GIT Infections Hagni20141

8/10/2019 GIT Infections Hagni20141

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GASTROINTESTINALTRACT INFECTIONS

E Hagni Wardoyo

Mataram, 16 Oct 2014

1



3



Importance of gut microbiota4

Almost 99% highly populated with anaerobic bacteria acidity prevent pathogen to colonize

Gut receive nearly 800grams of food and 8 liters ofwater everyday just make sure the first defensemechanisms rely on gastric juice

Gut’s microbiota exposed to all kinds of oral antibioticsand most parenteral antibiotics potent to spreadresistance clone

Surveillance study to describe resistance to antibiotics in thecommunity is well-defined by investigate resistance toantibiotics pattern of certain of microbiota such as E. coli



5



Food-associated infection vs food poisoning

6

Food poisoning Food-associatedinfection

True food poisoning occurs afterconsumption of food containing toxins,

which may be chemical (e.g. heavy metals)or bacterial in origin (e.g. from Clostridium

botulinum or Staphylococcus aureus)

Infection

associatedwith

consumptionof

contaminatedfood



Cause of disease Karakteristik

Food

infection

Infeksi m.o Makanan sebagai

vehicle patogen

multiplikasi infeksiFood

poisoning

Kerja toksin

(kemis, berasal

dari bakteri

m.o penghasil toksin

mungkin mati saat food

processing tetapi toksin

tetap ada

7



Diare, dipertimbangkan sebagai :8

Mekanisme host untukmenghilangkan m.o penyebab

Mekanisme penyebaraninfeksi ke host lain

Diare



PATHOGENIC MECHANISMS9

Inoculum Size

AdherenceToxin Production

Invasion




Inoculum Size


Invasion

Shigella, enterohemorrhagic Escherichia coli 10 – 100

bacteria can produce infection, Salmonella may have to

grow in food for several hours before reaching an effective

infectious dose




Inoculum Size


Invasion

V. cholerae, adheres to the brush border of small-

intestinal enterocytes via specific surface adhesins,including the toxin coregulated pilus and other

accessory colonization factors

ETEC produces an adherence protein called

colonization factor antigen that is necessary for

colonization of the upper small intestine




Inoculum Size


Invasion

cholera toxin, increase activity of cAMP in the intestinal

mucosa, which increases Cl – secretion and decreases

Na+ absorption, leading to loss of fluid and the

production of diarrhea

ETEC produce a protein called heat-labile enterotoxin

(LT) that is similar to cholera toxin/ heat-stable

enterotoxin (ST) which causes diarrhea by activation of

guanylate cyclase and elevation of intracellular cyclicGMP

Enteric pathogens that produce cytotoxins (destroy

intestinal mucosal cells dysentery): Shigella

dysenteriae type 1, Vibrio parahaemolyticus, andClostridium difficile. and Shiga toxin – producing strains of

E. coli produce potent cytotoxins and have been

associated with outbreaks of hemorrhagic colitis &HUS




Inoculum Size


Invasion

Shigella and EIEC caused invasion of mucosal epithelial cells,

intraepithelial multiplication, and subsequent spread to

adjacent cellsSalmonella causes inflammatory diarrhea by invasion of

the bowel mucosa

Salmonella typhi and Yersinia enterocolitica can penetrate

intact intestinal mucosa, multiply intracellularly in Peyer’s

patches and intestinal lymph nodes, and then disseminatethrough the bloodstream to cause enteric fever



14

Harrisons Infectious Diseases, p261



15

HOST DEFENSES



Intestinal damage

Infection of the gastrointestinal tract can cause damage locally or at distant sites

16



Many cases of diarrheal disease are

not diagnosed

Self limiting

medical and laboratory facilities are unavailable

patient's recent food and travel history, and

macroscopic and microscopic examination of the

feces for blood and pus can provide helpful clues

17



E.coli, Salmonella spp

Enterobacteriaceae18



Enterobactericeae

http://faculty.irsc.edu/FACULTY/TFischer/images/enterobacteriaceae.jpg



Enterobactericeae

General characteristic

Gram negative rods

Facultative anaerob

Ferment glucose

Oxidase-negative

Reduce nitratenitrit

+ -



Biochemical Test:

Analytic Profile Index Test

Biochemical Test for

Enterobactericae

Before performing test, should

be confirmed:

- Gram – rod

- Oxidase -

Image of API Test

Interpretation



Antigenic structureO Antigens

- Are Ag of the outer membrane

lipopolysaccharide (LPS)- Its antigenic specificity is determined by the

composition of the sugars that form the longterminal polysaccharide side chains linked tothe core polysaccharide and lipid A.

H Antigen

- Are Ag from Motile strains that have proteinperitrichous flagella, which extend well beyond thecell wall

- Many of the Enterobacteriaceae have surface pili,

which are antigenic proteins but not yet part ofany formal typing scheme.

K Antigen

- Are Ag from well-defined capsule or an

amorphous slime layer



Pathogenecity Determinants

AdhesionFactors

Attachmentfimbriae

attachmentpili

colonizingfactor

antigens(CFAs).

Invasivefactors

Proteinslocalized inthe outer

membrane(invasins)

thatfacilitatethe invasionof target

cells.

Toxins

Exotoxin

Cytotoxin

Enterotoxin

Endotoxin

Serumresistance Phagocytosis

resistanceCumulation

of Fe+

Resistanceto the

membrane

attack

complex of

the

complement

system

Makessurvival in

phagocyte

s possible.

Resistance

against

defensins

and/oroxygen

radicals

Active

transport

of Fe2+

by sidero-

phores in

the

bacterial

cell



E. coli24



GENERAL CHARACTERISTICS

• The Gram-negative• straight rods are

peritrichously flagellated

• Lactose is broken downrapidly.

• The complex antigenstructure of these bacteriais based on O, K, and Hantigens. Fimbrial antigenshave also been described.

• Specific numbers havebeen assigned to theantigens, e.g., serovarO18:K1:H7



GENERAL CHARACTERISTICS (2)

A member of the normalintestine flora in humansand animals indicatorfor faecal contaminationof drinking water

The bacteria becomespathogen either:

- Reach tissue outsidenormal intestinal (UTI90% caused by E.coli

- Cause diarrhea in theintestine due to specificvirulence properties

Guideline regulation

Drinking water Bathing water

100 ml of drinkingwater must not

contain any E. coli

100 ml of Surfacewater approved for

bathing should notcontain more than

100 (guideline

value) to 2000

(absolute cutoffvalue) E. coli

Havelaar, et al,2001, WHO Guidelines: The current position



There are six distinct groups of E. coli with different

pathogenetic mechanisms

1. enteropathogenic E. coli (EPEC),

2. enterotoxigenic E. coli (ETEC),

3. enterohemorrhagic E. coli (EHEC),

4. enteroinvasive E. coli (EIEC),

5. enteroaggregative E. coli (EAEC), and

6. diffuse-aggregative E. coli (DAEC)

27



28

Bailey & Scott p879



PATHOGENESIS: EPEC

Enteropathogenic E. coli

(EPEC).

EPEC attach themselves to the

epithelial cells of the smallintestine by means of the EPEC

adhesion factor (EAF), then

inject toxic molecules into the

enterocytes by means of atype III secretion system



PATHOGENESIS OF EHEC

Enterohemorrhagic E. coli (EHEC).

These bacteria are the causative pathogens in the hemorrhagic

colitis and hemolytic-uremic syndrome (HUS) that occur in about

5% of EHEC infections, accompanied by acute renal failure,

thrombocytopenia, and anemia. EHEC possess specific, plasmid coded fimbriae for adhesion to

enterocytes. They can also produce prophage-determined

cytotoxins (shigalike toxins or verocytotoxins). Some authors

therefore designate them as VTEC (verotoxin-producing E. coli).

EHEC strains have been found in the O serogroups O157, O26,

O111, O145, and others. The serovar most frequently

responsible for HUS is O157:H7.



PATHOGENESIS: EIEC

Enteroinvasive E. coli (EIEC).

These bacteria can penetrate into the colonic mucosa,

where they cause ulcerous, inflammatory lesions. The

pathogenesis and clinical picture of EIEC infections arethe same as in bacterial dysentery



PATHOGENESIS OF ETEC

Enterotoxic E. coli(ETEC).

The pathogenicity ofthese bacteria is dueto the heat-labileenterotoxin LT(inactivation at 60 0Cfor 30 minutes) and the

heatstable toxins STaand STb (can toleratetemperatures up to100 0C).

Some strains produceall of these toxins,some only one.

LT is very similar to

cholera toxin. Itstimulates the activityof adenylate cyclase



STa stimulates the activity of guanylate cyclase. (cGMPmediates the inhibition of Na+ absorption and stimulates Cl –

secretion by enterocytes.)

ETEC pathogenicity also derives from specific fimbriae, so-

called colonizing factors (CFA) that allow these bacteria toattach themselves to small intestine epithelial cells, thuspreventing their rapid removal by intestinal peristalsis.

The enterotoxins and CFA are determined by plasmid genes.The clinical picture of an ETEC infection is characterized by

massive watery diarrhea. The disease can occur at any age.Once the illness has abated, a local immunity is conferredlasting several months.



PATHOGENESIS OF EAEC

Enteroaggregative E. coli (EAggEC).

These bacteria cause watery, and sometimes

hemorrhagic, diarrhea in infants and small children.

Adhesion to enterocytes with specific attachmentfimbriae. Production of a toxin identical to STa in ETEC.



DIAGNOSTIC LABORATORY

SPECIMENS

Collection of specimens depend on

localization of disease Urine

Blood

Pus Spinal Fluid



IDENTIFICATION AND DIAGNOSIS

Diagnosis

Like the rest of the Enterobacteriaceae, E. coli is readily

isolated in culture. For the diagnosis of intestinal

disease, separating the virulent types discussed abovefrom the numerous other E. coli strains commonly found

in stool presents a special problem.

Methods to detect virulence factors are expensive



A screening test for EHEC takes advantage of the

observation that the O157:H7 serotype typically fails to

ferment sorbitol.

Incorporating sorbitol in place of lactose in MacConkey

agar provides an indicator medium from which suspect(colorless) colonies can be selected and then confirmed with

O157 antisera. This procedure has become routine in areas

where EHEC is endemic.



DRUG RESISTANCE

Overussed/missussedof AB

Incorporation of ABinto animal feeds

transmission ofresistance plasmidsamong different

genera



TREATMENT

E. coli diarrheas aremild and self-limiting,treatment is usually notan issue

rehydration andsupportive measures arethe mainstays of therapy

AB therapy appear toincrease toxin release

and therefore increasethe risk of hemolytricuremic syndrome (HUS)

AB + AB -

ETEC EHEC

EIECEPEC

trimethoprim/sulfamethoxazole

(TMP-SMX) or quinolones reduces

the duration of diarrhea

Antibiotic usage should take intoconsideration AB resistance pattern



Salmonella40



EPIDEMIOLOGY

WHO reports: 16-17 million annual cases resulting

in 600.000 deaths

In the developing world mortality rate: 5-30%

The overall cases are under-reported

An accurate figure of S. Typhimarium infection is

difficult to determine only large outbreaks are

investigated whilst sporadic cases are less reported

Pui et al, 2011, International Food Research Journal 18: 465-478



Epidemiology




Morphology and Identification

Motile with peritrichousflagella

Non-fastidious grow onsimple media

Survive freezing in water for

long periods Optimum growth temp 35-

37 ⁰C

Sensitive to heat of 70⁰C orabove

Resistence: brilliant green,sodium tetrathionate, sodiumdeoxycholateinclusion inselective media



Classification of Salmonellae

Basis of Classification

Host range epidemiology

Biochemicalreaction

Structure ofO, H, Vi Ag

Common Misinterpretation

S. Typhi /S.typhimarium

Generallyused BUT

INCORRECT

S. entericasubspecies

entericaserotype

Typhimarium

Shorten:Salmonella

Typhimarium



Classification of Salmonellae

S. enterica

Subspecies

enterica(subspecies I)

Subspecies

salmae(Subspecies II)

Subspecies

arizonae(Subspecies IIIa)

Subspecies

diarizonae(Subspecies IIIb)

Subspecies

houtenae(Subspecies IV)

Subspecies

Indica(subspecies VI)

S. Bongori

(subspecies V)

Bases of classification:Phylogenetic tree by comparison with 16S rRNA sequence

Used by WHO and CDC

(Pui et al, 2011, International Food Research Journal 18: 465-478;Brooks et al, 2010, Jawets Medical Microbiology 25th Edition)



Characteristic of Salmonella sp

Charcteristic S. enterica subsp enterica

Usual habitat Warm blooded animals

Gram stain -

moltility +

Shape rodSize width; lentg (um) 0-7-1.5; 2.5

Bismuth sulphite agar Black colonies surrounded by brown to balck zone --.

Metallic sheen

Eosin-methylen blue

agar

Translucent amber to colorless colonies

Hektoen enteric agar Blue to green colonies, mostly black centers (H2S

producers)

Pui et al, 2011, International Food Research Journal 18: 465-

478



Charcteristic

• Bismuth Sulphite Agar

• Dark zone around metalic black colonies

• Hektoen Agar

• Blue to green colonies, mostly black centres (H2S

producers)

Image: Biokar, 2010; MDC, n.d

• Methylene Blue Agar

• Translusent amber to colorless colonies



STAGES OF PATHOGENESIS

(O’Connor, 2010)

Survival in

environment

transmission Adherence

Colonization

invasion

Spread in hostSurvival in host

Mechanism of disease

production



Survival in the environment

Biofilm formation- Mechanism of quorum

sensing (cell to cellcommunication)

- Survive on plastic cuttingboard

Biofilm formationgenetic elements:bcsABZC and bcsEFGoperon required forsynthesus ofexopolysaccharide

Salano et al, 2002, MolecularMicrobiology, 43(3), 793-808



Transmission

GENERAL DESCRIPTION

Primery infective to humans:

- Salmonella Typhi

- Salmonella choleraesuis,- Slamonella Paratyphi A & B

Reservoir:

- poultry

- pigs- rodent

- cattle

- pets (turtle &parrots)

GENERAL DESCRIPTION

Mean infection dose is

105- 108 (some as few as

103 ) Salmonella Typhi



Transmission

Salmonella in theenvironment

Transmit to vector:flies, rat, birds(shed in faeces)

Transmit toreservoir: cattle,swine, poultry,

eggs

Transmit to human(direct or indirect

contact)

- Contaminatedfood or drinks

- Improperhandling of food

Callaway et al, 2008, J.ournal of aAnimal Sciences, doi:10.2527/jas.2007-0457; Pui et al, 2011, International Food

Research Journal 18: 465-478

Salmonella outbreak:



Salmonella outbreak:

Source of food contamination




Pathogenesis

Host FACTOR

Gastric acidity

Normalintestinal

microbial flora

Local intestinalimmunity

VIRULENCE FACTOrS

Attachment factor

- adhesion molecules

involving fimbriae of S.Typhimarium

Invasion factor

- Type III secretion systemencoded by:

- Spi-1: enables . Typhimariumenter the intestinal

- SP-2 promote survival in themacrophages



Pathogenesis: Invasion

TRIGGER MECHANISM

- Bacteria injectsmolecules into the hostcell via Type III secretion

apparatus- These causes changes in

the host cell’s actincytockeleton causing

membrane rufflesleading to bacterialuptake



Pathogenesis



Clinical Manifestation

Enteric fever Enterocolitis

Becteriaemia ChronicCarrier state



57



IDENTIFICATION AND DIAGNOSIS

Diagnosis

The method of choice is detection of the pathogens in cultures. Serovar

classification is determined with specific antisera in the slide

agglutination test.

Culturing requires at least two days. Typhoid salmonelloses can be diagnosed indirectly by measuring the

titer of agglutinating antibodies to O and H antigens (according to

Gruber-Widal). To provide conclusive proof the titer must rise by at

least fourfold from blood sampled at disease onset to a sample taken at

least one week later.



Specimen collection

Isolation

Final identification:Serologic methodand biochemical

methods

PCR



THERAPY

EMERGING OF RESISTANCE

STRAIN

Increase resistance to firstline therapy:

- Ampicillin- Chloramphenicol

- Trimethoprim-sulfamethoxazole

MDR Salmonella enterica

FACTORS ASSOCIATED WITH

RESISTANCE

Use of antibiotic infood animals

Overused/missusedof antibiotic

Inadequate use ofantibiotic ( dosage

and duration)



TREATMENT

Ciprofloxacin 500mg (child 10 mg/kg upto 500mg)orally’ 12 hourly for 5-7 days

Azithromycin 1 g (child 20mg/kg upto 1 g) on the firstday, followed by 500 mg (child 10mg/kg upto 500mg)daily for a further 6 days (total initial tretament 7 days)



TREATMENT: CARRIAGE STATE

Eliminating the infection in chronic stool carriers of typhoidsalmonellae, 2 – 5% of cases, presents a problem.

Chronic carriers are defined as convalescents who are still

eliminating pathogens three months after the end of the

manifest illness. The organisms usually persist in the scarifiedwall of the gallbladder.

Success is sometimes achieved with high-dose administration

of anti-infective agents, e.g., 4-quinolones or aminopenicillins.

A cholecystectomy is required in refractory cases.



PREVENTION

PREVENTION

Typhoid vaccines have been available since before the turn of the

century. An intramuscular killed whole bacterial vaccine was widely used

by the military and in travelers but gave poor protection against

exposure to large doses of organisms.

Recently, a live oral vaccine containing an attenuated Typhi strain has

been licensed. Probably as effective as the injectable vaccine, it protects

as many as 70% of children in endemic areas. No human vaccine is

available for the other Salmonella serotypes.

When all is said and done, the provision of clean water supplies and the

treatment of carriers will lead to the disappearance of typhoid.



Reading task! Not to written down nor to

compile. But it is included in the exam!

Shigella sp65



Campylobacter66



Campylobacter

Campylobacter spp. are still responsible for sporadicinfections following improper manipulation of

poorly cooked meat. Poultry is a major source of

infection. Unpasteurized dairy products and water have been

found to be sources of limited outbreaks

Campylobacter jejunii and Campylobacter coli are

the most frequently encountered species responsible

for diarrhea.

67



68

Signs and symptoms vary from asymptomaticinfections and may include fever, abdominal cramps

and diarrhea with or without blood and fecal white

blood cells. Although generally self-limited, relapses and

chronic diarrhea are possible, as well as

extraintestinal infection including bacteremia.

Campylobacter jejunii infection is the most frequently



recognized infection preceding the development of

Guillain –Barré syndrome69

The mechanisms rely on the cross-reactivity betweenganglioside-like motifs present in Campylobacter

jejunii lipopolysaccharide and those of peripheral

nerves. Also, this species has been associated with

immunoproliferative small intestinal disease



V. cholera70

EPIDEMIOLOGY: MORTALITY RATE



Age-specific mortality rates for at-risk populations by WHO stratum in cholera-endemic

countries, 2005

EPIDEMIOLOGY:



The Global Burden of Cholera

Age

(years)

Kolkata, India

(May 2003 –Apr 2005)

Jakarta, Indonesia

(Aug 2001 –Jul 2003)

Beira, Mozambique

(Jan –Dec 2004)

Population Cases Rate Population Cases Rate Population Cases Ratea

< 1 698 10 7.16 3 121 25 4.01 – – –

1 – 4 3 782 53 7.01 12 620 39 1.55 1 686b 9 8.8

5 – 14 11 440 50 2.19 29 093 17 0.29 17 861c 38 3.5

> 14 42 143 78 0.93 115 423 62 0.27

Total 58 063 191 1.64 160 257 143 0.45 19 547 47 4.0

Mohammad Ali, Anna Lena Lopez, Young Ae You, Young Eun Kim, Binod Sah, Brian Maskery & John Clemens

Volume 90, Number 3, March 2012, 209-218A

Table 1. Cholera annual incidence rates (per 1000), by age group, in two Asian and one African site11



GENRAL CHARACTERISTIC

Gram negative, rods curved aerobic

motile, possessing a

polar flagellum V cholerae serogroups

O1 and O139 causecholera in humans,

while other vibriosmay cause sepsis orenteritis.

IDENTIFICATION CULTURE



IDENTIFICATION: CULTURE

Characteristic Description

Growth temp 37 °C

Growth condition aerobic or anaerobic

Optimum Ph 8.5 – 9.5

Other oxidase-positive,which differentiates

them from enteric

gram-negative

Non spore

convex, smooth, round

colonies that are

opaque and granular

in transmitted light

Colonies of V. cholerae O1 isolated from

bloodculture

on 5% sheep blood

IDENTIFICATION:



Thiosulfate Citrate Bile Sucrose

Selective media for V.cholera

Incubation 18-24 hourat 35 deg aerobically

Positive results:

thymol blue-bromothymol blue

yellow (acid is formed)against greenbackground

Stages of Pathogenesis:



g g

SURVIVAL IN ENVIRONMENT EXAMPLE : V. cholera

In the environment V.cholerahas a symbiotic relationship

with chitinous animal such as

crustaceans

The toxin-coregulated pilus

is required for thisassociation by mediating

biofilm formation on

chitinous surfaces



A person with normal gastric acidity may have to ingestas many as 1010 or more V cholerae to become

infected when the vehicle is water, because the

organisms are susceptible to acid

When the vehicle is food, as few as 102 – 104 organisms

are necessary because of the buffering capacity of

food. Any medication or condition that decreases

stomach acidity makes a person more susceptible to

infection with V cholerae.

PATHOGENESIS



PATHOGENESIS

Colonization Secretion of Cholera toxin

Colonization of the

upper intestine by

toxigenic V. cholera

Secretion of Cholera

toxin (CT) potententerotoxin that is

capable causing

profuse watery diarrea

PATHOGENESIS OF DISEASE:



VIRULENCE FACTOR

Virulence

factor

CT Cholera toxin

RT RTX toxin

HAP HA protease

T3SS & T6SS Type-III

secretion gene

cluster

Type-IV

secretion

systemTCP Toxin

regulated pilus

(adherence)

Mekalonos, J.J, 2011 The evolution of Vibrio cholera as a Pathogen

Pathogenesis:



g

Invasion

Toxin causes secretory diarrea by altering ioninfluxes across the intestinal by accomplishing

elevated cAMP in intestinal through activation of G

protein Toxin contains 2 sub unit: subunit B and subunit A

Sub unit B: binds to GM1 ganglioside receptor

Sub Unit A: catalyzes the ADP ribosylation of hostG protein activates adenylate cyclase Cl-

and HCO3- tranpsport into the lumen

P th i



Pathogenesis



82

Bailey & Scott p878

ANTIGENIC STRUCTURE



ANTIGENIC STRUCTURE

H antigen O lipopolysaccharide

H antigen flagellar

antigen

Heat labile.

Antibodies to the H

antigen are probably

not involved in theprotection of

susceptible hosts

V cholerae has Olipopolysaccharides that conferserologic specificity.

There are at least 139 O antigengroups.

V cholerae strainscause classiccholera:

- O group 1

- O group 139

Antibodies to the O antigens tendto protect laboratory animalsagainst infections with V cholerae



The V cholerae serogroup O1 antigen has determinantsthat make possible further typing; the serotypes are

Ogawa, Inaba, and Hikojima.

Two biotypes of epidemic V cholerae have been

defined, classic and El Tor. The El Tor biotype produces

a hemolysin, gives positive results on the Voges-

Proskauer test, and is resistant to polymyxin B.



V cholerae O139 is very similar to V cholerae O1 El Torbiotype. V cholerae O139 does not produce the O1

lipopolysaccharide and does not have all the genes

necessary to make this antigen. V cholerae O139 makes

a polysaccharide capsule like other non-O1 V choleraestrains, while V cholerae O1 does not make a capsule.

Cholera



Cholera

Vibrio cholerae serotype O1, the cause of cholera, can be subdivided into different biotypes with

different epidemiologic features, and into serosubgroups and phage types for the purposes of

investigating outbreaks of infection. Although V. cholerae is the most important pathogen of the

genus, other species can also cause infections of both the gastrointestinal tract and other sites

86



The production of an enterotoxin is central to the pathogenesis of cholera, but the organisms

must possess other virulence factors to allow them to reach the small intestine and to adhere

to the mucosal cells.

87



Specific Tests V cholerae organisms are further identified by slide

agglutination tests using anti-O group 1 or group 139

antisera and by biochemical reaction patterns.

The microscopic appearance of smears made from

stool samples is not distinctive. Dark-field or phase

contrast microscopy may show the rapidly motile

vibrios.

TREATMENT



TREATMENT

The most important part of therapy consists ofwater and electrolyte replacement to correct the

severe dehydration and salt depletion.

Many antimicrobial agents are effective against Vcholerae. Oral tetracycline tends to reduce stool

output in cholera and shortens the period of

excretion of vibrios.



90



Diarrheal disease is a major cause of illness and death in children in developing countries. This

illustration shows the proportion of infections caused by different pathogens. Note that in as many

as 20% of infections a cause is not identified, but many of these are likely to be viral. (Data from

the WHO.) (EPEC, enteropathogenic Escherichia coli; ETEC, enterotoxigenic E. coli.)

91





Rotavirus92

93



FOOD POISONING

Staphylococcus aureus



Staphylococcus aureus

Staphylococcus aureus produces at least eight immunogically distinct enterotoxins, the most

important of which are listed here. Strains may produce one or more of the toxins simultaneously.

Enterotoxin A is by far the most common in food-associated disease

94

Botulism



Botulism

There are three forms of botulism foodborne botulism;

infant botulism;

wound botulism

In foodborne botulism, toxin is elaborated by organismsin food, which is then ingested.

In infant and wound botulism, the organisms arerespectively ingested or implanted in a wound, andmultiply and elaborate toxin in vivo.

Infant botulism has been associated with feeding babieshoney contaminated with Cl. botulinum spores

95

Patogenesis



Patogenesis

flaccid paralysis progressive muscle weakness andrespiratory arrest.

Intensive supportive treatment is urgently required, and

complete recovery may take many months.

Improvements in supportive care have reduced the

mortality from around 70% to approximately 10%, but

the disease, although rare, remains life-threatening.

In addition, since botulinum toxin is one of the mostpotent biological toxins known to man, there is concern

regarding its potential use as an agent of biowarfare

96

Laboratory diagnosis



Laboratory diagnosis

Demonstrating the presence of toxin by injectingsamples of feces and food (if available) into mice

that have been protected with botulinum antitoxin

or left unprotected.

Culture of feces or wound exudate for Cl. botulinum

should also be performed.

PCR-based assays for toxin sequences and ELISA

tests for functional toxin activity.

97

Treatment



Treatment

antitoxin ↙ difficulty in breathing ↙ difficulty in swallowing

Antibiotics are generally used only for treatment of

secondary infections

98

Prevention



Prevention

It is not practicable to prevent food becomingcontaminated with botulinum spores, so prevention

of disease depends upon preventing the

germination of spores in food by:

maintaining food at an acid pH;

storing food at less than 4°C;

destroying toxin in food by heating for 30 minutes at

80°C.

99



100

Harrison’s Infectious Disease, p265

HELICOBACTER PYLORI AND GASTRIC



ULCER DISEASE

Virulence factors: a cytotoxin,

acid-inhibiting protein,

adhesins,

urease (which aids survival in the acidic environment) other factors which disrupt the gastric mucosa.

Studies suggesting that H. pylori may actually provideprotection from some esophageal and gastric cancers

The interrelationship between H. pylori and gastricdisease is thus complex and remains to be furtherclarified

101

Eradication of H. pylori



Eradication of H. pylori

Eradication of H. pylori to promote the remissionand healing of ulcers requires combination therapy

such as

a proton pump inhibitor and two antibiotics such as clarithromycin and amoxicillin

102





Antibiotic-associated diarrhea103



Sekian dan terimakasih104

GIT Infections Hagni20141

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