Parasitosis y síndrome de intestino irritable / Parasitosis and irritable bowel syndrome

El síndrome de intestino irritable (SII) es un trastorno funcional digestivo de etiología multifactorial. En su fisiopatología se describen diversos factores, tanto biológicos, como psicológicos y ambientales, que afectan el estado de activación de células inmunes en la mucosa intestinal. Entre los factores ambientales se incluye la presencia de alguna parasitosis intestinal. El síndrome de intestino irritable post-infeccioso (SII-PI) es reconocido como un subgrupo de estos trastornos, cuya aparición de los síntomas es posterior a una infección intestinal provocada por agentes microbianos. A pesar de que en Chile hay pocos estudios respecto a la relación entre SII y parasitosis intestinal, se ha descrito la existencia de una asociación positiva entre SII e infecciones por Blastocistis hominis, uno de los parásitos prevalentes en Chile. En otros países, se ha descrito además una relación entre SII, amebiasis y giardiasis. Por la alta prevalencia de parasitosis en nuestro país, existe la necesidad de ampliar los estudios para clarificar la fuerza de la asociación entre parasitosis y SII.

Irritable bowel syndrome (IBS) is a functional disorder of the gastrointestinal tract characterised by multi-factorial aetiology. In IBS physiopathology are involved diverse factors between them biological, psychosocial, and environmental components which affect the immune activation status of gut mucosa. Among these factors is recognized the intestinal parasitosis. Post-infection IBS (PI-IBS) is recognised as a subgroup of functional disorders whose symptoms onset appear after a symptomatic intestinal infection caused by microbial agents. There are few studies regarding of relationship between IBS and intestinal parasitosis in Chile. However, is has been well described a positive association between IBS and Blastocystis hominis infections, one of prevalent parasites in Chile. In other countries, is also described a relationship between IBS and amebiasis and giardiasis. Both, characterized by a common mode of transmission through water as well as contaminated food. Because the high prevalence of parasitosis in our country it is necessary to expand the association studies to clarify the strength of the parasites ethiology in IBS.

Perfuração do colo por colite amebiana invasiva durante terapia anti-TNF para espondiloartrite / Colonic perforation due to invasive amebic colitis during anti-TNF therapy for spondyloarthritis

O bloqueio do TNF tem tido sucesso no tratamento de algumas doenças reumáticas, como a espondiloartrite. Relatam-se muitas complicações infecciosas com a terapia anti-TNF, principalmente infecções bacterianas, micobacterianas, virais e fúngicas. A Entamoeba histolytica é um protozoário extracelular que causa principalmente colite e abscesso hepático, sendo que a perfuração intestinal é uma complicação rara, com alta mortalidade. O TNF é considerado o principal mediador da imunidade celular contra a amebíase. Inicialmente, é quimiotático para a E. histolytica, potencializando sua adesão ao enterócito por meio da lectina galactose-inibível, e depois ativando os macrófagos para matarem a ameba pela liberação de NO; assim, o bloqueio do TNF poderia ser prejudicial, aumentando a virulência amebiana. Descreve-se o caso de uma mulher de 46 anos com espondiloartrite que apresentou uma perfuração do colo por colite amebiana invasiva durante uso de anti-TNF.

TNF blockade has been successful in the treatment of some rheumatic diseases such as spondyloarthritis. Many infectious complications have been reported with anti-TNF therapy, mainly bacterial, mycobacterial, viral and fungal infections. Entamoeba histolytica is an extracellular protozoan parasite that mainly causes colitis and hepatic abscess; bowel perforation is an uncommon complication with high mortality. TNF is considered the principal mediator of cell immunity against amebiasis. Initially, it is chemotactic to E. histolytica, enhancing its adherence to enterocyte via galactose inhibitable lectin, and then activating macrophages to kill ameba though the release of NO, so that TNF blocking could be harmful, increasing amebic virulence. We describe the case of a 46-year-old woman with spondyloarthritis who presented a colonic perforation due to invasive amebic colitis during anti-TNF use.

Brain abscess due to Entamoeba histolytica.

A patient of cerebral amoebiasis due to Entamoeba histolytica with no evidence of disease elsewhere is described. He made a complete recovery after surgical excision of the abscess along with metronidazole therapy.

Diagnostic dilemma in coinfection.

A Fifteen years girl belonging to a low socioeconomic status was admitted with peritonsillar abscess caused by methicillin resistant Staphylococcus aureus (MRSA), high fever, diarrhoea and septicaemic shock. Initial blood cultures and widal test, stool cultures and routine stool examination were non-contributory to the diagnosis. A bone marrow culture in the second week confirmed the diagnosis of Salmonella typhi infection. Examination of a fresh stool sample showed cysts of Entamoeba histolytica. She was treated with ciprofloxacin, metronidazole, augmentin and ceftriaxone. She had no clinical evidence of immunosuppression prior to this episode and her HIV test was negative. This case report highlights the presence of community acquired MRSA infection causing perititonsillar abscess, and the diagnostic dilemma of fever and diarrhoea due to coinfection with Salmonella typhi and Entamobea histolytica.

Does Entamoeba histolytica cause irritable bowel syndrome?

BACKGROUND: Symptoms of patients with irritable bowel syndrome (IBS) closely mimic those of patients with non-dysenteric amebic colitis. AIM: To examine the clinical relevance of presence and types of Entamoeba histolytica in stools of patients with IBS. METHODS: IBS was diagnosed by Manning's criteria. Stool examination was done 4-weekly for 48 weeks to detect E. histolytica cysts or trophozoites. Patients underwent initial sigmoidoscopy. Sera of 22 IBS patients, 23 asymptomatic cyst passers and 36 healthy volunteers whose stools were also examined were tested for presence of antiamebic antibodies. Stools were cultured for amebae; positive cultures were subjected to polyacrylamide-gel electrophoresis (PAGE) using hexokinase (HK) isoenzyme to distinguish between pathogenic (fast-moving band) E. histolytica infection and nonpathogenic (slow band) species of Entamoeba dispar. RESULTS: E. histolytica cultured from stool samples of four IBS patients had slow-moving band of HK on PAGE. All patients spontaneously eradicated the infection during the next eight to 24 weeks; all had negative serology for antiamebic antibodies, and normal rectal mucosa on sigmoidoscopy. No change in symptom score occurred on follow up in IBS patients, although all of them cleared the infection. Three additional E. histolytica isolates from IBS patients obtained from another laboratory also showed nonpathogenic isoenzyme pattern. CONCLUSION: Bowel symptoms in IBS patients were not related to E. histolytica infection. The term non-dysenteric amebic colitis thus appears to be inappropriate, since it may be used erroneously for patients with IBS with nonpathogenic ameba, leading to injudicious treatment with antiamebic drugs.