Meral SÖNMEZOĞLU MD Yeditepe University Hospital Associate Professor Department of Infectious Diseases and Microbiology Learning Objectives Describe and classify of ID: 806540
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Slide1
GASTROENTERITIS
And FOOD POISINING
Meral SÖNMEZOĞLU, MDYeditepe University HospitalAssociate ProfessorDepartment of Infectious Diseases and Microbiology
Slide2Learning
Objectives Describe and classify of gastroenteritis and food poisoningExplain the epidemiology of gastroenteritis and possible etiologic agents in various clinical settings
Know the pathophysiology of gastroenteritisDevelop an information on diagnosis and management plan for gastroenteritis
Slide3With
the exception of Helicobacter pylori gastritis, the term gastroenteritis is
applied to syndromes of diarrhea or vomiting that tend to involve noninflammatory infection in the
upper
small
bowel
or
inflammatory
infection
in
the
colon
Slide4Risk
of acquiring a gastrointestinal infection varies greatly with age
, living conditions, personal and cultural habits, and group exposuresThe second epidemiologic determinant of risk for enteric infection is where you are
T
he
third
determinant of risk is
when
you
are
there
.
The
majority
of
enteric
illnesses
in
temperate
climates
occur
during
winter
months
.
The
opposite
is
true
in
tropical
countries
,
where
distinct
summer
peaks
of
illnesses
are
common
.
The
role of
rainfall
is
uncertain
,
and
some
adjacent
areas
with
similar
monsoon
climates
have
opposite
seasons
of
major
diarrheal
illnesses
, as
illustrated
by
the
peak
seasons
for
cholera
Slide5Host defense factors
Gastric acidityIntestinal motilityIntestinal microfloraMucusSystemic and local immune mechanismsOthers (e.g. breast feeding)
Slide6Bacterial virulence factors
AdherenceEnterotoxin productionCytotoxin productionMucosal invasion
Slide7Mechanisms of infection
Ingestion of preformed toxin (food poisoning)Fecal-oral contamination Food, flies, fingers, feces, and fomitesContaminated foodAnimal reservoirFecal-oral contamination of foodInfectious dose varies (~100 to 109
)
Slide8Infectious
Doses of Enteric
Pathogens Shigella
10 to 10
2
Campylobacter
jejuni
10
2
to
10
6
Salmonella
10
5
Escherichia
coli
10
8
Vibrio
cholerae
10
8
Giardia
lamblia
10 to 10
2
cysts
Entamoeba
histolytica
10 to 10
2
cysts
Cryptosporidium
parvum
1
to
10
3
oocysts
Slide9DIARRHEA
Alteration in a normal bowel movementCharacterized by an increased in the water content, volume, or frequency of stools
>3 or more stools and at least 200 grDecrease in consistency (soft or liquid) and an increase in frequency of bowel movement to >3 stools per day
Slide10INFECTIOUS DIARRHEA
3-5 billion episodes yearlyMajor cause of worldwide morbidity and mortality5 million deaths yearly, 80% < 1 year of ageMajor cause of work/school absenteeism
Major economic burden, especially in developing countries
Slide11INFECTIOUS DIARRHEA
Due to an infectious etiology
Accompanied by symptoms of nausea, vomiting, or abdominal cramps. Acute diarrhea is an episode of diarrhea of <14 days in duration
Persistent
diarrhea
is of >14
days
in
duration
Chronic
diarrhea
lasts
>30
days
Slide12INFECTIOUS DIARRHEA
Second leading cause of morbidity
and mortality worldwideMore than 2 million deaths annuallySome causes of infectious diarrhea result in serious long term sequelae (HUS-STEC,G-B Campylobacter)
Slide13Etiology of Diarrhea
Infective
Non infective
Viruses
Bacteria
Parasites
Fungi
Allergic
Symptomatic
Inappropriate
feeding
Food
intolerance
Climate
Slide14Major Pathogens
Bacterial infection
Campylobacter, Shigella, and Salmonella
Protozoal
infection
Cryptosporidium
species
,
Giardia
lamblia
,
Isospora
belli,
Entamoeba
histolitica
,
Microsporidium
species
Toxin induced
E. coli and Clostridium
difficile
Mycobacterial
infection
M. tuberculosis, M.
Avium
co
mplex
Helminthic
infection
Strongyloides
stercoralis
Fungal infection
Candida species
(seldom a
cause of diarrhea)
Slide15Etiology of Infectious Diarrhea
(in (((8developed countries)
• 70-80% is viral • 10-20% is bacterial– Bacterial are responsible for most severe cases• < 10% is parasitic
Slide16Infectious Causes – Foodnet 2005
44.5 million persons (15% of the US pop.)Laboratory confirmed infections – 16,614
Microorganism#
Incidence
(
per 100,000
)
Salmonella
6,471
14.55
Campylobacter
5,655
12.72
Shigella
2,078
4.67
Cryptosporidium
1,313
2.95
STEC 0157
473
1.06
Yersinia
159
0.36
STEC non-0157
146
0.33
Listeria
135
0.3
Vibrio
119
0.27
Cyclospora
65
0.15
Salmonella Subtypes
Typhimurium
19%
Enteritidis
18%
Newport
10%
Heidelberg
6%
Javiana
5%
Slide17Slide18Slide19Slide20Slide21Türkiyede
Tifo vakaları
Slide22Mechanisms of infection
Ingestion of preformed toxin (food poisoning)Fecal-oral contamination Food, flies, fingers, feces, and fomitesContaminated food
Animal reservoirFecal-oral contamination of foodInfectious dose varies (~100 to 109)
Slide23Slide24Host defense factors
Gastric acidityIntestinal motilityIntestinal microflora
MucusSystemic and local immune mechanismsOthers (e.g. breast feeding)
Slide25Defense Barriers of the
Enterocytes
Physical barrier: mucus 2. Bacteriological (flora) 3. Immunological: Secretory IgA1
2
3
Slide2626
Morphology of Intestinal Mucosa
Villi
covered mainly (90%) by tall columnar absorptive cells (
Enterocytes
) having a
micrevillar
brush border
Crypts of lieberkuhn
Covered mainly by short columnar secretory cells
Goblet cells
without brush border
Slide27Bacterial virulence factors
AdherenceEnterotoxin productionCytotoxin production
Mucosal invasion
Slide28Diarrhea
Non-inflammatoryWatery diarrhea, no blood or mucus or pus in stool, no fever or systemic signs
Secretory or osmotic mechanismDehydration may occurGenerally self-limited and more benignTherapy generally supportiveInflammatoryFrequent lower volume stool, mucoid, bloody, or purulent. Often with fever or systemic signs, tenesmus, urgencyExudative mechanismDehydration rareLess benign
Slide29Osmotic Diarrhea
Interferes with absorption of waterSolutes are ingestedMagnesium sulfate or citrate or magnesium containing antacids
SorbitolMalabsorption of foodLactase deficiencyCeliac sprueVariety of infectious organisms (particularly viruses)Definition: Increased amounts of poorly absorbed, osmotically active solutes in gut lumen
Slide30Secretory Diarrhea
Excess secretion of electrolytes and water across mucosal surfaceUsually coupled with inhibition of absorptionClinical featuresstools very watery
stool volume largefasting does not stop diarrhea
Slide31Secretory Diarrhea
Bacterial or viral enterotoxinsCholera, enterotoxigenic E. coli, B. cereus, S. aureus,
Rotavirus, Norwalk virusHormonal secretagoguesCertain laxatives (castor oil, senna)
Slide32Exudative Diarrhea
Intestinal or colonic mucosa inflamed and ulceratedLeakage of fluid, blood, pusImpairment of absorption
Increased secretion (prostaglandins)The extent of bowel involved determinesSeverity of diarrheaSystemic signs and symptoms (abdominal pain, fever, etc)
Slide33Exudative Diarrhea
Infectious, invasive organismsShigella, Campylobacter, Yersinia, E. histolytica, EHEC, C diffIdiopathic inflammatory bowel diseaseCrohns disease
Ulcerative ColitisIschemia
Slide34Associated Signs & Symptoms
• Systemic illness/fever – invasive pathogen involvement
•
Vomiting
as
predominant
symptom
–
likely
viral
organism
or
food
poisoning
•
Abdominal
pain
–
inflammatory
process
(
Shigella
,
Campylobacter
,
EHEC)
•
Persistent
abdominal
pain
and
fever
:
Yersinia
Slide35When to Consider ABXMost cases of diarrhea resolve spontaneously and do not require treatment with antibiotics. Antibiotic
therapy may be considered however, in the following circumstances:– When signs and symptoms include:• Fever• Bloody stools• Presence of fecal leukocytes or occult blood;– To reduce fecal excretion and environmental contamination by a highly infectious agent like Shigella;– For persistent or life-threatening diarrheal infections such as cholera;– For immunocompromised patients.
Slide36Antibiotics
•
Most helpful for:– Shigella, ETEC, ameobiasis, Giardia, cholera, S. typhi•May help for:– non-typhi Salmonella &
Camplyobacter
• Can
prolong
fecal
shedding
,
use
only
if
severe
case
• Not
useful
for
viral
, EIEC
•
Can be
harmful
in EHEC
(O157:H7)
•
Multi
-
Drug
resistance
is a rapidly growing problem
Slide3737
Acute infectious diarrheaBacterial infectionCommon nonbacterial infection HKO antigensCommon among population – particular day care centersDeveloping countries – serious health effects, fatalIn the U.S., 1/3 due to contaminated food
Slide3838
HKO antigensH = flagellar antigenK= capsular antigenO= cell wall antigenEx. E. coli O157:H7
Slide3939
BacterialSalmonellaShigellaShiga-toxin producing Escherichia coliNon-shiga-toxin E. coliCampylobacterYersiniaClostridium difficile
Vibrio cholerae
Slide40A
cute Diarrhea in Children
The most important infective causes of acute diarrhea in developing countries in children are:Rotavirus Enterotoxigenic escherichia coli Shigella
Campylobacter
jejuni
Salmonella
typhimurium
40
Slide4141
SalmonellaContaminated animal products Salmonellosis - mildTyphoid fever – severeNormal flora in animals
Slide4242
Cases of typhoid fever and salmonelloses.Fig. 22.10 Data on the prevalence of typhoid fever andother salmonelloses
Slide43Nontyphoidal Salmonella
Salmonella typhimurium and enteritidisClinical syndromes
Gastroenteritis and colitisBacteremia and endocarditisEnteric fever (typhi and paratyphi)Localized tissue infectionCarrier state (> 1 year)Food-borne illness (poultry, meat, eggs)
Slide44Bacterial infection:
Salmonella
Clinical Symptoms may evolveFever; general malaise Sometimes no GI symptomsIf there are GI symptoms, will see:
Bloody diarrhea
Abdominal pain
Weight loss
Presenting Signs and Symptoms
Slide45Salmonellosis
Fever, cramping, abdominal pain, and diarrhea within 8-48 hours after ingestion of infective dose (contaminated poultry, shell eggs, dairy products, beef, exotic pets such as reptiles)Inflammatory (neutrophilic
) enteritis most typically involving the small bowel mucosa, occasional cause of colitis with crypt abscesses and erosive ulceration of colonic mucosa (Salmonella serotype Typhimurium)Moderate number of fecal neutrophils, usually fewer than in shigellosis except colitis with blood and pus in stool
Slide46Complications of
SalmonellosisDiarrhea usually self-limited (3-7 days), if persists >10 days another microbial etiology likely
Occasional dehydration requiring hospitalizationBacteremia (1-4% immunocompetent cases) (persistent bacteremia suggests endovascular infection site such as atherosclerotic plaques and aneurysms) After resolution of diarrhea mean duration of carriage in stool is 4-5 weeks
Slide47Stool culture
Salmonella bacilli may be found in stool/blood cultures
Serology: positive Widal test with increased titers Bacterial infection: Salmonella Diagnostics
Slide48Management and Treatment
TMP/SMX 960 mg bid or
Chloramphenicol 250 mg qid for 3 weeksIn case of sepsis, IV therapy is necessary Shorter regimens are: ciprofloxacin 500 mg bid or
ofloxacin
400 mg bid or
ceftriaxone
2 g IV for 7-10 days
Many patients often relapse after treatment and
chronic maintenance therapy (TMP/SMX 1 DD daily) is sometimes necessary.
Slide4949
ShigellaPrimarily a human parasiteInfects the large intestineNo perforation of intestineDysenteryExotoxin (shiga-toxin)
Enterotoxin
Slide50Shigella
Presenting Signs and Symptoms
Clinical Symptoms may evolveHigh feverAbdominal painBloody diarrhea
Slide51Shigella
dysenteriae, flexneri,
boydii, sonneiWatery or bloody diarrheaMay be complicated by reactive arthritis and rarely HUSVery infectious ( ~100 organisms cause disease)
Slide52Stool microscopy— fresh examination and after concentration
Multiple stool samples may be necessary
Shigella bacillus found in stool Shigella-
Diagnostics
Slide53Shigella
Management and Treatment TMP/SMX 960 mg bid x 5 days
or
amoxicillin 500 mg
tid
x 5 days
If resistant to the above, give
or
norfloxacin
400 mg bid x 5 days
or
nalidixic
acid 1 g
qid
x 10 days
ciprofloxacin 500 mg bid
Slide5454
Infection of the large intestine by Shigella dysenteriae.Fig. 22.11 The appearance of the large intestional mucosa
In Shigella dysentery.
Slide55© University of Alabama at Birmingham, Dept. of Path.
Shigella
colitis (Campylobacter or Salmonella would look much the same
.)
Slide56Diarrhea of Shigella – WBCs & RBCs
CDC
Slide57E. coli
Type
Clinical Features
Complications
ETEC
(
Enterotoxigenic
)
Watery diarrhea, travelers diarrhea
rare
EHEC
(
Enterohemorrhagic
)
Bloody diarrhea
Hemolytic uremic syndrome, TTP (mostly 0157:H7)
EIEC
(
Enteroinvasive
)
watery diarrhea or bloody diarrhea
rare
EAEC
(
Enteroaggregative
)
watery diarrhea or bloody diarrhea
rare
EPEC (
Enteropathogenic
)
Watery diarrhea or bloody diarrhea, mainly in children
May be protracted
Slide58Enterohemorrhagic
Escherichia coliNon-sorbitol fermenting Escherichia coli
(Escherichia coli 94% + for sorbitol fermentation) Majority of enterohemorrhagic strains positive for somatic O157 and flagellar H7 antigens (O104 and O111 strains have caused outbreaks in the US)Bacteriophage-mediated production of Shiga-like toxin (Stx1 or Stx2) which are cytotoxic (verotoxin)Accounts for 15% to 36% of cases of bloody diarrhea
Slide59Enterohemorrhagic
Escherichia coliAbdominal cramps and watery diarrhea 3 to 8 days following ingestion of contaminated food (undercooked beef, raw milk, fresh produce) or water
Shiga toxin absorbed from intestine and damages vascular endothelial cells (intestinal mucosa and kidney) Watery diarrhea followed by grossly bloody diarrheaUncomplicated illness lasts 1 to 12 daysUse of antibiotics contraindicated (phage-mediated production of Shiga toxin enhanced by ampicillin, norfloxacin, and other antibiotics)
Slide60Complications of Hemorrhagic
Escherichia coli ColitisFever and neutrophilic leukocytosis herald hemolytic uremic syndrome (HUS) (thrombocytopenia,
oliguria, hematuria, microangiopathic hemolytic anemia)HUS in 8% of infections in children with a 3% to 5% mortality
Slide6161
Shiga-toxin (E. coli)O157:H7 Enterohemorrhagic E. coli (EHEC)Serious manifestations – hemolytic uremic syndrome, neurologic symptomsShiga-toxin gene present on bacteriophage genomeType III secretion system
Slide6262
The Type III secretion is a complex bridge formed by the bacteria, enabling binding to the host cell, thereby allowing the bacteria to insert its products in the host cell. Fig. 22.12 Type III secretion system.
Slide6363
Non-shiga-toxin (E. coli)Enterotoxigenic – traveler’s diarrheaEnteroinvasive – no exotoxinEnteropathogenic – similar to EHEC
Enteroaggregative – chronic diarrhea
Slide6464
CampylobacterMost common bacterial cause of diarrheaRelated to Guillain-Barre syndrome (GBS) – paralysis
Slide65Campylobacter
Mainly C. jejuniTransmission from infected animals or food products, fresh or salt waterWatery diarrhea or dysenteryMay be complicated by Guillain-Barr
é and IPSID (Immunoproliferative small intestinal disease)
Slide66Bacterial infection:
Campylobacter
Clinical Symptoms may evolveFever and general malaise, sometimes without GI symptomsWhen present, GI symptoms include bloody diarrhea, abdominal pain and weight loss. Presenting Signs and Symptoms
Slide67Campylobacter
jejuni…Spirilla morphology
Gram Negative StainMotileRole as an Enteric Pathogen© 2007 Aichi Prefectural Institute of Health
Slide68Relatively fragile
Microaerophilic organism.Seems to be well adapted to birds
Campylobacter jejuni
Slide69C
ampylobacteriosisKnown as campylobacter enteritis or gastroenteritis.Infection causes watery or sticky diarrhea, which contain blood and fecal leukocytes.
Other symptoms include: fever, abdominal pain, nausea, headache and muscle pain.
Slide70Erythromycin 500 mg bid x 5 days (1st choice)
Fluoroquinolones are also effective, but resistance rates of 30-50% have been reported in some developing countries CampylobacterManagement and Treatment
Slide71Complications of
CampylobacteriosisEnteritis usually self-limiting (1 day to 1 week or longer)Guillain-Barré syndrome (structural homology of LPS O-antigen with human nerve gangliosides)
Post-infectious reactive arthritis (associated with HLA-B27)Bacteremia (rate of 1.5/1,000 intestinal infections)
Slide7272
Campylobacter jejuni has a unique S-shaped and spiral morphology, and is closely related to H. pylori.
Fig. 22.13 Scanning micrograph of Campylobacter jejuni, Showing comma, S, and spiral forms.
Slide7373
YersiniaHigh degree of abdominal painMistaken for appendicitisInfects the small intestineSome can affect the lymphatic system (intracellular)
Slide74Yersinia
enterocoliticaFermentative, rod-shaped or coccoid gram-negative bacteria, non-motile and metabolically inactive at 37
oC but motile and metabolically active at 22-30oCEnteropathogenic strains cytotoxic by penetratating human epithelial cellsInfection results in inflammatory ileitis (generally) and colitis (occasionally involving ascending colon) with mixed neutrophilic and mononuclear cell responseNecrosis of Peyer’s patches, mesenteric lymph node enlargement, and in severe cases thrombosis of mesenteric blood vessels with intestinal necrosis and hemorrhage
Slide75Yersinosis
Febrile diarrhea with abdominal pain 16 to 48 hours following ingestion of an infectious inoculumDuration of illness ranges from 1 day to a prolonged diarrhea of 4 weeks
Slide76Complications of
YersinosisCan simulate acute appendicitis (mesenteric lymphadenitis)Bacteremic dissemination with hepatic and
splenic abscess formationReactive arthritis associated with HLA-B27 histocompatibility antigen (10-30%)Exudative pharyngitis (8% of infections accompanied by fever but no diarrhea)
Slide77Treatment
Safe food handlingY. enterocolitica
is suscestible to amg,chloram, tetra, TMP/SMZ,pip, cipro, ß lactamase, resis to pen, ampi, 1. gen. ceph
.
Patients
with
septicemia
should
receive
antb
.
Y.
pseudotuberculosis
usually
not
require
antb
, but
with
septicemia
ampi
or
tetra
Slide7878
Clostridium difficilePseudomembranous colitis or antibiotic associated colitisCapable of superinfecting the large intestine due to drug treatmentsEnterotoxins
Slide79Slide8080
A mild and more severe case of antibiotic-associated colitis.Fig. 22.14 Antibiotic-associated colitis.
Slide81Pseudomembranes:
Irregular yellow plaques of necrotic debris (black arrow) with intervening edematous bowel mucosa (white arrow) in an 87-year-old woman. These findings are consistent with pseudomembranes caused by Clostridium difficile infection.
Schroeder, 2005
Slide82♦ Pathogenesis
Accountable for 15-25% of antibiotic-associated diarrhea.Fecal-oral route transmission.Three steps to C. Difficile diarrhea:
Alteration of the normal fecal flora↓ Colonic colonization of C. difficile↓ Growth and production of its toxins LaMont, 2006Poutanen & Simor, 2004
Slide83Pathogenesis of C. difficile infection
Uncolonized patient↓Antibiotic exposure↓
Disruption of colinic microflora↓C. Difficile ingestion & colonization ↓ ↓ Good IgG Poor IgG ↓ ↓ Asymptomatic carrier Production of toxins ↓ Colonic mucosal damage ↓ Clinical Disease
Schroeder, 2005
Slide84♦ Risk Factors
Antibiotics – fluoroquinolones, cephalosporins, clindamycins, penicillinsMedications:Proton pump inhibitorHistamine-2 receptor blockersNon-steroidal anti-inflammatories (except aspirin)LaxativesNarcoticsAntiperistaltic drugs
Advanced age ( ≥ 65yrs.)Chemotherapy
Slide85Medical/Surgical procedures
Gastrointestinal surgeryEnemasEnteral tube feedingsEndoscopyUnderlying illness and its severityInflammatory bowel diseaseDiabetes mellitus/HyperthyroidismLeukemia/Lymphoma
Liver/Renal failureHistory of C. difficile associated diarrheaProlonged hospital stay/Nursing home resident Louie & Meddings, 2004McDonald, Owings, & Jernigan, 2006Melillo, 1998Poutanon & Simor, 2004
Slide86Toxic Megacolon
LaMont, 2006
Slide87♦♦ Diagnostic Testing
LaMont, 2006
Slide88♦ Treatment
Discontinue the offending agentIf unable:Choose an antibiotic less frequently associated with antibiotic-associated diarrhea (aminoglycosides, sulfonamides, macrolides, vancomycin, tetracyclines)Prescribe Metronidazole 500mg PO TID throughout the needed course of antibiotic therapy and for 7 days after.
LaMont, 2006Schroeder, 2005
Slide8989
Vibrio choleraeCholeraUnique O and H antigensCholera toxin (CT) – A-B toxinBacteria never enter host cellsHeavy lost of fluid “rice-water stool”Untreated cases can be fatal
Slide9090
Vibrio cholerae has a unique curved shaped and single polar flagellum.Fig. 22.15 Vibrio cholerae
Slide91Slide9292
Common nonbacterialCryptosporidiumRotavirus
Slide9393
CryptosporidiumProtozoan infectionZoonoticOocystsIntracellularAIDS patients are at riskAssociated with fresh water outbreaks
Slide9494
A SEM of Cryptosporidium shows attachment to the intestinal epithelium, prior to intracellular invasion. Fig. 22.16 Scanning electron micrograph of Cryptosporidium
Slide9595
Acid-fast staining enables oocysts to be identified, as they stain red or purple.Fig. 22.17 Acid-fast stain in Cryptosporidium
Slide9696
RotavirusResponsible for most morbidity and mortality from diarrheaBabies lacking maternal antibodies are at risk Unique morphological appearance
Slide9797
A feces sample containing Rotavirus, which has a unique “spoked-wheel” appearance.Fig. 22.18 Rotavirus visible in a sample of feces from
A child with gastroenteritis.
Slide98Acute
diarrhea is an episode of diarrhea of <14 days in duration
Persistent diarrhea is of >14 days in durationChronic diarrhea lasts >30 days
Slide9999
Features of acute diarrhea.Checkpoint 22.5 Acute diarrhea
Slide100100
Acute diarrhea with vomitingFood poisoning - toxinStaphylococcus aureusBacillus cereusClostridium perfringens
Slide101Classic Syndromes: Acute food poisoning
Similar illness in 2 or more personsEpidemiologic evidence of common food sourceOnset of symptoms typically within 6 hours of ingestionNausea and vomiting prominent
Preformed toxin of S. aureus or B. cereusLonger incubation periods for C. perfringens
Slide102102
Features of acute diarrhea with vomiting.Checkpoint 22.6 Acute diarrhea with vomiting
Slide103103
Chronic diarrheaEnteroaggregative (EAEC) E. coliCyclospora cayetanensisGiardia lambliaEntamoeba histolytica
Slide104104
EAEC E. coli can be identified by its ability to adhere to human cells in aggregates.Fig. 22.19 Enteroaggregative E. coli adhering to epithelial cells.
Slide105105
The protozoan Cyclospora can be identified by the acid-fast stain, in which large cysts stain pink to red and have a wrinkled outer wall.
Fig. 22.20 An acid-fast stain of Cyclospora in a human Fecal sample.
Slide106106
The protozoan Giardia is typically transmitted by its cysts, which eventually germinates into the trophozoite and damages the jejunum.
Fig. 22.21 The “face” of a Giardia lamblia trophozoite.
Slide107107
Entamoeba histolytica have different cellular forms, which includes a trophozoite that contains a karyosome and hosts cells (rbc) and bacteria, and a mature cyst which undergoes excystment.
Fig. 22.22 Cellular forms of Entamoeba hystolytic
Slide108108
Features of chronic diarrhea.Checkpoint 22.7 Chronic diarrhea.
Slide109Slide110History
Onset and duration of diarrheaTiming of exposure to potential pathogensTravel, ingestion history, environment, recent medications, ageCharacter of stool
Volume, presence of blood, mucus, or pusAssociated symptoms and signsAbdominal pain, fever, vomiting, dehydration
Slide111Physical examination
Vital signs: Fever, tachycardiaAbdominal tenderness or painSigns of dehydration
Blood in stool
Slide112Evaluation of Infectious Diarrhea
Stool studiesfecal leukocytes and RBC/bloodBacterial cultureInclude
C. difficle toxin assayMay need to request EHEC screenEndoscopic evaluation may be useful in someespecially for bloody diarrhea or chronic diarrhea
Slide113Laboratory investigations
Stool WBC may be
ABSENT
PRESENT
VARIABLE
V.
cholerae
Enterotoxigenic
E. coli
Virus
E.
Histolytica
Food poisoning
Shigella
Campylobacter
Invasive
E. coli
Salmonella
Non-cholera
vibrio
Yersinia
C.
difficile
Slide114Laboratory investigation
Not routinely indicated
Low yield 1.5 -2.4%Not useful in initial managementMore sensitive and specific in stool with WBC
Slide115Fecal PMNs
Common in
Shigella, Campylobacter, EHEC, EIEC, C. diff Rare in Salmonella, Yersinia, ETEC, EAEC
Slide116MANAGING INFECTIOUS DIARRHEA
Initial rehidrationPerform thorough clinical and epidemiological evaluation
Perform selective fecal studiesInstitute selective therapy for Traveler’s diarrheaShigellosis Campylobacter infectionAvoid administering antimotilty agentsSelectively administer available vaccines
Slide117Oral rehydration solutions
Slide118Treatment of Diarrhea
Treatment of specific etiologyNon-specific treatmenthydrationAbsorptions (Kaopectate®)
Bismuth Antiperistaltics/opiate derivativesFiber supplementation
Slide119TUS 2010
Kırk iki yaşında erkek hasta akut karın bulguları ile acil servise başvuruyor. Hastanın sağ alt karın bölgesinde belirgin olmak üzere tüm karın bölgelerinde hassasiyet ve defans saptanıyor. Ayakta karın grafisinde serbest hava bulunan hastanın öyküsünden 3 hafta önce yaptığı bir seyahat sonrası ishal başladığı öğreniliyor. Bu hasta için en olası tanı aşağıdakilerden hangisidir?A) Akut apandisit
perforasyonuB) Meckel divertiküliti perforasyonuC) Tifo enterit perforasyonuD) Tüberküloz enterit perforasyonuE) Campylobacter enfeksiyonu perforasyonu
Slide120TUS 2010
Kırk iki yaşında erkek hasta akut karın bulguları ile acil servise başvuruyor. Hastanın sağ alt karın bölgesinde belirgin olmak üzere tüm karın bölgelerinde hassasiyet ve defans saptanıyor. Ayakta karın grafisinde serbest hava bulunan hastanın öyküsünden 3 hafta önce yaptığı bir seyahat sonrası ishal başladığı öğreniliyor. Bu hasta için en olası tanı aşağıdakilerden hangisidir?A) Akut apandisit perforasyonu
B) Meckel divertiküliti perforasyonuC) Tifo enterit perforasyonuD) Tüberküloz enterit perforasyonuE) Campylobacter enfeksiyonu perforasyonu
Slide121TUS 2012
Rotavirus enfeksiyonlarının en sık görüldüğü yaş grubu aşağıdakilerden hangisidir?A) 4 aydan küçük olanlarB) 4 ay ile 2 yaş arasında olanlarC) 2 yaş ile 4 yaş arasında olanlarD) 5 yaş ile 7 yaş arasında olanlarE) 8 yaşından büyük olanlar
Slide122TUS 2012
Rotavirus enfeksiyonlarının en sık görüldüğü yaş grubu aşağıdakilerden hangisidir?A) 4 aydan küçük olanlarB) 4 ay ile 2 yaş arasında olanlarC) 2 yaş ile 4 yaş arasında olanlarD) 5 yaş ile 7 yaş arasında olanlar
E) 8 yaşından büyük olanlar
Slide123TUS 2013
45 yaşında erkek hasta akşam yemekle beraber alkol aldıktan 1 saat sonra ani başlayan karın krampları, baş dönmesi, bulantı, yüzde kızarma ve sıcak basması şikayetleriyle acil servise başvurdu. Öyküsünden 4 gündür diş enf nedeniyle adını hatılamadığı bir antibiyotik aldığını söyledi. Fizik muayenesinde kan basıncı 80/40 mmHg nabzı 140/dk. Aşağıdaki ilaçlardan hangisinin buna yol açması en olasıdır?
a) Tetrasiklin b) Klaritromisin c) Klindamisin d) Amoksisilin e) Metronidazol
Slide124TUS 2013
45 yaşında erkek hasta akşam yemekle beraber alkol aldıktan 1 saat sonra ani başlayan karın krampları, baş dönmesi, bulantı, yüzde kızarma ve sıcak basması şikayetleriyle acil servise başvurdu. Öyküsünden 4 gündür diş enf nedeniyle adını hatılamadığı bir antibiyotik aldığını söyledi. Fizik muayenesinde kan basıncı 80/40 mmHg nabzı 140/dk. Aşağıdaki ilaçlardan hangisinin buna yol açması en olasıdır?
a) Tetrasiklin b) Klaritromisin c) Klindamisin d) Amoksisilin e) Metronidazol
Slide125TUS 2013
45 yaşında erkek hasta akşam yemekle beraber alkol aldıktan 1 saat sonra ani başlayan karın krampları, baş dönmesi, bulantı, yüzde kızarma ve sıcak basması şikayetleriyle acil servise başvurdu. Öyküsünden 4 gündür diş enf nedeniyle adını hatılamadığı bir antibiyotik aldığını söyledi. Fizik muayenesinde kan basıncı 80/40 mmHg nabzı 140/dk. Aşağıdaki ilaçlardan hangisinin buna yol açması en olasıdır?
a) Tetrasiklin b) Klaritromisin c) Klindamisin d) Amoksisilin e) Metronidazol
Slide126One
of the most common alcohol-antibiotic interactions
is with the antimicrobial agent metronidazole (Flagyl). Metronidazole is used for a variety of infections, including gastrointestinal, skin, joint and respiratory tract infections
.
Taking
metronidazole
with
alcohol
may
result
in a
reaction
called
a “
disulfiram
-
like
reaction
”. A “
disulfiram
-
like
reaction
”
may
include
nausea
,
flushing
of
the
skin,
stomach
cramps
,
vomiting
, headaches, rapid heart rate, and difficulty breathing.A similar reaction may occur with other antibiotics.
Slide127TUS 2013
Gastroenterit kliniği olan bir hastanın dışkısından clostridum dif. toksin a/b izole edilmiş. EN OLASI neden nedir? a) antibiyotik kullanımıb) besin zehirlenmesi
c) rotavirüs enteritid) Stafilokok zehirlenmesi
Slide128TUS 2013
Gastroenterit kliniği olan bir hastanın dışkısından clostridum dif. toksin a/b izole edilmiş. EN OLASI neden nedir? a) antibiyotik kullanımı
b) besin zehirlenmesic) rotavirüs enteritid) Stafilokok zehirlenmesi
Slide129TUS 2013
Pirinç suyu ishali olan hastada yapılan dışkı yaymasında sinek uçuşması görüntü var? a) Rotavirüsb) Salmonellac) Campylobacterd)
Vibrio
Slide130TUS 2013
Pirinç suyu ishali olan hastada yapılan dışkı yaymasında sinek uçuşması görüntü var? a) Rotavirüsb) Salmonellac) Campylobacterd)
Vibrio
Slide131TUS 2013
8 haftadır günde 6-7 kez süren ishal yakınması. tenezm hissi var. geceleri ishalden dolayı uyuyamıyor. Gaita mikroskopisinde lökosit eritrosit gözlendi . tanı? a- kolon tipi- enflamatuar
b- kolon tipi nonenflamayuar c-i barsak tipi enflamatuar d- i. barsak tipi non inflamayuar
Slide132TUS 2013
8 haftadır günde 6-7 kez süren ishal yakınması. tenezm hissi var. geceleri ishalden dolayı uyuyamıyor. Gaita mikroskopisinde lökosit eritrosit gözlendi . tanı? a- kolon tipi- enflamatuar
b- kolon tipi nonenflamayuar c-i barsak tipi enflamatuar d- i. barsak tipi non inflamayuar
Slide133TUS 2013
Aşağıdaki bakterilerden hangisinin insanda oluşturduğu hastalıkların patogenezinde, bakteri tarafından üretilen ekzotoksin rol oynamaz?A) Vibrio
choleraeB) Corynebacterium diphtheriaeC) Haemophilus influenzaeD) Staphylococcus aureusE) Shigella dysenteriae
Slide134TUS 2013
Aşağıdaki bakterilerden hangisinin insanda oluşturduğu hastalıkların patogenezinde, bakteri tarafından üretilen ekzotoksin rol oynamaz?A) Vibrio
choleraeB) Corynebacterium diphtheriaeC) Haemophilus influenzaeD) Staphylococcus aureusE) Shigella dysenteriae
Slide135TUS 2013
Aşağıdaki gastroenterit etkenlerinden hangisinin tek doğal kaynağı insandır?A) Campylobacter jejuni
B) Escherichia coli O157:H7C) Salmonella TyphimuriumD) Vibrio parahaemolyticusE) Shigella dysenteriae
Slide136TUS 2013
Aşağıdaki gastroenterit etkenlerinden hangisinin tek doğal kaynağı insandır?A) Campylobacter jejuni
B) Escherichia coli O157:H7C) Salmonella TyphimuriumD) Vibrio parahaemolyticusE) Shigella dysenteriae
Slide137TUS 2013
Otuz altı yaşındaki erkek hasta, dışarıda yemek yedikten 24 saat sonra ani kusma, ishal ve baş ağrısı ile acil servise başvuruyor. Daha sonra aynı şikâyetlerle 6 hastanın daha acil servise başvurduğu öğreniliyor.Bu hastada gastroenterite neden olan virus büyük olasılıkla aşağıdakilerden hangisidir?
A) CoronavirusB) Hepatit A virusuC) NorovirusD) AdenovirusE) Echovirus
Slide138TUS 2013
Otuz altı yaşındaki erkek hasta, dışarıda yemek yedikten 24 saat sonra ani kusma, ishal ve baş ağrısı ile acil servise başvuruyor. Daha sonra aynı şikâyetlerle 6 hastanın daha acil servise başvurduğu öğreniliyor.Bu hastada gastroenterite neden olan virus büyük olasılıkla aşağıdakilerden hangisidir?
A) CoronavirusB) Hepatit A virusuC) NorovirusD) AdenovirusE) Echovirus
Slide139TUS 2014
Slide140STEC’in
ürettiği Shigalike toksinleri ilk olarak Vero hücre kültüründe gözlenmiş olduğundan verotoksin olarak da adlandırılmaktadır. Shigalike toksini Vero hücrelerine
toksik etki gösteren, protein sentezini inhibe eden ve lizojen bir bakteriyofaj tarafından kodlanan sitotoksinlerdir. Bunlar; Shigella dysenteriae tip 1’in oluşturduğu toksin ile aynı olan shigalike toksin1 (stx 1; verotoksin 1) ve daha az benzeyen
shigalike
toksin 2’dir (
stx
2;
verotoksin
2).
Slide141TUS 2014
Slide142TUS 2014
Slide143TUS 2015
Slide144TUS 2015
Slide145TUS 2015
Slide146TUS 2015