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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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diarrhea
Diarrhea
  • Stool consistency – liquid , half-liquid , mushy
  • Abnormalstoolvolume >300g/ 24 h
  • Abnormalfrequency
  • Containspus, blood, mucus , flakedepithelium
  • Green, grey, grey-yellow
common causes of acute community aquired infective diarrhea
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
infective diarrhoeas
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
infectious diarrhea features
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
host factors
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
slide7

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 .
microbial factors
MicrobialFactors
  • Invasivness
  • Attachment
  • Cytotoxin
  • Enterotoxin
  • Neurotoxin
complications
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
slide10
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

slide11

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

slide12

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

distinguishing features of inflammatory and non inflamatory diarhea
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

explore history for

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.

slide15

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.
the principles of oral rehydratation
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.

persisting diarrhea after an acute onset
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
management of acute diarrhea
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 )
slide19

Shigellaspp.

  • Salmonella spp.
  • Escherichia coli : EHEC,EIEC, EPEC, ETEC, EAgEC
  • Campylobacterjejuni
  • Amebicdysentery
  • Yersinios
  • Vibriosis
salmonellosis non typhoid sallmonella infection
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

slide21

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%
salmonellosis non typhoid sallmonella infection complitactions
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
slide23

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
typhoid and parathyphoid fevers enteric fever
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
slide25

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.
typhoid and parathyphoid fevers enteric fever clinical features
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.

slide27

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)
typhoid and parathyphoid fevers enteric fever invasigations and diagnosis
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

shigella infection
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
shigella infection pathogenesis
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
shigella infection1
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
campylobacter infection
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

slide33

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)
verotoxin producing escherichia coli vtec ehec
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
slide35

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
other e coli
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

other e coli1
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
cholera
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

slide39

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

yersinia enterocolitica
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
slide41

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
entamoeba histolitica
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
entamoeba histolytica
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
slide44

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
entamoeba histolityca v s shigellosis salmonellosis
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
haemolitic uraemic syndrome
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
slide47

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

clostridium dificile
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

slide49

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
antibiotics by the risk of causing clostridium difficile related disease examples
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
clinical features
CLINICAL FEATURES
  • In 90 % previousantibiotycotherapy 1-8 weeksbeforesymptomesoccured
  • Even one dose of antibioticmaycauseCdD.
  • Symptomsoccure :-most oftenbetween 5-10 day of theraphy

-may be presentafter one dayor 10 weeksafterfinishingantibiotic

            • Milddiarrhea ; severe colitis ,megacolontoxicum
  • Abdomianalcramps, not very high fever, leukocytosis
  • Diarrheaisaccompained by fever

– 30-50%

-Leukocytosis 50-60%

-Ambdominalpain 20-33%

slide52

WBC on average 15.000/mm3

  • Pseudomembranous colitis in 25% patientswithC.difficile
  • Veryseverecoursein 3%- megacolontoxicum,shock,colectomia,death
  • Severe and complicatedC.difficileinfectionin 37% casesis not accompainedwithdiarreha
  • Recurrancerate 20%

Patientwith C. difficileshould be isolated for 48 afterdiarrehahasfinished

treatment
TREATMENT
  • STOP ANTIBIOTIC isenough to relief symptomsin 23% of patientsin 48-72h and may be enoughwhenmildinfection
  • Metronidazol 4 x 250 mg or 3 x 500 mg
  • Vancomycin 4 x 125-500 mg
  • Whentreatmentiseffectivesymptomslasts for 4,6 days –metro and 3 days –vanko.
  • Recurrence – usethe same drugthat was used to treatlastepisode
  • Ifrecurrenceismoresevere –usevanko
slide54
FOODBORNE DISEASEResult from ingestion of a wide variety of foods contaminated with pathogenic organisms, microbial toxins or chemicals.
  • An outbreak occurs when 2 or more people consuming the same food develop identical ilness, usually gastro intestinal sometimes neurological
  • Most commonly in developd countries : Salmonella, C.perfrigens, E .coli O157 and NLVs
  • Pathogens vary according to the food involved
  • Short periods of less than 6 hours suggest ingestion of performed toxin
  • IP >12 h ,the presence of fever and symptoms continuing beyond 24h suggest actual infection by living organisms
slide55

Foodborne disease –features

  • Vomitting , nausea, retch
  • Diarrhea
  • Abdominalpain
  • Fever
  • Headache
  • Irritability
slide56

Outbreaks of staphylococcal food poisoning -ham,poultry,potato and egg salads,cream-filled pastries which are thought to be contaminated during preparation by a food handler.

Food handler’s hand has a purulent skin lesion (true in minority).

  • B.cereus of the short incubation type-fried rice that has been cooked and held warm for extended periods.
  • C.perfrigens-beef, poultry and gravies. Outbreaks occur when these items are prepared in large quantities for banquets or in institutional setting, without final adequate reheating.
slide57

Long incubation Bacillus cereus-meat or vegetable dishes. BUT ALSO this bacteria is being a frequent contaminant of raw meats,vegetables,milkproducts.

It has been isolated from 25% of dried foods such as seasoning mixes,spices,dried potatoes and from more than 50% of dried beans and cereals.

  • E.coli O157-H7-

Undercooked ground beef, lettuce, apple cider, alfaalfa sprouts, venison, and salami.

Healthy cattle commonly carry E.coli O157 –H7 in their intestines and execrate it in manure. Produce may be contaminated with E.coli O157 –H7 through use of manure as fertilizer or use water in processing that has been contaminated with fecal matter. Consumption of contaminated swimming water or drinking water.

slide58

Salomenlla- poultry , beef, egg, dairy products or produce. Internally contaminated shell eggs cause many outbreaks of infections with Salmonella serotype Enteritidis.

Fresh produce melons, tomatoes, raw milk, unpasteurized orange juice, alfalfa sprouts, contaminated chocolate candy, peanut snacks, cereals.

  • Shigella- cool , moist foods, that require much handling after cooking; raw vegetables, at salad bar, parsley, scallions, lettuce.
slide59

V.parahaemoliticus – bivalve mollusks, crustaceans

  • V.cholerae O1 and non O1 outbreaks have been traced to contaminated shellfish eaten raw or inadequately cooked.

Crabs brought in travelers language from Latin America have caused cholera in the US.

  • Yersiniaenterocoliticahave been casused by consumption of raw pork and contaminated milk and by cross-contamination from the preparation of pork chitterling in the household.
  • Travelers diarrhea caused by ETEC associated with consumption of salads in Mexico and foodborne outbreak of ETEC occurred after ingestion of imported cheese.In recent years outbreaks of traveler’s diarrhea at home related to consumption of fresh produce have become more common.
slide60

Botulism

most of ten associated with the ingestion of low-acid ph>4.4 home canned vegetables, fruits, fish. Honey was the source of Clostridium botulinum in some cases of infant botulism.

Norovirus –contamination of food by an ill food handler. Less commonly contaminations of shellfish, salads, imported frozen raspberries.

Cyclospora- infections were linked to consumption of raspberries imported from Central America.

Outberaks have been also associated with mesclun lettuce mix.

slide61

NAUSEA AND VOMITING WITNIN 1 TO 6 HOURS–caused by a performed enterotoxin

Staphylococcus aureus

  • Vomiting 86% + diarrhea 68% + fever 16%
  • Staphyloccoci responsible for episodes of food poisoning produce enterotoxines ( A to Q) but not all are emetic.
  • TSST-1 –pyrogenicsuperantigenes
  • B and C- nonmenstrual toxic shock syndrome. Enterotoxines produces its emetic action after interaction with abdominal viscera.

Bacillus cereus-type 1- short incubaton

  • Causes two types of food poisoning disease.
  • Type one characterized primarily by nausea and vomiting. Incubation period is 1-6 h.
  • Vomiting 100% + abdominal cramps 100% + diarrhea 33%
abdominal cramps and diarrhea within 8 16 hours caused by toxin produced in vivo
ABDOMINAL CRAMPS AND DIARRHEA WITHIN 8-16 HOURS- CAUSED BY TOXIN PRODUCED IN VIVO.

In these two-vomiting and fever infrequently.

Vomiting in 1/3 of affected persons suggests that these organisms are not involved.

Bacillus cereus- type -2 long incubation

Incubation 8-16 hours.

Diarrhea 96% + abdominal cramps 96% + sometimes vomiting and rarely fever

Clostridium perfrigens- toxins produced in vivo, accounting for the longer incubation period.

The most common symptoms are abdominal cramps and diarrhea although nausea may occur, vomiting and fever are uncommon- less then <10%

5 types of toxin have been described. Type A is almost always the toxin causing food poisoning. The enterotoxin is active throughout the small intestine, with greatest activity in ileum in which net serretion of sodium and fluid and inhibitition of chloride and glucose absorption occur. ; it damages epithelial cells at villus tips.

fever abdominal cramps diarrhea within 16 48 h
FEVER, ABDOMINAL CRAMPS, DIARRHEA WITHIN 16-48 H

Salmonella, Shigella, Campylobacter jejuni, Vibroparahaemoliticus, E.coli.

bloody diarrhea and vomiting occur in a varying proportion of patients

C.jejuni is most common foodborne bacterial pathogen-in contrast to the illnesses caused by other org. food poisoning caused by C.jejuni is chracterizied by longer incubation period, 3-4 days

Salmonella is second most common bacterial pathogen

associated with foodborne outbreaks ; median incubation period 6-48 h

E.coli O157-H7 like C.jejuni 3-4 days.

abdominal cramps and watery diarrhea 16 72 h
ABDOMINAL CRAMPS AND WATERY DIARRHEA <16-72 H

enterotoxigenic strains of E.coli, V.parahaemoliticus, V. cholera non O1 and in endemic areas V.cholerae O1 and O 139, C.jejuni, Salmonella, Shigella.

enterotoxines synthesized in vivo are responsible for the syndrome caused by V.cholerae O1 and V.cholerae non O1 and enterotoxigenic strains of E.coli.

when Salmonella, Shigella, V.parahaemoliticus –enterotoxigenic or cytotoxic substances

severe cholera : profuse watery diarrhea accompanied by musclar cramps

Cholera -5 days

V.cholerae non O1-2-12 days

other resolve within 72-96 h

vomiting and nonbloody diarrhea 24 72 h
VOMITING AND NONBLOODY DIARRHEA <24-72 H

Norovirusesthe most common of known foodborne pathogens

causing 2/3 of all foodborne illnesses caused by known pathogens.

vomiting and diarrhea are often the presenting symptoms, onset 1-2 days after exposure

watery, nonbloody diarrhea, abdominal pain, nausea.

vomiting more common among children, diarrhea more likely to predominate in adults.

fever 1/3 to ½ and is low grade

It is impossible to distinguish beweennoroviruses and some bacterial causes of gastroenteritis, such as ETEC for a single patient based on clinical course.

Criteria that suggest noroviruses:

1) failure to detect a bacterial or parasitic pathogen in stool specimens

2)occurance of vomiting >50% of patients

3)mean duration 12-60 h

4)mean incubation 24-48 h

fever and abdominal cramps 16 48h without diarrhea
FEVER AND ABDOMINAL CRAMPS <16-48H WITHOUT DIARRHEA
  • Yersiniaenterocolitica-foodborne outbreaks in the US ,more common cause in Northern Europe and Canada.
  • Young children –febrile diarrhea is the most common presentation.
  • Older children and adults may closely resemble acute appendicitis.
bloody diarrhea without fever 72 120 h
BLOODY DIARRHEA WITHOUT FEVER <72-120 H

The syndrome of hemorrhagic colitis has been linked to Shiga toxin-producing strains of E.coli most often serotype O157-H7.These strains produce cytotoxins that affect Vero kidney cell cultures and are neutralized by antiserum to Shiga toxin. (Shiga toxins and verotoxines)

The toxins are absorbed from the gut and damage vascular endothelial cells in target organs such as gut and kidney.

Severe abdominal cramps and diarrhea which is initially watery but may be grossly bloody.

uncomplicated infection remain afebrile

mean incubation 3-8 days

Duration of uncomplicated 1-12 days

development of fever and leukocytosis may herald HUS.Children mortality 3-5 %

HUS occurs in 8% of infections in children,with onset about 1 week after the beginning of diarrheal illness.

other E.coliserogroups that produce Shiga toxins can also cause hemorrhagic colitis and HUS.

nausea vomitting diarrhea pralysis 18 36h
NAUSEA, VOMITTING, DIARRHEA PRALYSIS <18-36H
  • Acute gastroenteritis + symptoms simultaneously with or just before onset of descending weakness or paralysis strongly suggests the diagnosis of foodborne botulism.
  • The botulinal toxins which inhibit acetylocholine release from nerve endings.

Atneuromuscularjunction

  • The disease in humans is caused by one of three toxins A,B,E which are produced after germination of Clostridium botulinum spores in inadequately processed food.
  • In older children and adults results from ingestion of performed toxin.
  • Infant botulism results from ingestion of spores with subsequent toxin production in vivo.

Rarelyinfantsayswallowsporeswhichlatergerminate and producetoxin.toxigenesiscannotoccurinmatureadultguts.

  • Foodborne and infant botulismareveryrarein UK but a smllnumber of cases of woundbotulismoccureachyearininjectingdrugusers
  • Diagnosisisprimarlyclinical
  • Confirmation by demonstratingtoxininthebloodorfaeces.
  • Teratement:botulinumantitoxin.
  • Wound and infant :penicilin and metronidazole to stop toxigenesis
  • Ventilatorysupport.
slide69

Guillan-Barre syndrome- in contrast to botulism,this syndrome is usually manifested by an ascending paralysis accompanied by sensory findings ad abnormal nerve conduction velocity.

  • This syndrome has been associated with serologic evidence of recent C.jejuni infection . In a multicenter study of 118 patients in the US 36% had serologic evidence of a preceding C.jejuni infection.
systemic illness
SYSTEMIC ILLNESS

Listeriosis typically affects pregnant women, fetuses, persons with compromised immunity-fever, myalgis, bacteriemia, meningitis.

foods cold processd meats and dairy products.

incubation period 2-6 weeks

Vibriovulnificuscause fulminate myonecrosis or primary bacteriemia after ingestion of raw oysters