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Gastrointestinal tract infections

Gastrointestinal tract infections. Diarrhea. S tool consistency – liquid , half-liquid , mushy Abnormal stool volume >300g/ 24 h Abnormal frequency Contains pus , blood , mucus , flaked epithelium Green, grey , grey-yellow.

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Gastrointestinal tract infections

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  1. Gastrointestinaltractinfections

  2. Diarrhea • Stool consistency – liquid , half-liquid , mushy • Abnormalstoolvolume >300g/ 24 h • Abnormalfrequency • Containspus, blood, mucus , flakedepithelium • Green, grey, grey-yellow

  3. Commoncauses of acutecommunity-aquiredinfectivediarrhea Developing countries Developedcountries CHILDREN Rotavirus Adenovirus SLVs Campylobacter Shigella Salmonella Cryptosporidum VTEC ADULTS Campylobacter Salmonella NLVs Giardia Cryptosporidium VTEC CHILDREN • rotavirus • ETEC • Adenovirus • EPEC • Giardia • Shigella • EAggEC • Campylobacter • Salmonella ADULTS • ETEC • Salmonella • Shigella • NLVs • Vibrios • Cryptosporidium • giardia

  4. Infectivediarrhoeas • Major cause of morbidity and mortalityinthe developing countries, particularyamongchildren • Theresponsiblefactorsare : poorstandards of hygiene and sanitation, malnutrition, overcrowding , poormedical resources • In thedevelopedcountriesthediseaseisalsocommon but of lowmortality

  5. Infectious diarrhea features • Sudden onset • Suspected food consumption • Other people ,who where eating the same food have similar symptoms • Diarrhea accompanied by vomitting • Travels prior to onset of diarrhea

  6. Host Factors • Host species,age-ex.rotaviruses,EPEC-children ;Clostridium difficile-eldery • Personalhygiene • Gastricacidity • Physical barriers –mucus and mucosal tissue integrity. Continuous removal and renewal of gastrointestinal mucus may bind organisms and toxins and further aid in protecting the intact mucosa from enzymatic and microbial attack. • Intestinalmotility • Normalenteric flora The loss of normal flora or a shift in the balance of these organisms caused by the use of antibiotics leads to their replacement by Pseudomonas, Klebsiella, Clostridium, Candida. When these organisms take up residence they may cause serious systemic infections • Intestinalimmunity

  7. Most bacterial pathogens that are ingested never reach the intestinal tract  the normal gastric acid barrier. • Neutralization of this barrier  increase of susceptibility and the severity of bacterial and parasitic infections. • Normal gastric pH <4 >99,9% of ingested coliform bacteria are killed within 30 min. • H.pylori infections may in themselves alter gastric acidity and thereby increase host susceptibility to other enteric pathogens. • Salmonella bacteremia may develop in patients after opiates were taken to mild gastroenteritis. • The antimotility drugs abolished antibiotic effectiveness in reducing diarrhea and positive cultures and was associated with prolonged fever and shedding of Shigella • Complications of Campylobacter or Clostridium difficile were more common in patients who received antimotility agents. • These drugs also predispose to HUS after infection with EHEC .

  8. MicrobialFactors • Invasivness • Attachment • Cytotoxin • Enterotoxin • Neurotoxin

  9. Complications • Dehydratation and renalfailure • Septicaemia (Salmonella , Yersinia , Campylobacterfetus) • Toxiccolonicdilatation ( Salmonella, Campylobacter, Shigella, Clostridium difficile) • Haemolytic-ureamicsyndrome (enterohaemorrhagicE.coli O157, Shigelladysenteriae) • Reactivearthritis ( Shigella, Salmonella, Campylobacter ; particularyin HLA-B27 positiveindividuals) • Erythemanodosum (Salmonella, Campylobacter, Yersiniaenterocolitica) • Persistentdiarrhea • Hypernatremicdehydratation of infants-high serum sodium>150 mmol/l despiteoverall body deficit of sodium,becausegreaterloos of watertahnsodium

  10. Enteric disease can be produced by microbe-host interactions that alter normal intestinal physiology in one of three fundamental ways: 1)by a shift in delicate balance of bidirectional water and electrolytes fluxes in the upper small bowel by intraluminal toxins or minimally invasive organisms 2)by inflammatory of cytotoxic destruction of the ileal or colonic mucosa 3)by penetration through an intact mucosa to the reticuloendothelial system

  11. These three types can be distinguished by a quick simple examination. Mucus from a fresh stool specimen is mixed with a drop of methylene blue and examinated for the presence of fecal leucocytes. • No leukocytes are noted  suggests non-inflammatory process. Diarrhea usually arises from the upper small bowel by the action of true enterotoxin or agents such as Giardia or viruses. 2) The presence of polymorphonuclear leucocytes documents an inflammatory or invasive process that usually arises from colon or distal small bowel. Agents that cause an inflammatory colitis may require specific antimicrobial intervention as well as supportive fluid therapy

  12. 3)Caused by organisms that penetrate the intact intestinal mucosa often in the distal small bowel to multiply in the lymphatic or reticuloendothelial cells. This usually results in a febrile systemic illness with or without diarrhea The classic example is Salmonella typhi. If diarrhea is present mononuclear leukocytes may be found in the stools of these patients

  13. DISTINGUISHING FEATURES OF INFLAMMATORY AND NON-INFLAMATORY DIARHEA Inflammatory • Stolls:smallvolume,blood,pus • Pathology: inflammation of colonic and distalilealmucosa • Mucosalinflammationimpairsabsorption of fluid and possiblesecretagogueeffect on inflammatory products Shigella, Salmonella, Campylobacter E.coli O157 EIEC, Clostridium difficile Yersiniaenterocolitica E.histolitica Non-inflammatory • Largevolume,waterywithoutpus,blood • Proximal ,smallintestine • Secretory osmoticdiarrhoea. mucosalinflammationabsent Cholera, ETEC, EPEC, toxin-typefoodpoisoning, rotavirus, adenovirus, Cryptosporidia, Giardia non-inflammatoryintheearlystageswhendueto Shigella, Salmonella and Campylobacter

  14. Explorehistory for: Fever,tenesmussuggests an inflammatory protocolitis Blood-EHEC or amebiasis Seafood-Vibrio or Norwalk-like viruses Antibiotics- Clostridium difficile, salmonellosis. Travel-ETEC, Norwalk-like, rotaviruses, parasitic (Giardia, Strongloides, Entamoeba, Cryptosporidium) Outbreak- Staphyloccousaureus, Bacillus cereus, anisakiasis, Clostridium perfrigens ,Cryptosporidium, ETEC, Vibrio, Salmonella, Campyolobacter ,Shigella, EIEC.

  15. Spring and summer months Cyclospora. • Unexplained abdominal pain and fever suggesting an appendicitis-culture for Yersiniaenterocolitica should be taken. • Immunocompromised hosts- viral(CMV, Herpes simplex, coxackievirus, rotavius) , bacterial (Salmonella , MAC) and parasitic (Cryptosporidium, Isospora, Strongyloides, Entamoeba, Giardia) • Duration >10 days + weight loss- should prompt consideration giardiasis, cyclosporiasis, cryptosporidiosis.

  16. Theprinciples of oralrehydratation 1) 3,5 gNaCl + 2.5g NaHCO3 + 1.5g KCl + 20g glucose /1 liter of boiledwater 2) 3 leveltablespoons of sugar + ¾ teaspoon salt + ½ teaspoonsodiumbicarbonate 1 cup orangejuice and water to 1 liter 3) 1 levelteaspoon salt + 8 levelteaspoon of sugar per liter of water 1 cup orangejuiceortwobananas for potassium 40g cerealflour (rice,maize,wheat,potato) for glucose Caution : beforegivingthe drink tasteit and be sureitis no moresaltythantears.

  17. PERSISTING DIARRHEA AFTER AN ACUTE ONSET • Infective diarrhea >2 weeks is rare, exept in parasitic infections and tropical infantile due to EPEC and EAggEC In othercasessuspect : • Underlying inflammatory bowel disease-if stools are bloody • Postinfctive irritable bowel syndrome • Postinfectivemalabsorption (if history of travel to the tropics) • Secondary lactose malabsorption

  18. Management of acutediarrhea • Most – mild - short onlyattention to hydratation • Arrangestoolculture and faecalmicroscopyifsevere, watery, bloodyor high –risk for complications ( eldery, debiliated, immunocompromised, otherconcurentillnesses) • Antibioticsshould be avoidedinaveragecases of bacterialdiarrhea –thedurationisatbestonlymarginallyshortened ; mayencouragebacterialrestistance • Considerempiricalfluoroquinoloneifsevereinfllmatoryorhigh-risk group • ConsiderfluoroquinoloneifstoolcultureshowsSalmonella, Shigella, Campylobacterand diarrheastillpresent • Antimicrobialtherapyindicatedinfollowingcirumstances : Invasivesalmonellosis , cholera, severeyersiniosis, giardiasis, amoebiasis, traveller’sdiarrhea • Empiricaltherapyrarelyindicatedininfantilediarrhea as most is of viraletiology • Avoidantimotilitydrugs ( exept for veryshortcoursesinadulttraveller’sdiarrhea )

  19. Shigellaspp. • Salmonella spp. • Escherichia coli : EHEC,EIEC, EPEC, ETEC, EAgEC • Campylobacterjejuni • Amebicdysentery • Yersinios • Vibriosis

  20. Salmonellosis – non-typhoidSallmonellainfection • Gram-negative small bacilli • Primarily inhibit animals intestines • S.typhimurium DT 104 mayhaveemergeddue to heuse of antibioticsinanimalhusbandry; moreoftensevere and invasive • About 2000 serotypes.Only a small number account for the vast majority of human infections.Common examples are:S.eteritidis,S.typhimurium, S.virchow,S.hadar,S.heidelberg,S.indiana • The second commonest cause of bacterial diarrhea in developed countries • The incidence has increased substantially in last 3 decades Transmission : inadequately cooked contaminated food , hen’s eggs (infected via the oviduct) raw milk ; turtles

  21. Salmonellosis – non-typhoidSallmonellainfection Pathogenesis • invades lower intestinal mucosa,multiplying locally and producing inflammation and fluid secretion. • Transient bacteriemia is not uncommon • Significant invasive disease with organ involvement is commoner in infancy and old age, with immunosupresion,debility, achlorhydria . Clinical features • IP – 12-48h • May remain inapparent • Begins abruptly with nusea, vomitting, malaise ,cramp-like abdominal pains, diarrhea • Initially stools are large-volume and watery without blood but later may become blood-stained and mucoid • Diarrhea usually settles within a few days ; persistance beyond 3 weeks is rare • After recovery patients excrete salmonella for 4-6weeks , longer in exremes ages . • Chronic carriage beyond 1 year is rare <1%

  22. Salmonellosis – non-typhoidSallmonellainfectioncomplitactions • Severe diarrhea , dehydratation, real failure . Prone to occur in the eldery, the immunocompromised, persons with gastric achlorhydria. • Colitis, withseverebloodydiarrhea,may be segmentalmimickingCrohn’ disease, toxicmegacolonmaydevelop • Ileitis, pain and tendernesslocalizingovetherightiliacfossa,may be confusedwithappendicitis • Invasive salmonellosis: septicemia, typhoid-like illness without significant diarrhea ,metastaticc infections in extraintestinal sites – kidneys,spleen,heart valves,joints, lungs. • Postinfective irritable bowel syndrome • Reactive arthritis,particulary in individuals with HLA-B27 antigen

  23. Salmonellosis – non-typhoidSallmonellainfection Diagnosis : stool culture Treatment • Most cases have a short lasting , self-limiting illness and require only attention to hydratation • Patients with high risk for invasive illness ,those with severe symptoms should receive antibiotics (ciprofloxacion, ceftriaxone) • Ciprofloxacin 2 x 500mg p.o/ 5days • Xifaxan 2 x 2 tbs a 200mg / 3 days • Children – azytromycin

  24. Typhoid and parathyphoidfevers (entericfever) Epidemiology • Causative organisms S.typhi , S.parathypi A,B,C ; human pathoges • The infections are most prelevant in south and south-east Asia,the Middle East, Central and South Africa. • A low level of edemicity in south and eastern Europe (mostly paratyphoid B ) • In developed countries typhoid enteric fever is largely imported infection Transmission • Food and water contaminated with faeces and urine of patient carrier • IP- 10-21 days

  25. Typhoid and parathyphoidfevers (entericfever) Pathogenesis • The organisms penetrate the intestinal mucosa and travel to the regional glands to multiply , then enter bloodstream in a large numbers, marking the onset of fever. • The Peyer’s patches of the ileum are infected during this bacteraemia and also later through infected bile • They become inflamed and later during 2nd or3rd week of illness may ulcerate,causing haemorrhage and perforation • Liver and gall bladder are also involved • After recovery persist indefinitely in the billary and urinary tracts • After recovery , localintestinal,cellural and humoralimmunities develop and second attacks are rare.

  26. Typhoid and parathyphoidfevers (entericfever)-clinicalfeatures • Untreated typhoid fever is often a severe prolonged illness lasting for 4 weeks or more 1st week- fever , headache, malaise, constipation, unproductive cough, relative bradycardia 2nd week- continuous fever, apathy, diarrhea, abdominal distension, ‘rose spots’ (30%), splenomegaly (75%) 3rd week- continuous fever, delirium, drowsiness, gross abdominal distension, ‘pea soup’ diarrhea 4th week- gradual improvement in all symptoms.

  27. Typhoid and parathyphoidfevers (entericfever) • After recovery relapse may occur in up to 10% of cases • Mild and inapparent cases occur • Paratphoid is similar to typhoid but generally milder. Complications • Intestinal haemorrhage and perforation • Myocarditis • Neuropsychiatric: psychosis, encephalomyelitis • Cholecystitis,cholangitis, hepatitis • Pneumonia • Abscesses in spleen, bone or ovary • Chronic carrier state in 3% (less after fluoroquinolone)

  28. Typhoid and parathyphoidfevers (entericfever)Invasigations and diagnosis • White cell count in normal or leucopenic.Leucocytosis occurs when there is hemorrhage or pyogenic complication • Definitive diagnosis requires isolation from blood or bone marrow • Blood culture is positive in80% in 1st week, less common thereafter or when there is prior antibiotic use • Stool and urine cultures are often positive from 2nd week • Widal test-measurement of O and H antibodies – unreliable and often difficult to interpret n the previously immunized or infected with other Salmonella groups. Antibiotics: ciprofloxacin in adults or third-generation cephalosporin in children (ceftriaxone), chloramphenicol ,TMP/SMX

  29. Shigellainfection Epidemiology • Gram-negative shigellabacilli,strict human pathogenes • 4 sub groups :S. dysenteriae, S.flexnerii, S.boydii, S.sonnei • Occurs world wide ; the third commonest cause of bacterial diarrhea in developed countries • Developed countries –most cases S.sonnei; tropics- endemic dysentery is most commonly due to S.flexnerii • Epidemic dysentery is due to S.dysenteriae type I (Shiga bacillus ,Sd I ),mainly tropical countries Transmission: faecal-oral, waterborne, foodborne, sexually –oral-anal contacts Flies may spread infection in the tropics. • Infecting dose :10-100organisms • Overcrowding and poor personal hygiene encourage transmission • Incubation period 2-4 days

  30. ShigellainfectionPathogenesis • Entryinvade the colonic mucosa inflammationulceration and sloughing and fluid secretion • Sd I elaborates enterotoxin (Shiga toxin) which causes microangiopathy leading to HUS syndrome and thrombotic thrombocytopenic purpura Clinical features • May be inapparent or mild • Malaise,abdominaldyscomfort, watery diarrhea • S.sonnei-diarrhoea may remain watery, settles within 3-5 days • S.flexneri, S.boydii, Sd I blood and mucus appear in stools • Severe cases - classic picture of dysentery: fever, severe abdominal cramps, tenesmus,small volume stools with blood, mucus, pus. • Carriage after clinical recovery:is common but ceases by 8 weeks

  31. Shigellainfection Complications • Rare in S.sonnei • Toxic dilatation and/or perforation (S.flexneri,Sd I) • Haemolitic-uraemic syndrome Treatment • Most cases are mild ,require only adequate oral fluid intake • Severe : antibiotics –ciprofloxacin for adults, thrimetoprim for children

  32. Campylobacterinfection Epidemiology • Gram-negative bacilli • Ocurrs worldwide • The commonest cause of bacterial diarrhoeanin the developed countries • Zoonotic infection ; resorvoirs are gasrtointestinal tracts of birds (poulutry),animals,cattle,pets • Transmission : raw or unndercookedmeet,unpasterized milk or water, infected pets • Person to person is rare • IP 3-5 days Pathogenesis Invasion of lower intestines,ileum and colon,mucosal inflammation and secretion

  33. Campylobacterinfection Clinical features • May be inapparent • Fever, myalgia, abdominal pain may precede diarrhea by 1-2 days • Stools are initially large-volume , watery .May become small volume, bloody, mucoid • Vomiting common in children • Diarrhea ceases within 1 week • Low grade abdominal pain may continue for several more days • Most patients cease to execrate organisms in their faeces within 3-4 weeks Complications • Acute ileitis • Severe colitis • Guillain-Barre syndrome • Rarely : acute cholecystitis, erythemanodosum Treatment • Most cases require only correction of dehydratation • Antibiotics only if severe or prolonged diarrhea ( erythromycin, ciprofloxacin)

  34. VerotoxinproducingEscherichia coli VTEC (EHEC) Epidemiology • VTEC strains –an important cause of diarrhea in Europe and North America, and of diarrheal hemolytic –uremic syndrome (HUS) • VTEC O 157 is the strain most commonly involved ,other serotypes are occasional causes • Incidence is the highest among children <5 years • It is zoonotic infection : reservoir is the intestines of cattle ,sheep and other • Infecting dose <100organisms • Transmitted is by consumption – contaminated food (undercooked beefburgers),unpasteurized milk and milk products or water; contaminated swimming pools,fruit juices • Incubation period 3-4 days Pathogenesis • Verotoxin elaborated is similar to Shiga toxin of S.dysenteriae type I • Destruction of colonic cells and damage to capillary endothelium, producing hemorrhagic colitis and microvascularangiopathy, particularly affecting glomeruli and central nervous system

  35. VTEC Clinical features • Mild non- bloody diarrhea to haemorrhagic colitis (50%) • Severeabdominalpains and passing of frank bloodystools • Feverisrare • Usuallyself-limiting,resolveswithin 7 days Complications • HUS Diagnosis • All diarrhoealstoolsamplesshould be examined for E.coli O157 • Patientswithsuspectedacuteinflammatoryboweldiesase,patientspassingbloodystools and patientswith HUS should be investigated for non-O157 VTEC iftheirstoolsarenegativefoeE.coli O157 Treatment • Hydratation.monitoringrenalfunction • Antibioticsmay not be effective

  36. OtherE.coli Epidemiology • Affecthumansonly • EPEC –enteropathogenic (enteroadherent)-major cause of infantile diarrhea in developing countries • ETEC-enterotoxigenic-infantile diarrhea in developing countries and traveler’s diarrhea • EAggEC-enteroaggregative-childhoodpersistent diarrhea • EIEC-enteroinvasive –an uncommoncause of dysenteriaelikeillnessinthe developing countries • Transmission- fecal-oral,contaminated infant feeds, contaminatedfood, water • Incubation period 1-2 days Pathogenesis EPEC-adhere to smallintestinalmucosalcellsdissolution of microvilli ETEC action of twotoxins-A net increaseinintestinalsecretion Heat-labile-LT-stimulatesadenylatecyclase Heat-stable-ST-stimulatesguanylatecyclase EIEC-invadesileal and colonicmucosainflammation and dysenterylikeillness

  37. OtherE.coli Clinical features • EPEC, ETEC- acute onset watery diarrhea, fever is absent.EPEC may cause severe and protracted diarrhoea in hospital outbreaks • EAggEC- fever,abdominal pains ,watery stools becoming small volume,mucoid and bloody.Short lasting Treatment • Most cases require oral rehydration only • In severe protracted diarrhea co-trimoxazole • A single dose of ciprofloxacin and loperamide at the onset of symptoms is often effective for travelers diarrhea

  38. Cholera Epidemiology • Gram negativemotilecurvedbacillibelonging to speciesVibriocholerae • Epidemic cholera iscausedonly by theserogroup O1 (classical and Eltorbiotypes) and O 139 • Pockets of classical cholera existintheGangetic delta • In natureV.choleraeexistsinaquaticenvironments. • Humansareonly natural hosts • Transmissionthroughcontaminatedfood and water • Childrenmorecomonnlyaffected • Incubation period 2-3 days Pathogenesis Action of cholera toxin (enterotoxin)throughstimulation od adenylatecyclase Localintestinalimmunityagainstthespecificserogroupfollowsrecovery

  39. Clinical features • Sudden onset of vomiting and profuse watery diarrhea with abdominal cramps • Fever is absent • Stools are white-yellow with mucus flecks (rice water) • Daily volume often reaches several liters • Mild and inapparent cases also occur • Diarrhea subsides and resolves within a few days Complications • Rapid dehydratation ,shock and death within hours • Death rates may reach 50% when cholera strikes a previously unaffected and unprepared country • Organized diarrhea disease control programs reduce fatality <1% Treatment • Early use of oral rehydratation supplement to correct fluid and electrolyte loss • Ciprofloxacin and norfloxacin are effective in shortening the duration of the clinical ilness,eliminating vibrios from faeces Important : adequate disposal of human faeces during an epidemic

  40. Yersiniaenterocolitica Epidemiology • Gram-negative • Most human infections :serotypes O:3,O:5,O:8 and O:9,which cause primarlyzoonotic infections of domestic and wild animals and are often asymptomatic • Y.enterocolitica after Campylobacter,Samonella,Shigella ranks in frequency of faecal isolation in Eu and America but clinical case reports are less common • Scandinavian countries report a higher incidence of clinical cases than other developed countries • Transmission :fecal-oral,contaminated food,milk,water,contact with animals • Incubation period 5 days • Highest incidence is among children Pathogenesis • Invading the small intestinal mucosa,multiply in the reticuloendothelial cell’s of Peyer’s patches • Ielitis and less commonly colitis and mesenteric adenitis • Possible bloodstream invasion in patients with iron overload or immune deficiency

  41. Clinical features • Acutefebrilewatery diarrhea inyoungchildren • Olderchildren and adults-rightlowerquadrantabdominalpain,mimickingappedicitis • Spontaneusreccoverwithin a fewdays Complications • Septicaemia • Reactivearthritis (particularyinindividualswith HLA B27) • Erythemanodosum Treatment • Most casesaremild and self-limiting. Severecasesshould be treatedwithcotrimoxazole and ciprofloxacin

  42. Entamoebahistolitica Thethridleadingparasiticcause of deathafter malaria and schistosomatosis 40.000-100.000 deathsannuallyinthe developing countries • Humansareonlyreservoir • Occursthroughouttropical and subtropicalAsia,Africa,the Middle East, Central and SouhAmerica,particularyinpoorsocioeconomiccondtions • Developedcountries:immigrants,travellers,mentalinstitutions,malehomosexuals • Transmission by ingestion of cystsincontaminatedwaterorfood • Person-to-person • Incubation period 2-6 weeks • 90% of infectedpersonsareasymptomatic cyst passers

  43. Entamoebahistolytica . Pathogenesis • In thesmallintestinethe cyst isdigestedreleasing 4 trophozoites,whichmigratedownwards to live on thecolonicsurface and multiplyinbinaryfission • Trophozoites do not transmitinfection • Onlytrophoziitescaninvadetissues • Attachement to intestinalmucosacauseinflammation and ulceration. • Trophozoitesmayinvadelocalveins and migrate via portal venouscirculation to liver and produceabscess • Immunity to futureinvasivediseasedevelopesfollowingrecovery but not to freshcolonization of intestines

  44. Enatmoebahistolytica Clinical features • Gradually worsening bloody mucoid diarrhea over 1-3 weeks,cramp like abdominal pains and variable pyrexia • The symptoms usually persist for several weeks before subsiding,even if no treatment is given • Relapses are common • Cyst passing may continue for years -cystsoutsidethehuman body cansurvive for a long time, inmoistconditions Complications • Fulminant colitis • Amoeboma • Chronic amoebiasis • Amoebic liver abscess-less <1% diefromliverabscessifdiagnosed and treatedearly. Treatment • Metronidazole is the drug of choice for active colonic disease and for liver abscess • Aspiration of liver abscess is required only if rupture is likely or when distinction from pyogenic abscess is necessary • A 10 day follow-up course of diloxanidefuorate is necessary to destroy colonic cysts

  45. Entamoebahistolitycav.sShigellosis,salmonellosis • Slow onset • Incubation >7 days , 21 days • Painfullcaecum • No fever • no painfulltenesmus • Bloodinstoolls , not fresh • Veryodorousstools • Absenceon not many WBC instools • Abruptusonset • IP 7 days • Painfullesica • High fever • Painfulltenesmus • Freshblood • Non-odorousstools • many WBC instools

  46. Haemolitic –uraemicsyndrome • Complication of E.coli O157 and Shigelladysenteriae • Devlopes 2-7% cases overall • Between 2-14 days of diarrhea • Oliguria,renal failure, thrombocytopenia,microangiopathic anemia • Seizures,coma • Dissaminated endothelium lesion

  47. POSTINFECTION SYNDROMES Reiter’s syndrome (reactive arthritis) may develop after infection with Salmonella,Yersinia,Campylobacter,Shigella as well as after nonfoodborne infections such as nongonococcalurethritis and Cyclospora infections. Reiter’s syndrome: 1) polyatrhritis 2) urethritis 3) conjunctivitis

  48. Clostridium dificile • Gram –positiveanaerobicbacilli • Transmition : fecal-oral ,directcontactbetweenpatients,fromtheenvironmnet DIAGNOSIS : diarrhea ormegacolontoxicumwithoutanyotherreason plus one of threebelow : 1)Demonstration of C.difficiletoxininstoolspecimen 2)Sigmoidoscopicchanges –colitis pseudomembranosa 3)Histopathologicallyconfirmed colitis pseudomembraosa

  49. CARRIERS • 3%- population • 20-40%-hospitalized • 50-60%- newborn and infants ; 3% after first year • 15-25% reasons of postantibioticdiarrhea RISK FACTORS • Previousantibioticotherapy • Age : >65 years 20 x moreoftenthan <20 years • Hospitalization

  50. Antibiotics by therisk of causing Clostridium difficile relateddisease-examples High risk • Cephalosporines II and III generation • Clindamycin • Fluoroquinolones • Wide spectrum penicilines Medium risk • Macrolides • Cotrimoxazole • Carbapenemes • Amoksycylin • Ampicilin Lowrisk • Aminoglikozides • Rifampicin • Metronidazole • Vankomycine • Tetracyclines

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