shown in Fig 910

■ Symptomatic intestinal amebosis. Following peroral ingestion of a mature E. histolytica cyst, the tetranuclear ameba is released, divides to produce four or eight uninucleate trophozoites, which then continue to multiply and encyst (Fig. 9.10). The trophozoites colonize the large intestine mucosa or lumen. Their potential for invading and destroying tissue is high and is based on the following characteristics and processes: adhesion of trophozoites to intestinal cells by means of surface lectins, killing of cells with pore-forming peptides (amebapore, types A-C) and dissolution of the extracellular matrix by cysteine proteases. This enables the amebas to penetrate into the intestinal wall, where they multiply and cause pathological changes (necrotic foci, ulcers, inflammatory reactions) (see below).

■ Asymptomatic intestinal amebosis. This condition is usually caused by E. dispar, less frequently by E. histolytica. Characterizing E. dispar as "apathogenic" is not entirely accurate, since these organisms can cause slight intest-

Fig. 9.10 1 Cyst of E. histolytica, following peroral ingestion, in stomach; 2 ameba emerging from a cyst; 3 dividing stage of ameba; 4 uninucleate trophozoites result from division; 4a invasive stage with phagocytosed erythrocytes, extraintestinal; 4b lesions in the intestinal wall; 5 the amebas encyst; 6 cysts excreted with feces and different transmission routes; 7 peroral ingestion of cysts. ►

— Entamoeba histolytica: Life Cycle

Histolytica
9

inal lesions in experimental animals. E. dispar adheres to host cells in very much the same way as E. histolytica, but it produces only very small amounts of amebapore A and B and none of the particularly potent type C at all. E. dispar is lacking several genes that code for certain cysteine proteases. Also, the activity of certain proteases in E. dispar is greatly reduced compared to E. histolytica.

■ Extraintestinal amebosis. E. histolytica can disseminate to other organs from the intestinal wall, most particularly to the liver (Fig. 9.10). As a result of the destruction of parenchymal cells, small necrotic foci, so-called abscesses, form and gradually become larger and can even affect major portions of the organ. Bacteria are involved in only about 5 % of cases, so that the inflammatory reactions at the edges of the foci are usually mild. The decomposing lesion contains a brownish or yellowish, puslike liquid, in most cases bacte-riologically sterile, later becoming a necrotic mass; amebas are often only detectable in the transition zone between the lesion and intact hepatic tissue. Liver abscesses sometimes perforate into the pleural space or lung; less often a hematogenous dissemination of amebas results in an invasion of the spleen, brain, and other organs. Cutaneous amebosis most frequently occurs in the perianal area, associated with rectal changes.

Epidemiology. Humans are the reservoirs for E. histolytica (rarely also: monkeys, dogs, cats). The infection is due to transmission of mature cysts with contaminated foods (fruit, vegetables), drinking water or fecally contaminated hands. Flies and cockroaches can function as intermediaries by carrying cysts from the feces of an excretor to foods. In contrast to the vegetative forms, the cysts are quite resistant in a moist environment (i.e., they survive at 28-34 °C for about eight days, at 10 °C for about one month); under conditions of desiccation and temperatures exceeding 55 °C they are quickly killed. The amounts of chlorine normally added to drinking water are insufficient to kill the cysts. Monkeys have been shown to be hosts of E. histolytica and E. dispar.

Clinical manifestations. Clinical symptoms can develop as early as two to four weeks after infection with E. histolytica or after asymptomatic periods of months or even years.

■ Intestinal forms

— Asymptomatic intestinal form. E. histolytica can colonize the intestinal mucosa, reproduce, and persist for long periods without becoming invasive or causing any changes. The apathogenic E. dispar is more frequent than E. histolytica, so that most asymptomatic infections are probably caused by the former. Trophozoites, and more frequently cysts, of the E. histolytica/E. dispar type are excreted, antibodies to E. histolytica antigens are usually not found in serum.

— The invasive intestinal form results from the invasion of the intestinal wall by the pathogenic E. histolytica and reflects large intestine disease. The intestinal parts affected (colon, cecum, rectum, sometimes terminal ileum) show either circumscribed or more expanded lesions of varying intensity, ranging from edematous swelling and reddening to pinhead-sized foci with central necrosis or larger, bottle-shaped ulcers extending deep into the intestinal wall with swollen edges and large decomposing foci. The ulcers sometimes perforate into the peritoneal cavity. Healing processes with scar formation may reduce the intestinal lumen; pronounced inflammatory processes can lead to a tumorlike thickening of the intestinal wall (ameboma). The acute disease usually begins with abdominal discomfort and episodes of diarrhea of varying duration, at first mushy then increasing mucoid, including blood-tinged, so-called "red currant jelly stools" in which amebas can be detected, including trophozoites containing erythrocytes. In such cases, antibodies are usually present in serum. The symptoms may abate spontaneously, but fairly often a recidivat-ing chronic colitis develops that can last for months or even years.

■ Extraintestinal forms

— Extraintestinal forms develop because of hematogenous dissemination of E. histolytica originating in the intestine. The most frequent form is the so-called "liver abscess," which may develop in some infected persons. Only about 10% of patients with liver abscesses are also suffering from amebic colitis; coproscopic methods often do not reveal amebas in stool. The liver abscess causes remittent fever (sometimes high), upper abdominal pain, liver enlargement, elevation of the diaphragm, general weakness, and other symptoms. Large liver abscesses that are not treated in time are often lethal. Antibodies are detectable in most cases (around 95%) (see also Diagnosis). Other forms of extraintestinal amebosis are much rarer and include involvement of the lungs, brain, and skin.

Immunity. Reinfections are possible since sufficient immunity is not conferred in the course of an infection. Antibodies are usually detectable in serum in invasive intestinal and extraintestinal amebosis caused by E. histolytica.

Diagnosis

■ Intestinal amebosis

— Coproscopic diagnosis. For diagnosis of intestinal amebosis a body-warm stool specimen must be fixed without delay in SAF solution and examined microscopically following laboratory processing (p. 621). A single stool analysis has a statistical sensitivity of only 50-60%, but this can be raised to 95% by examining stool specimens from three consecutive days. Since E. histolytica and E. dispar are morphologically indistinguishable, a finding is classified as E. histolytica/E. dispar complex.

Differential Diagnosis of Intestinal Protozoa abc d

Differential Diagnosis of Intestinal Protozoa abc d f e

Enteromonas Hominis

Microspora spores

Blastocystis hominis

Cryptosporidium oocysts

Cyclospora oocycts

Sarcocystis Isospora belli oocyst

Sporocyst

Microspora spores

Blastocystis hominis

Cryptosporidium oocysts

Cyclospora oocycts

Sarcocystis Isospora belli oocyst

Sporocyst

Sporulated Oocyst

Sporulated Oocyst f e h k g

— Differential diagnosis. It is important to differentiate the E. histolytica/E. dispar complex from intestinal epithelia, granulocytes, macrophages, and fungi as well as from other, apathogenic, intestinal protozoa (amebas: Entamoeba coli, E. hartmanni, E. polecki, iodamoeba biitschlii, Endolimax nana; flagellates: Dientamoeba fragilis, Enteromonas hominis, Chilomastix mesnili, Pentatrichomonas hominis (Fig. 9.11). D. fragilis is classified by some authors as potentially pathogenic. Blastocystis hominis is frequently found in stool samples (Fig. 9.11h): this intestinal inhabitant is considered a fungus or a protozoon; some authors ascribe it a certain significance as causative agent of diarrhea. It is important to remember that a number of drugs reduce the excretion of intestinal protozoa.

a Giardia intestinalis (pathogenic): trophozoites: 9-21 x 5-12 im; cysts: 8-14 x 8-10 |im (see also p. 478).

b Dientamoeba fragilis (apathogenic or facultatively pathogenic): trophozoites: 5-15 im, 3/4 of stages with two nuclei, the rest with one; karyosome consisting of four to six granules; cysts: none.

c Entamoeba histolytica (pathogenic):

trophozoites: small form (1) 10-20 im, with Entamoeba nucleus and small number of vacuoles containing bacteria; larger form (2) 20-60 im, with phagocytosed erythrocytes; (3) cysts: 10-16 im, one to four nuclei. Here binuclear cyst with glycogen vacuole and cigarshaped chromidial bodies and (4) a tetranuclear cyst. Entamoeba dispar (apathogenic): morphologically identical with E. histolytica (see text).

Entamoeba hartmanni (5) (apathogenic): similar to E. histolytica, but smaller. Trophozoites and cysts approximately 3-10 im. d Entamoeba coli (apathogenic):

trophozoites: with Entamoeba nucleus, 10-50 im, in most cases numerous vacuoles containing bacteria and particles.Cysts: 15-25 im, one to eight nuclei, chromidial bodies slender, splinter-shaped. e lodamoeba bütschlii (apathogenic):

trophozoites: 6-20 im, nucleus with large karyosome, either centrally located or contiguous with the nuclear membrane.

Cysts: 5-18 im, one nucleus, rarely two.

f Endolimax nana (apathogenic):

trophozoites: 6-15 im, nucleus with karyosome.

cysts: usually oval, 8-12 im long.

g Microsporia (pathogenic):

spores: very small (!), 1-3.5 im long depending on species, oval shape; spores often not stained homogeneously by chromotropic staining according to Weber (see also Fig. 9.20c, p. 539). h Blastocystis hominis (facultatively pathogenic?): single cells: 5-20 im. i Cryptosporidium species (pathogenic): oocysts: 4-5 im (see also Fig. 9.14a, p. 516). j Cyclospora cayetanensis (pathogenic):

oocysts: 4-5 im, spherical, unsporulated in fresh stool; after sporulation two spor-

ocysts with two sporozoites each (see also Fig. 9.14a, p. 516).

k Sarcocystis species (pathogenic):

l Isospora belli (pathogenic):

— Differentiation of E. histolytica and E. dispar. A new type of PCR is now used in specialized laboratories that facilitates direct detection of these amebic species in stool specimens as well as a differential diagnosis.

— Detection of coproantigen. E. histolytica antigen can be detected in stool specimens using an ELISA based on monoclonal antibodies with high levels of sensitivity and specificity.

— Serological antibody assay. Antibodies can be detected serologically in 95-100% of patients with amebic liver abscess. This is also frequently the case in invasive intestinal amebosis caused by E. histolytica. On the other hand, antibodies are produced far less often in E. dispar infections. When stages of the E. histolytica/E. dispar complex are detected in stool, the presence or absence of serum antibodies can be used in differential diagnosis of invasive vs. noninvasive intestinal amebosis.

■ Extraintestinal amebosis. This type of amebosis is diagnosed with the help of clinical methods (ultrasound, computer tomography, etc.) and serological antibody detection (see above).

Therapy. Nitromidazole derivatives are effective against symptomatic intestinal and extraintestinal forms of amebosis. On the other hand, amebicides with only luminal activity are effective against asymptomatic intestinal amebosis (e.g., diloxanide furoate) (Table 9.5). A new drug against intestinal amebic infections is nitazoxandide. Besides chemotherapy, other measures may also be required, e.g., surgery and symptomatic treatment for liver abscesses.

Prevention. Travelers to endemic areas should decontaminate drinking water by boiling or filtering it (e.g., with Katadyn filters), not eat salads, eat only fruit they have peeled themselves and exercise caution when it comes to changing their diet. Chemoprophylactic dugs are not available.

Table 9.5 Chemotherapy in Amebosis (examples)

Group of amoebicides*

Active substance

Indication

Luminal amebicides

Diloxanide furoate

Asymptomatic cyst excreters,

Paromomycin

follow-up treatment of invasive

Nitazoxanide

intestinal form

Systemic amebicides

Nitroimidazoles:

Invasive intestinal and extrain

Metronidazole

testinal forms

Ornidazole

Tinidazole

*Application per os

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  • ana
    What is life cycle of entamoeba histolytica and its pathogenesis?
    8 years ago
  • mezan
    What is a enamoeba histolytic cyst classified as?
    8 years ago
  • falco sackville-baggins
    How much time it will take to kill E hominis cysts?
    7 years ago

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