Bloody Diarrhea
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اسهال خونی دکتر مجیذ اصغرزاده فوق تخصص بیماری های عفونی کودکان Dysentery is defined as • acute bloody diarrhea • typically with abdominal pain and fever • caused by invasive microbial infection Diarrhea Dysentery Diarrhea is presented as watery stool Dysentery is presented as a mucoid with no blood and mucus. stool that may be accompanied by blood. may or may not be accompanied by The patient usually complains of cramps or a pain. cramps and pain in the lower abdominal area Fever is less common Fever is more common affects the small bowel affects the colon Diarrheal infection is located and Dysentery not only upper epithelial targets only intestinal lumen and cells are targeted but colon ulceration upper epithelial cells also results There is no cell death in diarrhea and When a person gets dysentery, the the infection is only caused because of upper epithelial cells are attacked and the release of some toxins by the destroyed by the pathogen or disease infecting agent causing agent. Diarrhea Dysentery The antimicrobial that are used to treat Treatment for dysentery can eradicate diarrhea do not eradicate the toxin left the pathogen that is causing the behind infection and stop the inflammation. The effects of diarrhea are not that Dysentery can cause a lot of, serious apart from a risk of complications, if left untreated dehydration Diarrhea is mostly viral. E.coli can Dysentery is mostly bacterial. E coli, also cause watery diarrhea Shigella, and Salmonella are the most common causative organisms Diarrhea does not need antibiotics . Dysentery may requires antibiotic Oral rehydration solutions or treatment. Intravenous antibiotics may intravenous fluid therapy may be used be needed in severely ill children The child with bloody diarrhea is at higher risk for complications, including sepsis and other systemic diseases therefore the threshold for admission of such children to the hospital for close observation is lower may be associated with growth shortfalls in young children in developing areas The four major causes of bloody diarrhea (including both dysenteric and nondysenteric forms) in the US , in descending order of frequency of occurrence, are • Shigella • Campylobacter • nontyphoid Salmonella • STEC Other organisms may also cause dysentery, including • Aeromonas species • Vibrios(Noncholeraic) • Yersinia enterocolitica A history of antibiotic intake and/or recent admission to a health care facility strongly suggest C. diffcile. When typhoid fever is present with diarrhea in an endemic area, the diarrhea is ofen inflammatory, with many fecal PMN or mononuclear leukocytes seen on microscopic examination. A history of travel to areas of poor sanitation may implicate any of the aforementioned pathogens. venereal exposure, particularly among men who have sex with men, may implicate • gonococci • herpes simplex virus, • Chlamydia trachomatis (lymphogranuloma venereum) • Treponema pallidum as a cause of proctitis Bloody diarrhea and abdominal cramps after a 72-120 hr incubation period are associated with infections from Shigella and STEC , such as E. coli O157:H7. Organisms associated with dysentery or hemorrhagic diarrhea can also cause watery diarrhea alone without fever or that precedes a more complicated course that results in dysentery. Unusually low inoculum required for infection by organisms such as shigellae or amebas. As few as 100 shigellae or 10 cysts of enteric parasites, such as Entamoeba coli or Giardia lamblia substantial risk of person-to-person spread in daycare centers, institutions other areas where Nonhygienic conditions may allow direct fecal-oral spread. Te cysts of parasites such as Entamoeba histolytica or Balantidium coli ofen resist chlorination and therefore may cause waterborne outbreaks of dysenteric illnesses. Salt- water or seafood exposure should lead to consideration of Vibrio parahaemolyticus as a potential cause of infammatory colitis or of watery diarrhea Farm or domestic animal exposure might lead to consideration of nontyphoid Salmonella species, Campylobacter jejuni, or Yersinia enterocolitica. diarrhea contain blood fecal leukocytes in association with abdominal cramps tenesmus fever In the stool specimen Examination for fecal leukocytes ofen reveals • sheets of polymorphonuclear leukocytes • in clumps of mucus, • even in the absence of gross blood Fewer pyknotic leukocytes are reported in amebic dysentery ; this may be attributable to the • deeper undermining ulcers characteristic of amebiasis • cytolytic efect of the ameba on leukocytes. Stool cultures are indicated in the setting of acute bloody diarrhea and are helpful for guiding therapy Stool cultures should be obtained as early in the course of disease as possible from children with • bloody diarrhea in whom stool microscopy indicates fecal leukocytes, • in outbreaks with suspected HUS • in immunosuppressed children with diarrhea Te use of fresh specimens promptly plated onto appropriate enteric culture media is very important in the isolation of shigellae. Specialized techniques are required to isolate • Vibrio (thiosulfate citrate bile salts [TCBS] agar), • Yersinia (cold enrichment), • C. jejuni Te identifcation of toxigenic C. difcile is done by • immunoassay for either C. difcile toxin A or B • cell culture cytotoxicity • PCR assay for C. difcile toxin B. Leukocytosis or even a leukemoid reaction has been described in colitis caused by C. difcile may be useful in the diagnosis of a • pseudomembranous enterocolitis or in the • identifcation of parasites such as E.histolytica (with special [PAS] stain) B. coli. Amebic colitis is associated with • discrete small ulcerations with • undermined edges amid relatively normal mucosa. Acute shigellosis causes • more widespread, shallow, 3- to 7-mm ulcers • more intense infammatory exudate Barium studies are unnecessary and are relatively contraindicated for toxic patients with acute colitis. presence of biomarkers of acute or prolonged intestinal infammation, such as • Fecal myeloperoxidase • Neopterin • Fecal calprotectin Terapy consists of • careful supportive fuid management with • specifc antimicrobial therapy directed at a specifc pathogen if suspected on the basis of the • Epidemiologic setting or • Microbiologic test results. Once laboratory diagnosis is made, pathogen-specific antimicrobial therapy should be initiated for all forms of infectious colitis (Shigella, Salmonella, and Campylobacter) other than STEC. Treatment of dysentery in cases in which stool culture is not available should be targeted at Shigella. Mild symptoms are self-limited more severe cases antibiotics are recommended for cure and for preventing complications and relapse The progressive development of antibiotic resistance in Shigella isolates is not new Ampicillin and TMP-SMX, once affordable mainstays of therapy, have long ago lost efficacy in most Shigella-endemic regions Resistance to nalidixic acid, fluoroquinolones, ceftriaxone, and azithromycin and multidrug-resistant strains are also being reported in many countries. Therefore regularly updated local or regional antibiotic sensitivity patterns to different species and strains of Shigella are required to guide empiric therapy In the absence of local data, the recommendations from the WHO should be followed. First-line therapy is ciprofloxacin (in all age groups, including pediatrics) second-line therapy is pivmecillinam (where available), ceftriaxone, or azithromycin. Azithromycin has the added advantage of also treating most isolates of Campylobacter, a second major cause of dysenteric diarrhea in children younger than 2 years in developing countries The antibiotics recommended by the WHO are effective in reducing the clinical and bacteriologic signs and symptoms of dysentery and thus can be expected to decrease diarrhea mortality attributable to dysentery clinical manifestations range from • watery or loose stools • with minimal or no constitutional symptoms to • more severe symptoms, including high fever, abdominal cramps or tenderness, tenesmus, mucoid stools with or without blood Septicemia • by Shigella organisms or • by other gut flora Neonates malnourished children people with S dysenteriae serotype 1 infection but may occur in healthy children with nondysenteriae shigellosis Generalized seizures • self-limited • associated with high fever or electrolyte abnormalities Reactive arthritis HLA-B27 often causes a more severe illness than other shigellae with a higher risk of complications • septicemia • pseudomembranous colitis • toxic megacolon • Intestinal perforation • HUS rare in industrialized countries Shigella sonnei 85% Shigella flexneri 14% Shigella boydii, 1% other species less than 1% resource-limited countries outbreaks • S flexneri • S dysenteriae Shiga toxin a potent cytotoxin produced by S dysenteriae serotype 1 small number of strains • S flexneri type 2a • S dysenteriae type 4, • S sonnei HUS has not been associated with infections attributable to these serotypes Humans are the natural host fecal-oral route • via contact with a contaminated inanimate object • ingestion of contaminated food or water • sexual contact Houseflies also may be vectors 10 organisms Prolonged organism survival • water (up to 6 months) • food (up to 30 days) incubation period varies from 1 to 7 days but typically is 1 to 3 days S/E Cary-Blair media correction of fluid and electrolyte mild episodes do not require AB therapy Severe disease immunosuppressive