AMEBIASIS INTESTINAL Y EXTRAINTESTINAL PDF

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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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Amebiasis, due to the pathogenic parasite Entamoeba histolytica, is a leading cause of diarrhea globally. Largely an infection of impoverished communities in developing countries, amebiasis has emerged as an amebiwsis infection among returning travelers, immigrants, and men who have sex with men residing in developed countries.

Severe cases can be associated with high case fatality. Polymerase chain reaction—based diagnosis is increasingly available but remains underutilized. Nitroimidazoles are currently recommended for treatment, but new drug development to treat parasitic agents is a high priority.

Diagnóstico de amebiasis intestinal y extraintestinal

Amebiasis should be considered before corticosteroid therapy to decrease complications. There is no effective vaccine, so prevention focuses on sanitation and access to clean water. Further understanding of parasite biology and pathogenesis will advance future targeted therapeutic and preventative strategies.

Amebiasis is caused by infection with the pseudopod-forming, nonflagellated protozoan parasite Entamoeba histolytica. Amebiasis can be asymptomatic or can lead to the development of severe infection with amebic colitis and amebic liver abscess. The significance of amebiasis is exemplified in several ways. Even in low-incidence settings, these properties of the parasite lead to outbreaks among military and general populations [ 5—7 ].

Advances in molecular diagnostic methodologies have improved our understanding and led to the recognition and separation of E. Of the many Entamoeba species that infect humans, 3 species are morphologically indistinguishable from E.

Of these 3, E. Earlier descriptions of amebiasis relying solely on microscopy may have been obscured by these nonpathogenic strains. There is no vaccine to prevent amebiasis. Nitroimidazoles are the mainstay treatment for invasive amebiasis.

Given the toxicity that can be associated with this class and potential concerns for development of resistance, as has already been reported for some anaerobic pathogens, new therapies are needed [ 10 ]. For these reasons, improved understanding of amebiasis pathogenesis is needed as a way forward toward enhanced treatment and prevention. This report reviews recent literature expanding our knowledge of the epidemiology, clinical presentation, and management of amebiasis, while providing important new insights into diagnostic evaluation and prevention.

The global significance of amebiasis is widespread, with the highest burden of amebiasis borne by those residing in developing countries, particularly the tropics and subtropics, where there is inadequate hygiene and access to sanitation.

Millions of people are infected with E. In the United States, the incidence of amebiasis is low, though amebiasis-related deaths still routinely occur, accounting for at least 5 deaths per year [ 11 ]. Amebiasis in the United States is seen mostly in returning travelers or immigrants from endemic countries [ 12 ]. Data from the GeoSentinel Surveillance Network, a large international surveillance and monitoring system, have shown that E.

Amebiasis accounts for Travelers to South Asia, the Middle East, and South America appear to have the highest risk, in particular those volunteering as missionary workers or doing other volunteering work.

Amoebiasis

Even travel of household or sexual contacts to an endemic area may pose a extaintestinal of infection [ 13 ]. Other industrialized countries including parts of Asia, Europe, North America, and Australia have highlighted gay men, bisexual men, and other men who have sex with men MSM as a population at higher risk of acquiring amebiasis than the general population.

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In developing countries, the exact burden of amebiasis is difficult to quantify, and reports can be affected by geographic region, study design, sample size, incubation, symptom severity, and the sensitivity of the diagnostic modality used Table 1. In addition, diagnostic capacities and surveillance are extraintestinla limited in areas where E.

Recent reports, however, have shown that the seroprevalence of E. By cross-sectional survey, E. A re-emergence of E. Using fecal antigen detection, E. The epidemiology on the incidence and prevalence of amebiasis in Africa is particularly limited, but it appears widespread, as exemplified in a cross-sectional study of patients attending gastroenterology clinics in South Africa, where E.

The life cycle of E. Transmission occurs after the ingestion of the infectious cyst.

This most commonly arises from fecally contaminated hands, food, or water, but there is a new appreciation that exposure to fecal matter may occur during sexual contact, in particular among MSM groups [ 24 ]. Following ingestion, excystation to trophozoites occurs, and the released trophozoites migrate to the large intestine, multiplying by binary fission to produce more cysts.

The trophozoite may invade the intestinal epithelium and even pass to extra-intestinal sites extrainttestinal as the liver via hepatic portal circulation or disseminate further to distant sites such as the brain and lungs hematogenously. Symptoms may occur within weeks after ingestion but may also develop years after infection.

Entamoeba histolytica in stool and pathological features of intestinal amebiasis. A, Cyst of E. Note the chromatoid body with blunt ends red arrow.

B, Trophozoite of E. The ingested erythrocytes appear as dark inclusions red arrow. The parasite shows nuclei that have the typical small, extrraintestinal located karyosome and thin, uniform peripheral chromatin.

C, Intestinal tissue from a patient with amebic colitis showing multiple ulcers. D, Classic flask-shaped ulcer of amebiasis courtesy of the Centers for Disease Control and Prevention. Cysts and trophozoites are passed in stools. Several properties of the cyst help it to remain hardy in the environment for weeks, whereas trophozoites do not survive. For example, cysts are resistant to gastric acidity and are also relatively resistant to chlorine.

The low infectious dose and environmental stability can predispose to the development of outbreaks [ 56 ]. Cysts can be killed by boiling. Contact with host cells is required for parasite-induced death. Trophozoites are able to kill host cells by several different mechanisms, which include inducing programmed cell death, phagocytosis, and trogocytosis [ 25 ]. The intestinal epithelium is the point of first contact for E.

Before cell adherence, trophozoites secrete immune modulators that stimulate epithelial cells, resulting in cytokine production and subsequent mucosal inflammatory cell infiltration [ 2627 ]. A positive correlation was recently found between Eh MIF levels and intestinal inflammation in persons with amebic colitis [ 28 ]. MMPs break down the extracellular matrix in the gut to promote cell migration and are overexpressed in all infections with protozoan parasites, including amebiasis [ 2930 ].

In a recent study, MMPs were shown to be necessary for E.

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It appears that Eh MIF is a parasite virulence factor that triggers inflammation, resulting in increased expression of MMPs, which promotes invasion of the host. Various host immune mechanisms are elicited in response to amebiasis extrainteetinal an attempt to clear or prevent infection. Infected children develop antibodies against Eh MIF, which are associated with protection from reinfection [ 2833 ].

Although the immune response is normally protective, it can also produce extraintestinall effects when the response is excessive. Another cytokine produced during infection is interleukin-8 IL-8a potent neutrophil chemoattractant. In response to IL-8, neutrophils infiltrate the intestinal tract as the first cells zmebiasis an innate immune response to amebic invasion [ 2730 ].

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Patients with severe amebic colitis have higher colonic tissue levels of IL-8 and neutrophils, suggesting that neutrophils might be responsible for collateral tissue damage during inflammation at the site of invasion [ amebiassis ]. The majority of E. The reasons for this are poorly understood but result from an interplay of several factors related to parasite, host, and environment. Recently, it was found that the gut microbiome is enriched in Prevotella copri in people with amebic diarrhea, indicating that dysbiosis may in part contribute to susceptibility to the development of colitis [ 22 ].

Asymptomatic wxtraintestinal is referred to as luminal amebiasis. A gender difference in amebiasis is not seen in children, but interestingly, in the adult population, inyestinal disease is more common in males than females, particularly for amebic liver abscess [ 12 ].

Symptomatic intestinal infection can have a wide spectrum of manifestations Table 2. Presentation may be acute or more gradual, and amebic colitis may also present similarly to inflammatory bowel disease IBD. It may not be possible to distinguish amebic colitis from IBD even by imaging, inflammatory markers, or endoscopy, and the colon may appear friable, with diffuse ulceration by gross examination Figure 1 [ 4 ]. Disease may be limited to kntestinal ascending colon or cecum.

Life-threatening manifestations of amebic colitis include fulminant infection, which can result in massive areas of colonic involvement with perforation and peritonitis, bowel necrosis, or toxic megacolon [ 4 ].

Corticosteroid use has been described as a risk factor for the development of fulminant forms of amebic colitis [ 4 ].

Patients may be toxic in appearance, extraimtestinal, and hypotensive, with profuse bloody diarrhea, abdominal pain, distension, and signs of peritonism.

Amebic colitis may also present as acute appendicitis Figure 2. The only distinguishing feature was a higher median neutrophil count in those with amebic infection compared with those without in this series [ 38 ].

Ameboma, the development of tumor-like granulation tissue in the colonic lumen, can mimic colonic cancer. The differential diagnosis of amebic colitis includes bacterial enteric infection, such as Salmonella spp.

The aid of stool PCR and culture can help to kntestinal several of these differentials. Immunohistochemical staining of trophozoites brown using specific anti— Entamoeba histolytica macrophage migration inhibitory factor antibodies in a patient with amebic appendicitis. Amebic liver abscess, which is the most common extra-intestinal manifestation, develops when trophozoites disseminate to the liver.

Extraibtestinal poorly understood reasons, amebic liver abscesses are 10 times more common in men than women, often presenting between the ages ihtestinal 20 and 40 years. Onset can be acute, subacute, or subtle. Hepatic amebiasis has been reported over 20 years after the last visit to an endemic area, so any travel history may be important in this diagnosis.

The majority will present with fever and right upper quadrant pain, typically without concurrent dysentery extriantestinal gastrointestinal symptoms Table 2 [ 12 ]. Hepatomegaly with point tenderness over the liver can often be detected. Cough and respiratory symptoms, including pleuritic right-sided chest pain, may occur, or even referred pain to the shoulder. Imaging more often reveals right lobe lesions, usually solitary, but left lobe or multiple lesions may extraintestinao less commonly seen Table 2 [ 12 ].

Amebic liver abscess may be difficult to clinically distinguish from pyogenic liver abscess. Echinococcal cysts of the liver are another important differential, but they tend to appear as multiple clustered fluid collections without surrounding enhancement on imaging. Peripheral eosinophilia is rare with amebic liver abscess and is more commonly associated with echinococcosis and hepatic fascioliasis liver fluke.

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