AMEBIASIS INTESTINAL Y EXTRAINTESTINAL PDF
Amoebiasis, also known amoebic dysentery, is an infection caused by any of the amobae of the Entamoeba group. Symptoms are most common during infection by Entamoeba histolytica. Amoebiasis can be present with no, mild, or severe symptoms. Symptoms may include abdominal pain, diarrhea, or bloody diarrhea. . can no longer be found in the feces once the disease goes extra-. Extra-intestinal amebiasis: clinical presentation in a non-endemic setting .. patogénicos complejos que le permiten invadir la mucosa intestinal y causar colitis. Although most cases of amebiasis are asymptomatic, dysentery and invasive extraintestinal disease can occur. Amebic liver abscess is the.
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In spite of a wealth of knowledge on the biochemistry and cellular and molecular biology of Entamoeba histolytica, little has been done to apply these advances to our understanding of the lesions observed in patients with intetinal amebiasis. In this review, the pathological and histological findings in acute amebic colitis are related to the molecular mechanisms of E. Infection of the human colon by E.
Although a complete picture has not ameboasis been achieved, the basic mechanisms involved in the production of focal lytic lesions include complex multifactorial processes in which lectins facilitate adhesion, proteases degrade extracellular matrix components, porins help nourish the parasite and may also kill incoming polymorphonuclear leukocytes and macrophages, and motility is used by the parasite to invade deeper layers of the colon. Nevertheless, much still needs to be unraveled to understand how this microscopic parasite has earned its well-deserved histolytic name.
Amebiasis is the infection of the human gastrointestinal tract by Entamoeba histolyticaa protozoan parasite that is capable of invading the intestinal mucosa and may spread to other organs, amebixsis the liver.
Entamoeba disparan ameba morphologically similar to Intestial. The acceptance of E.
Pathogenesis of Intestinal Amebiasis: From Molecules to Disease
Currently, there is no low-cost laboratory test available for the differentiation of E. The development of this valuable diagnostic tool for use in clinical laboratories and large-scale epidemiological studies has been made a priority 8 and is the subject of intense research 22057606396, Preliminary data obtained from the application of these methods confirm the presence of E. Of note, the prevalence rates of both species in different geographical areas is still difficult to estimate due to the small number of samples analyzed.
Invasive amebiasis due to E. In areas of endemic infection, a variety of conditions including ignorance, poverty, overcrowding, inadequate and contaminated water supplies, and poor sanitation favor direct fecal-oral transmission of amebas from one person to another. Being responsible for approximately 70 thousand deaths annually, amebiasis is the fourth leading cause of death due to a protozoan infection after malaria, Chagas’ disease, and leishmaniasis and the third cause of morbidity in this organism group after malaria and trichomoniasis, according to recent World Health Organization estimates The motile form of E.
Cysts are excreted in stools and may be ingested by a new host via contaminated food or water. The parasite excysts in the terminal ileum, with each emerging quadrinucleate trophozoite giving rise to eight uninucleated trophozoites.
Trophozoites may invade the colonic mucosa and cause dysentery and, through spreading via the bloodstream, may give rise to extraintestinal lesions, mainly liver abscesses. Depending on the affected organ, the clinical manifestations of amebiasis are intestinal or extraintestinal.
There are four clinical forms of invasive intestinal amebiasis, all of which are generally acute: Patients with dysentery have an average of three to five mucosanguineous evacuations per day, with moderate colic pain preceding discharge, and they have rectal tenesmus.
In patients with bloody diarrhea, evacuations are also few but the stools are composed of liquid fecal material stained with blood. While there is moderate colic pain, there is no rectal tenesmus. Fever and systemic manifestations are generally absent. These syndromes constitute the classic ambulatory dysentery and can easily be distinguished from that of bacterial origin, where the patient frequently complains of systemic signs and symptoms such as fever, chills, headache, malaise, anorexia, nausea, vomiting, cramping abdominal pain, and tenesmus reviewed in reference This condition, which results from the migration of trophozoites from the colon exttraintestinal the liver through the portal circulation, is 10 times more common in adults than in children and 3 times more frequent in males than in females In general, the onset is abrupt, with pain in the right hypochondrium radiating toward the t shoulder and scapular area.
The pain usually increases with deep breathing, with coughing, and while stepping on the right foot during walking. When the abscess is localized to the right lobe, symptoms include an irritative cough that is sometimes productive and a pleuritic type of chest pain. Abscesses in the upper left lobe can cause epigastric, sometimes dyspneic pain, at times spreading to the base of the neck and to one or both shoulders. The patient commonly has chills and profuse sweating in the afternoon and at night.
Other symptoms include anorexia, nausea, vomiting, diarrhea with or without bloodand dysentery. Aebiasis physical examination, the cardinal sign of amebic liver abscess is painful hepatomegaly. Digital pressure and fist percussion will often produce intense pain in the liver region. On palpation, the liver is soft and smooth, in contrast to the rough, hard, irregular character of the liver in amebiasie with cirrhosis and hepatocarcinoma. When jaundice is severe, multiple abscesses should be suspected.
Diarrhea or dysentery is seen in fewer than one-third of patients. Complications of amebic liver abscess include perforation to the pericardial space, pleura, or peritoneal cavity reviewed in reference The diagnosis of invasive intestinal amebiasis is still based on the microscopic identification of E.
Trophozoites are most likely to be found in the bloody mucus and in the yellowish exudate covering the mucosal ulcerations obtained during rectosigmoidoscopy. Diagnostic problems arise when only cysts are identified in stools of healthy or diarrheic individuals.
A commercially available laboratory test based on the identification of specific E. However, the high cost and lack of knowledge of this test have hindered its use in clinical laboratories, especially in countries where amebiasis is endemic. Until these new diagnostic tests are widely available to clinical laboratories, these samples should be reported as containing E.
The diagnosis of amebic liver abscess is sometimes difficult. In areas of endemic infection or when there is a history of travel to such amdbiasis, amebic abscess should be suspected in patients with spiking fever, weight loss, and abdominal pain in the upper right quadrant or epigastrium and in patients with tenderness in the liver area.
The presence of leukocytosis, a high alkaline phosphatase level, and an elevated right diaphragm suggest a hepatic abscess. The diagnosis is confirmed by ultrasonography or by computed tomography CT scans.
The CT scan is the most precise method for identifying hepatic abscesses, aamebiasis when they are small, and following intravenous injection of contrasting agents, it is of great value in the differential diagnosis of intestinall focal lesions of the liver The high cost of this method, however, limits its use to cases when there are doubts about the diagnosis.
Of all tests available, the Centers for Disease Control and Prevention has chosen the enzyme immunoassay exraintestinal its standard serological reference test for amebiasis. However, in areas of endemic infection, the high prevalence of antiamebic antibodies in the general extrintestinal reduces the usefulness amebixsis serological tests for diagnosis reviewed in reference The powerful lytic activity of E.
Most studies have focused on a single factor in an attempt to dissect the multiple mechanisms used by the parasite that ultimately result in tissue destruction. The aim of the present review is to provide an overview of the pathological lesions of human intestinal amebiasis and to discuss recent advances in the study of the molecular mechanisms of amebic pathogenicity.
Intestinal invasive amebiasis may be associated with a variety extraintestnial anatomical alterations such as acute ulcerative colitis, toxic megacolon, ameboma, or amebic appendicitis. Amebic ulcerative colitis is extraintestinao far the most frequent and is thus the focus of this discussion.
Typical intestinal amebic ulcers are found in the colon primarily in the cecumsigmoid colon, and rectum. Two types of ulcers, nodular and irregular, have been described. Nodular lesions appear as small 0. The necrotic center may appear depressed or hemorrhagic but more often is filled with a yellowish mucoid material Fig. When there are few ulcers, the intervening mucosal folds may appear normal. However, lesions can also cover most of the entire mucosa of the colon, with the uninvolved segments being congested and edematous.
Irregular or serpinginous ulcers 1 to 5 cm in length are usually found exrraintestinal the cecum and ascending colon. These ulcers are characteristically shallow with broad, elevated margins and are filled with fibrin.
Congestion and edema of the narrow strips of uninvolved mucosa and edematous thickening of the entire intestinal wall are frequently observed accompanying these large ulcers.
Pathogenesis of Intestinal Amebiasis: From Molecules to Disease
Both types of intestinal ulcers are often present in the same patient. In surgical specimens, extensive superficial mucosal denudation is observed reviewed in reference Intestinal specimen from a patient with acute amebic colitis.
Several nodular lesions show characteristic rounded, slightly elevated areas of the mucosa with irregular necrotic centers surrounded by extaintestinal hyperemic tissue. The necrotic centers are filled with a yellowish mucoid material, except in two ulcers, where the center is hemorrhagic.
The intervening mucosal folds have a mostly normal appearance, although one segment is congested and edematous.
CDC – DPDx – Amebiasis
The microscopic changes characteristic of amebic ulcerative colitis have been studied in human rectal biopsy specimens. Little has been added to the now classical description by Prathap and Gilman, published inwho found five types of lesions that seem to correspond to the progression of damage caused by E. In the initial stages, trophozoites produce nonspecific lesions characterized by thickening of the mucosa, due to glandular hyperplasia and stromal edema, with an intact although wavy surface epithelium.
Mild to moderate infiltration of neutrophils is observed within and around capillaries, but small collections can also be identified beneath the surface epithelium.
Lymphoid aggregates show reactive hyperplasia with numerous histiocytic cells.
intestnal Amebas are present in small numbers in the surface exudate. As the lesion progresses, there is a mucopenic depression due to loss of mucin from the surface and from glandular epithelial cells, which decrease in height from columnar to cuboidal and flattened dividing cells. A larger neutrophil infiltrate is evident, and plasma cells, eosinophils, macrophages, and lymphocytes can also be identified. Amebas may be present in large numbers on the luminal surface but are particularly abundant adjacent to the sites of epithelial lysis.
They are surrounded by a proteinaceous exudate composed mainly of fibrin, mucin, erythrocytes, and occasionally neutrophils and mononuclear cells. Invasion of the colonic and extraintesrinal mucosa by E. Depending on the extent of damage, these can be small interglandular foci of microinvasion, with little tissue necrosis and inflammatory cell response, or larger areas of superficial ulceration where amebic aggregates are separated from surviving tissue by a thin zone of necrosis and neutrophils.
Cell infiltration around invading amebas leads to rapid lysis of inflammatory cells and tissue necrosis; thus, acute inflammatory cells are seldom found in biopsy samples or in scrapings of rectal mucosal lesions Experimental intestinal amebiasis in the guinea pig. A large pseudopod is extended by the parasite during penetration to the lamina propria.
A semithin section stained with toluidine blue is shown. Scanning electron micrographs of experimental intestinal amebiasis in the guinea pig. A Trophozoites of E.
B A small interglandular region of microinvasion is observed in the early invasive lesion with superficial ulceration. C In a more advanced stage of invasion, numerous trophozoites are seen penetrating a colonic ulcer. The late invasive lesion with deep ulceration corresponds to the flask ulcer described in the classical monograph of Councilman and Lafleur The mucosal ulcer extends deep into a larger area of the submucosa, which seems to be particularly susceptible to the lytic action of the parasite, and produces abundant microhemorrhages.
This explains the finding of hematophagous amebas in stool amebiasie or in rectal scrapings, still the best indication of the amebic nature of a case of dysentery or bloody diarrhea.
A thick exudate containing acellular proteinaceous material, red blood cells, and strands t fibrin is seen on the floor of the ulcer, where groups of amebas are identified, especially in the deeper layers.
A deeply eosinophilic zone of fibrinoid necrosis separates the exudate from underlying viable submucosa. The latter is edematous, hyperemic, and heavily infiltrated inteshinal plasma cells.