The purpose of this manuscript is to provide a current overview on the Shiga Toxin / verotoxin-producing Escherichia coli (STEC) hemolytic uremic syndrome (HUS) with emphasis on the epidemiology, clinical and laboratory manifestations, pathogenesis, recommended assessment, treatment strategies and prognosis. Hemolytic uremic syndrome (HUS) is a cause of the community-acquired acute renal insufficiency in young children. The outbreak in Germany illustrated both the emerging importance of non-O157 serotypes as agents of human disease and the potential for large-scale methods of food production and distribution to result in widespread disease. Children with STEC-induced HUS typically have a prodromal illness that can rapidly develop severe and multisystem life-threatening complications. STEC infection is acquired through contaminated food or water. Thrombotic microangiopathy is the mechanism of the development of the characteristic pathologic lesion of HUS. Any patient with a recent history of diarrhea and signs of a multi-organ disorder requires a proper assessment for the possible development of HUS. Appropriate laboratory testing for both O157 and non-O157 serotypes, as well as prompt initiation of infection control procedures for confirmed or suspected cases, will facilitate follow-up investigation to identify the source of disease and will help to prevent secondary transmission. Currently, diagnostic test to predict which patients will develop HUS is not available. Supportive care and intravenous fluid replacement are the cornerstones of treatment because of the current lack of safe and specific therapeutic intervention. Culizumab and/or plasma treatment may be considered in patients with severe CNS involvement who have a poor prognosis. None of the multiple therapeutic agents including antithrombotic agents, plasma exchange and/or plasma infusion, tissue-type plasminogen activator, and oral Shiga toxin-binding agent that have been used is recommended. For most patients with uncomplicated STEC-associated gastroenteritis who are treated with supportive care, the prognosis was excellent. Public health interventions are the key to prevent STEC-associated diarrhea and HUS. Researches will improve the care of patients with different HUS types in the years to come. The identification of genetic factors associated with HUS will contribute to a better insight of the pathogenesis of HUS and will have potential therapeutic and preventive implications.

Vibrio cholerae O139 is well known as the causative agent of cholera. It is noninvasive but many reports suggested it to cause bacteremia which brings in a little controversy with the previously reported old literature especially after reported histopathological invasion pattern of Vibrio cholerae O139 and Vibrio cholerae O1 ElTor. The rabbits were processes for ileac loops inoculation of Vibrio cholerae O139 followed by biochemical and molecular analysis of the presence of Vibrio cholerae O139 in liver, gall bladder and bile. We concluded the presence of Vibrio cholerae in liver, bile and gall bladder homogenized tissue. Retrograde spreading of bacteria to the liver via the common bile duct was excluded by complete closure of the intestinal lumen distant to the duct in the intestinal lumen. However, the bacteria might traffic, probably via macrophages, to distant area in the body including the liver. Another study in future is a need to identify the lesions of Vibrio cholerae invasions within liver and gall bladder by immunohistochemistry and using GFP visibility for Vibrio cholerae passage.

The obesity epidemic is globally considered as one of the topmost health concern whose multifactorial etiology involves sedentary life style, poor dietary habit, individual's genetic peculiarity, environmental factors, adipose tissue inflammation and many more. More recently, researchers are intensively focusing on the role of gut microbiome in the manifestation and pathogenesis of obesity and associated complications. Microbiomes modulation of inflammatory responses associated to physiology of obesity implicated the involvement of the Toll-like receptors (TLRs), Short-chain fatty acids (SCFAs) response, gut fermentation mechanisms, as well as passive immune defense exerted by refining of mucous barriers in response to bacterial presence. We reviewhere the role of gut microbiota in the pathogenesis and management of obesity as it relates to metabolic inflammation. Accurate alteration of the gut microbiome appears to be a potential therapeutic intervention that may impede white adipose tissue inflammation and in the long run prevent obesity.

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