infeksi git by e.coli & salmonella spp rev 2016

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    GASTROINTESTINALTRACT INFECTIONS

    Ike Irmawati P.A

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    Introduction

    Gastroenteritis  gastrointestinal

    symptons : nausea, vomiting, diarrhea &

    abdominal discomfort

    Diarrhea 

    abnormal fecal discharge : frequent &/orfluid stool

    Resulting from disease small intestine

    ↑↑ fluid & electrolyte loss

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    Dysentry  An inflammatory disorder of G!

    Associated "ith : blood & pus in feces

    #ymptoms : pain in anus, fever, abdominalcramps

    Resulting from disease large intestine

    $nterocolitis  inflammation involving the

    mucosa small & large intestine

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    21/12/08

    Pathogenesis

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    nfections

    ingested in sufficient number 

    $lude host defenses of upper G! & reach

    the intestine

    Diarrhea the most common outcome of

    G! infection

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    anamnesis

    %atients recent food

    !ravel history

    'acroscopic & microscopic of the fecesblood, pus/ mucous

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    Escherichia coli 

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    Escherichia coli 

    (ormal gut flora

      'ay also inhabit female genital tract

    %ossess virulence factors intestinal

    tract or at other site )eg* +rinary tract

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    Escherichia coli 

    #pectrum of disease:

     – -acterimia

     – +rinary tract infection: caused .0 case1 hemolisin)2, virulensi factor pili %  +%$3 )uropathogenicE.coli 

     – (eonatal meningitis: E. coli  45  '($3

    )meningitis/ sepsis6associated E.coli)

     – Nosocomial infection

     – Gastroenteritis )Diarrea by E. coli 

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    7 classes )virotypes of E. coli  that

    cause diarrheal diseases : 

    5*enteroto8igenic E. coli  )$!$3

    9*enteroinvasive E. coli  )$$3

    *enterohemorrhagic E. coli  )$;$3

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    Mechanism of virulence

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    Patogenesis

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    ETEC

    >irulence

    fimbrial adhesins e*g* 3?A , 3?A , 4..,

    4@@non invasive

    produce ! and/or #! enteroto8in

    "atery diarrhea in infants and travelers1 noinflammation, no fever 

    !ransmitted by contaminated food and

    "ater 

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    ETEC

    Adult self6limited 56 day

    ! $Bsoto8in )subunit A & - activation ofadenilat cyclase cA'% hypersecretion of

    "ater & 3l6

     , as "ell as inhibiting the reabsorption(a2   hipermotilitas & diarrhea -e antigenicand similar to V. cholerae enteroto8in

    #! !o8in : activation of guanylate cyclase cG'% "ater secretion

    -acteria has coloniCation factor in the smallintestine epithelium gen faBtor Bolonisasi terBait

    plasmid

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    Patogenesis ETEC

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    EPEC

    non fimbrial adhesin )intimin & !ir  

    )translocated intimin receptor, -fp

    )bundle-forming pili  and

    $%$3 adherence factor )$A? enableslocaliCed adherence of bacteria to

    mucosal intestinal cells changes in cell

    surface )loss of microvilli

    does not produce ! or #!1 some reports

    of shiga6liBe to8in

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    EPEC

    usually infants diarrhea & child in

    developing country1 "atery diarrhea

    self6limited/ chronic diarrhea

    some inflammation, no fever1 symptoms

    probably result mainly from invasion

    rather than to8igenesis

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    EHEC

    >!$3 #!$3

    adhesins not characteriCed, probably fimbriae

    moderately invasive

    produce shiga to8in >eroto8in

    pediatric diarrhea,

    nflammation & bleeding mucosa of large

    intestine )hemorrhagic colitis

    may be complicated by hemolytic uremiasyndrome )to8in mediated damage to Bidneys

    characteriCed by: hemolytic anemia & lo" platelet

    count

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    EHEC

    after attachment at mucosa of colonproduce to8in effects on the intestinal

    epithelium diare

    3aused hemorrhagic colitis and hemolyticuremic syndrome );+#  veroto8in

    receptors found in renal epithelium

    Acute renal failure

    solate E. coli  E5=F:;F & E97 )epang,95, sorbitol )6

    !ransmitted by ingestion of undercooBed

    beef or ra" milB

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    EHEC

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    EIEC

    nonfimbrial adhesins

    possibly outer membrane protein

    invasive )penetrate and multiply "ithinepithelial cells

    dysentery6liBe diarrhea )mucous, blood

    necrosis, ulceration & inflammation of the

    large bo"el high fever, malaise, headache, abdominal

    pain

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    EIEC

    +sually seen in young children living in

    areas of poor sanitation

    !est aBtosa )6, test #ereny )2,

    leuBocytes in feses

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     E. coli  invade by endocytosis inside

    epithelial cell they lyse endocytic

    vakuola   multiply & spread to

    adjacent cells   tissue destruction,

    inflammation , necrosis & ulceration

      blood & mucus in stools

    Patogenesis EIEC

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    Patogenesis EIEC

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    EEC

    %robably involves binding by pilli

    non invasive

    produce #!6liBe to8in )$A#! and a

    hemolysin6liBe to8ins

    persistent "atery diarrhea in young

    children "ithout inflammation or fever 

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    EEC

    !he bacteria can attach in cultur cell &

    forming aggregates )stacked brick 

     plasmid-associated fimbriae

    associated with a global aggregativeregulator gene ( Agg) responsible for

    cellular adherence

    #tool specimen : no bloody & no "hite

    blood cell

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    !EC

    %roduce alpha hemolysin & cytoto8ic

    necrotiCing factor 5

    Diarrhea : children

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    diagnose

    3ulture : $ndo agar metalic colony

    Inflammatory gastroenteritis

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    Enteroto"igenic #ETEC$ E. coli %gram negative rod

    Ingestion of comtaminated&ater or food'

    ETEC has multi(le(athogenic mechanisms&hich include at least2 distinct to"ins) a heat%la*ile

    to"in #+T$ and a heat sta*leto"in #,T$' +T is similar tocholera to"in' The ,T acts*- stimulation of guan-latec-clase &ith resultant c-clic.MP accumulation inmucosal cells'

    Travelers !iarrhea) &ater-

    self%limited diarrheavomiting cram(s nausealo&%grade fever 1% da-sduration'

    Entero(athogenic #EPEC$ E. colialso called enteroadherent E. coli %gram negative rod

    Ingestion of comtaminated&ater or food'

    EPEC (roduces nodemonstra*le e"tracellularto"in' f( mediates looseattachment to microvilluscells &hich leads toincreases in Ca levels andthen rearrangements inactin Intimin (rotein neededfor intimate contact &illhuman cells and final stagesof cell destruction'

    Infant diarrhea &ith fevernausea vomiting non*lood-diarrhea

    Enteroaggregative #EEC$ E. coli %gram negative rod

    Ingestion of comtaminated&ater or food'

     ggregative (attern due tocertain thin (ili #.33P4fim*riae$

    !evelo(ing countries(ersistant &ater- diarrhea &ith vomiting anddeh-dration in infants' Canlead to *lood- stools

    Inflammatory gastroenteritis

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    Escherichia coliEnteroinvasive E. coli#EIEC$- gram negativerod

    Ingestion ofcontaminated foodand &ater'

    Plasmid mediatedinvasion of e(ithelialcells

    fever cram(ing&ater- diarrheafollo&ed *- scant*lood- stools

    Escherichia coliEnterohemorrhagic E.coli #EHEC$ includesserot-(e 5167H7-gram negative rod

    Ingestion ofcontaminated food#undercoo9edham*urgers$ and&ater 

    3eroto"in%*loc9s(rotein s-nthesis

    *lood- diarrhea and insevere cases can leadto hemol-tic uremics-ndrome #H:,$

    Invasive gastroenteritis

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    Thera(-

    #upportive therapy : oral rehydration

    ;+# by $;$3 : transfusion & hemodialysis

    Antimicrobial therapy may shorten theduration of illness, but many of these

    infection resolve "ithout such therapy

    Antimicrobial therapy for non6life6

    threatening infection contraindicated 

    develop resistance

    ?ood sanitation and environment

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    ,almonella

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    'orphology:

     – Rod, Gram )6, motile, facultativeanaerobic

     – (o fermentation lactose & sucrose

     – produce ;9#

     – ?reeCing temperature resistant

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    !he genus !almonella has three Binds ofmaHor antigens :

    5*somatic )E 

    heat stabile & alcoholresistant %#

    9*surface ) 4 >i antigen  virulence factor

    capsular polysaccharide

    *flagellar ); heat6labile protein!almonella enterica serovars )e*g*,$nteritidis, !yphi peritrich flagella

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    ;ospes:

     – ;uman !. typhi" !. paratyphi A, -, 3

     – %ig !. cholera-suis

     – 3o" !. dublin

     – #heep !. abortus suis

    nfective doses !. typhi : 57 6 5@

    the  Salmonella strains isolated from humans

    and other warm-blooded animals.

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    n humans, !almonella are the cause of

    three diseases called salmonellosis:

    5* enteric fever )typhoid, prolonged fever

    & multisystem involvement ) blood, lympnodes, liver & spleen

      caused by: #* serotype !yphi, %aratyphi

    A,- or 3

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    Cont'

    9* Gastroenteritis & diarrhea

      production infection limited to the

    mucosa & sub mucosa of the

    gastrointestinal tract

      caused by: #* serotype !yphimurium &

    #* serotype $nteritidis

    acute gastroenteritis, resulting from a

    foodborne infection/into8ication

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    * -acterimia & e8traintestinal infections

      occur by spread from G!

      $tiology: ! * choleraesuis

      !. dublin

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    Salmonella enterica serovar T-(hi'

    Also called !almonella !yphi

     the causative agent of typhoid fever*

      !he symptoms of typhoid fever include

      nausea, vomiting, fever and death*

    !. !yphi can only infect humans

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    !almonella enterica serovar !yphimurium #S. T-(himurium$

    the most common cause of food

    poisoning

    n humans !. !yphimurium does not causeas severe disease as !. !yphi,

    !he disease is characteriCed by diarrhea,

    abdominal cramps, vomiting and nausea,

    and generally lasts up to F days*

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    !almonella enterica serovar $nteritidis

    !. $nteritidis causes a disease almost

    identical to the very closely related !.

    !yphimurium*

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      !. enteritidisBakteri menempel pd

    epitel ilium terminal

    Bakteri berpenetrasi dlm sel &

     bermigrasi ke lamina propia pd

    ileocecal berkembangbiak pd

    folikel limfoid hiperplasia dan

    hipertrofi reticuloendothelial

    PMN Infeksi terbatas

     pada traktus

    gastrointestinal

    Respon inflamasi

     pelepasan Prostaglandin

    cMP meningkat

     sekresi cairan

    meningkat

    !IR"

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    ,almonellosis

    5 billion !almonella per gram of feces

    'ortality rate I 5 0

     – ;igher in infants and elderly

    Recovery in a fe" days

     – #ome may shed bacteria in feces for 7 months

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    ,almonellosis

    ncubation time 59 J 7 hours

    -acteria invade the intestinal mucosa and

    multiply

    'ay pass thru mucosa into lymphatic or

    circulatory system and become systemic

    ?ever, abdominal pain, cramps and

    diarrhea

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    Patogenesis ,almonellosis

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    Mucosa invasion *- ,almonella

    R t Ef ! i i A d Eth # Ef # l ll i

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    Routes Ef !ransmission And Ether #ources Ef #almonellosis

    5*!he most common route of infection is through oralingestion*

    9*nfection can occur through an open cut, sore or "ound

    into the bloodstream*

    *nfection can occur through splashing of contaminated

    material into the eyes*

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    Cont'

    7*mproperly cooBed meats, especially poultry and chopped

    beef/porB/turBey*

    F*Recontamination of cooBed meats through contact "ith

    ra" meats/fluids*

    .*3ontamination of foods by salmonella contaminated handsof servers/preparers*

    @*3ontact "ith, ingestion or inhalation of soil contaminated

    "ith animal feces*

    5*Ra" milB )especially among farm families and

    contaminated pasteuriCed milB*

    55*?ish meal, bone meal and meat meal1 fertiliCers and

    animal feeds*

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    Enterocolitis

    manifestation: vomiting, stomach ache,

    diarrea & fever 

    Enset: 76

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    Enterocolitis

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    +a*orator-

    -acterial isolation  e*g* Gaal culture, ##

    agar, 'ac3onBey agar, AD%, $ndo agar 

    #erologi e*g* !est Kidal enteriB fever 

    T i

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    Tera(i

    $nteric fever & -acteremia antibiotic: – 4hloramfeniBol, ampisilin, trimetoprim6

    sulfometho8aCol, sefalosporin

    $nterocolitis: – Diarrea fluid & electrolyte replacement

     – Antibiotic do not reduce the sympton & may

    prolong e8cretion of salmonella in the feces

    3arrier: BholisisteBtomi & antibiotiB

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    (revention

    ?ood sanitation & clean drinBing "ater 

    >acination

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    Salmonella typhi,Salmonella paratyphi  and C Salmonellacholerasuis

    ingestion of fecall-contaminated food or&ater 

    a*le to survive inneutro(hils

    t-(hoid fever (arat-(hoidor enteric fevers;

    anore"ia letharg-malaise general aches(ains dull continuousheadache usuall-confined to the frontalregions non(roductivecough nose*leed #10< of(atients$ vaguea*dominal (ain anddiscomfort consti(ation#20< of (atients havemild diarrhea$ a*dominaldistension due to gas inthe intestines *lood-feces

    Salmonella enteriditis(contains 7 subgroupsand 1500 serotypes)-gram negative rod

    =ecal%oral transmissionvia contaminated &aterfood#(oultr- eggs or dair-(roducts$ or directl- in-oung children

    nausea vomitingdiarrhea

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    ! E9t Mi *i l 21/1