Diarrheagenic e. Coli Official

8/13/2019 Diarrheagenic e. Coli Official

http://slidepdf.com/reader/full/diarrheagenic-e-coli-official 1/23

DIARRHEAGENIC

ESCHERICHIA COLI

(E.COLI)

ENTEROPATHOGENIC E.COLI

(EPEC)

ENTEROINVASIVE E.COLI (EIEC)

PROFESSOR : DOCTOR MARWA

MEHESSEIN

ASSESSOR : DOCTOR MALAKA MOF

(MICROBIOLOGY DEPARTMENT)

NOR SALEHAH SAZLI (10-3-271)

NUR ATHIFAH MOHAMMAD BASRI (10-3-272)

NUR ‘ADILAH FAISAL SABRI (10-3-273)

NUR EZZATI AIZA MAHAT (10-3-274)

NUR AQILAH TAJUDEEN (10-3-275)



Escherichia Coli

Escherichia Coli (E. Coli) is a gram negative, rod shaped bacterium. It is one of the normal floras

present in intestine of human. It can turn pathogenic to human by causing food poisoning and

diarrhea to human. However, most of strains of E. coli are not pathogenic to human and

harmless. But there are also some strains which are pathogenic to human. They are

Enteropathogenic E. coli (EPEC), Enteroinvasive E. Coli (EIEC), Enterotoxigenic E. Coli (ETEC), and

Enterohaemorrhagic E. Coli (EHEC).

NUR EZZATI AIZA MAHAT (10-3-274)

TYPICAL ENTEROPATHOGENIC ESCHERICHIA COLI

(TYPICAL EPEC)

1. DEFINITION

Enteropathogenic Escherichia coli (EPEC) are one of the Escherichia coli that are

pathogenic to human by producing diarrhea. It is characterized by action of attaching

and effacing (A/E) on intestinal cells (Figure 1). It does not produce Shiga toxin, Shiga-

like toxin or verocytotoxin. Generally pathogenesis of EPEC characterized by microvilli

destruction, close adherence of bacteria to the intestinal epithelium and also

aggregation of certain cytoskeleton at the sites of bacterial attachments. It is further

differentiated to typical EPC and atypical EPEC based on their genetic characteristics,

serotype and virulence factors.

Figure 1 show the attaching and effacing of EPEC to the intestinal cells.

2. SEROTYPE



Majority of EPEC fall into an O:H serotypes. The serotypes can be seen in Table 1.

Table 1 shows several serotypes of typical and atypical EPEC strains.

Table 2 shows the types of intimin present in typical and atypical strains of EPEC

3. VIRULENCE

Intimin that is a virulence factor (non fimbrial adhesin). It is attaching and

effacing (A/E) protein which helps in adhesion of bacteria. It is expressed by the

bacteria and bind to its receptor that is translocated intimin receptor (TIR) which

is present in cytoplasm of intestinal cell. Posses EAF (EPEC adherence factor) plasmid.

Typical EPEC strains only show localized adherence to cultured epithelial cells

which shows compact micro colonies of bacteria or bacterial clusters (Figure 2).

EAF not necessarily cause A/E lesion but presence of the plasmid could enhance

the efficiency of the lesion. Secondly, there is also gene to encode for the bundle

forming pilli (BFP) in EAF plasmid. These sequences provide stabilization to the

micro colonies of bacteria by interconnecting them together. This is shown after

bacteria are in contact with the cells for 3 hours. BFP play a role in bacterial cell

adhesion and somehow this could enhance the A/E lesion formation.



Figure 2 shows 4 types of adherence of Escherichia coli to the cultured epithelial

cells.

Figure 3 shows different pathogenesis of different E coli.



4. PREVALENCE

Typical EPEC cause outbreaks of infantile diarrhea in developing countries.

Usually typical EPEC serotype rarely cause diarrhea in industrialized countries.

It is strongly related to diarrhea in child below 1 year of age. The frequency of

this serotype of diarrhea of adult or children below 1 year of age was rarely seen.This condition maybe due to increased resistance, developed immunity or loss of

some specific receptors for adhesion.

First typical EPEC strains isolated in different countries were of serotypes O55:H6

and O111:H2. These strains also present in industrialized countries but rare.

Recently, several studies showed that the emergence of typical EPEC has

decreased compared to atypical EPEC. This is maybe due to development of

some developing countries resulting in proper sanitation and improved hygiene.

5. RESERVOIR Typical serotypes of EPEC are not founded in animals. So this indicates that

human is the only living reservoir for this organism.

NUR AQILAH TAJUDEEN (10-3-275)

6. PATHOGENESIS

After exposure to the small intestinemucosa, the typical EPEC [tEPEC] introduce an

arm-like structure called bundle-forming pilus

[BFP] which promotes localized adherence.

tPEC also carry the LEE (locus enterocyte &

effacement) that encodes intimin and other

factors responsible for initiation of

attachment. Lesions produced by the tEPEC

known as A/E ; attaching and effacing. The

tissue related to the lesion area have

characteristic morphological changes such asdissolution of intestinal wall binding surface

accompanied by loss of epithelial microvilli at the site of bacteria intimately attached.

According to the journal “Principle Of Bacterial Pathogenesis” by Eduardo A. Groisman

– published by Elsevier, this incident explained by the formation of cup-like projections or

pedestral by the rearrangement of the cytoskeleton in host acini once the tEPEC reside. The



tEPEC also is able to move from pedestral to pedestral across the exterior of mucosal cells by

utilizing compound that present at the human mucosal tissue.

The interruption of tissue arrangement and molecular interaction at the site of lesions

consequently lead to loss of absorptive surface area that eventually leads to diarrhea.

7. DIARRHEA CAUSED BY TYPICAL EPEC

tEPEC strains contribute to predominant case of

infantile diarrhea, worldwide and represent major endemic

health threat to children under 6 months of age living in

developing countries

In contrast to other diarrheagenic Escherichia, EPEC does not produce any classicalprotein toxins but induces diarrhea by intimate binding to intestinal cells. Diarrhea is the result

of a series of signals triggered by the pathogen-host membrane interaction, which in turn

provokes reorganization of the cytoskeleton of the affected cell, involving accumulation of

polymerized actin beneath the adherent bacteria, with a consequent loss in microvillus

structure and effacement of the intestinal villi.

The diarrhea caused is characterized by the transient watery diarrhea, profuse watery

diarrhea plus vomiting and also persistent diarrhea. Blood and mucus are rarely present in stool

while the fever is either very low or absent. Noted that vomiting is very prominent in diarrhea

produced by tEPEC and may render oral rehydration therapy.

8. DIAGNOSIS

Lab Diagnosis

Bacterial isolation and

characterization.The swabs are

streaked onto plates of

MacConkey agar, and the plates

incubated at 37°C for 24 h. Lactose-positive and lactose-negative

colonies are identified biochemically by standard techniques using EPM, MILi, and Simmons citrate. The colonies are subcultured on tryptic

soy agar and also stored in brain heart infusion agar plus 50% glycerol

at −70°C for further utilization.



Serotyping

The O serotyping method was used to identify the isolates belonging to O serogroups

defined commercially. Isolates that can agglutinate with one of the specific commercial

pathogenic O antisera were defined as “suspected DEC” (sDEC) isolates, and they were

collected for further testing to see if they carried any of the six virulence genes mentionedbelow. For O-antigen determination, suspend the bacterial culture in 3 ml normal saline, heated

the mixture to 100°C for 1 h, and used the boiled suspension as the antigenic mixture. Then

mixed 1 drop of a specific O poly- or monovalent antiserum of “pathogenic E. coli immune sera”

(Denka Seiken, Tokyo, Japan) with the antigen preparation on a glass slide for 1 min and

observed the slide for agglutination.

For H-antigen determination, pass the bacterial culture through the semisolid medium with a

Craigie's tube to enhance the motile ability and then grew the culture in liquid broth. After the

addition of a formalin solution to achieve a final concentration of 1%, the suspension could be

used as an antigenic mixture and was mixed with specific H-antigen monovalent antiserum

(Denka Seiken) in a plastic tube. The agglutination results could be observed after the tubes

were kept in a 50°C water bath for 1 h.

However this serotyping is neither sensitive nor specific.

Polymerase Chain Reaction (PCR)

This test is responsible to differentiate and ensure the type of EPEC (typical or atypical)

strains as it act on specific primers for each gene that encodes intimin, Stx-gene (Shiga- toxins)

and bFp (bundle-forming pilus)

9. PREVENTION AND THERAPY

- Cook all ground beef and hamburger

thoroughly. Because groundbeef can turn brown

before disease-causing bacteria are killed, thus try

not to eat ground beef patties that are still pink in

the middle.



- Drink only pasteurized milk, juice, or cider. Commercial juice with an extended shelf-life

that is sold at room temperature (e.g. juice in cardboard boxes, vacuum sealed juice in

glass containers) has been pasteurized, although this is generally not indicated on the

label. Juice concentrates are also heated sufficiently to kill pathogens.

- Wash fruits and vegetables thoroughly,

especially those that will not be cooked.

- Children under 5 years of age,

immunocompromised persons, and the elderly should

avoid eating alfalfa sprouts until their safety can be

assured. Methods to decontaminate alfalfa seeds and

sprouts are being investigated.

- Drink municipal water that has been treated with chlorine or other effective disinfectants.

- Avoid swallowing lake or pool water while swimming.

- Make sure that persons with diarrhea, especially

children, wash their hands carefully with soap after

bowel movements to reduce the risk of spreading

infection, and that persons wash hands after changing

soiled diapers. Anyone with a diarrheal illness should avoid swimming in public pools or

lakes, sharing baths with others, and preparing food for others.

- Rehydration either by oral or parenteral solutions.

#Human milk is proved to be able to inhibit tEPEC adherent and in addition it contains antibody

against several EPEC virulence factors. Studies conducted by Dr. Alfredo G.Torres, professor of

the Texas University, USA among community of Latin America, shows that breast-feeding

infants less than 6 months contribute to lower the risk of tEPEC infection related to diarrhea of

serotype O111:H2 (non motile) and O119:H6

##Vaccines for EPEC are still under development. Sherwold L. Gorbash stated in his book-

“Infectious Diseases” ;( published by Lipincott, Willsons & William) that enthusiasism for an

EPEC vaccine are based on the intimin, bFp or secreted proteins as these encode for the

virulence and pathogenicity of the infections.



NOR SALEHAH SAZLI (10-3-271)

ATYPICAL ENTEROPATHOGENIC ESCHERICHIA COLI

(ATYPICAL EPEC)

1. Serotype

Atypical EPEC is more closely related to Shiga toxin-producing E. coli (STEC), and like STEC these

strains appear to be emerging pathogens.

The most studied EPEC strains belong to a series of O antigenic groups known as EPEC O

serogroups. Twelve EPEC serogroups were recognized by the World Health Organization in

1987: O26, O55, O86, O111, O114, O119, O125, O126, O127, O128, O142, and O158. These

serogroups include both typical and atypical EPEC strains, as well as other diarrheogenic E.

coli categories, mainly enteroaggregative E. coli (EAEC) . Furthermore, most of the strains of

each category correspond to specific serotypes in each O serogroup. The division of EPEC

strains into typical and atypical has important implications that are not yet fully appreciated.

EPEC can no longer be considered as a single group of enteropathogenic organisms.(1)(8)

Strains Serotypes

Typical O55:H6, O86:H34, O111:[H2],a O114:H2, O119:[H6], O127:H6, O142:H6, O142:H34

Atypical O26:H[11], O55:[H7], O55:H34, O86:H8, O111ac:[H8], O111:H9, O111:H25, O119:H2,

O125ac:H6, O128:H2

a

Brackets denote the frequent occurrence of non motile strains.(2)



2. Prevalence

Atypical EPEC are prevalent in both developed and developing countries. They appear to causedisease in a broader range of ages and have been associated with outbreaks in developed

countries.(4) The main difference between tEPEC and aEPEC is the presence of the EPEC

adherence factor (EAF) plasmid in tEPEC .This plasmid encodes the bundle-forming pilus (BFP),

which mediates localized adherence to intestinal cells, which is an essential property to

differentiate typical EPEC from atypical EPEC strains .

3. Reservoir

For atypical EPEC, both animals and humans can be reservoirs such as dogs, cats, cattle, sheep,

rabbits and monkeys. (3)

4. Virulence Factor(2)

A subset of EPEC, known as atypical EPEC, do not carry EPEC adherence factor plasmid (pEAF)

and hence do not produce bundle-forming pili (Bfp). Accordingly, their role in disease is

controversial. Recently, people investigated the causes of community-acquired gastroenteritis.



Among the infectious agents that were sought in these studies was atypical EPEC, which

emerged as the single most frequent pathogen in the study population.

Atypical EPEC strains frequently express enteroaggregative heat stable toxin (EAST1) and other

potential virulence factors not encoded in the LEE region (Table 1). Accordingly, there are two

kinds of atypical EPEC strains: those that express only the LEE-encoded virulence factors and

those that express both LEE and the non-LEE encoded virulence factors. Usually both kinds of

strains belong to a single clone.

All atypical EPEC serotypes, with exception of O125ac:H6, include both kinds of strains. All

strains of this serotype examined thus far show the aggregative adherence pattern and the LEE

region. The occurrence of more than one kind of strain in most atypical serotypes is another

interesting difference between typical and atypical EPEC.

Table 1

Virulence characteristics not encoded on the locus of enterocyte effacement (LEE) of atypical

enteropathogenic Escherichia coli (EPEC) strains isolated in São Paulo, Brazil

Serotype Characteristics

O26:[H11]a EAST1, E-hly

b

O55:[H7] EAST1, Afa

O111ac:[H8] E-hly

O111:[H9] E-hly

O119:H2 EAST1

O125ac:H6 AA

O128:H2 EAST1

a Brackets denote the frequent occurrence of nonmotile strains.

bEAST, heat-stable toxin 1 of EAEC; E-hly, EHEC hemolysin; AA, aggregative adherence; Afa, afimbrial

adhesin.

Typical and atypical EPEC strains also differ in adherence patterns. The typical strains show only

the LA pattern, while atypical strains may show the LAL (localized-like adherence) pattern , the

DA (diffuse adherence) pattern, or the AA (aggregative adherence) pattern (Figure 1). The LALpattern is characteristic of the strains of most serotypes and is mediated mainly by intimin . The

DA pattern is mediated by the Afa adhesin and the AA is mediated by an aggregative adhesin.

Typical and atypical EPEC also have some interesting differences with regard to the intimin

types (Table 2).



Table 2

Intimin types of typical and atypical enteropathogenic Escherichia coli (EPEC) serotypes

Intimin

types

Typical Atypical

Alpha O55:[H6],a O127:H6, O142:H6,

O142:H34

O111:[H9], O125ac:H6

Beta O111:[H2], O114:H2, O119:[H6] O26:H[11], O119:H2,

O128:H2

Gamma O55:[H7], O111ac:[H8]

Delta O86:H34a Brackets denote the frequent occurrence of nonmotile strains.



FIGURE 1: Adherence patterns of enteropathogenic Escherichia coli (EPEC) strains. Localized

adherence (LA), diffuse adherence (DA), aggregative adherence (AA), and localized adherence-

like (LAL). Magnification: X100.

5. Pathogenicity associated and diarrheaAtypical EPEC seems to be a more important cause of diarrhea. Patients infected with atypical

EPRC experienced mild, nondehydrating and non inflammatory diarrhea that was not

particularly associated with fever, vomitting or abdominal pain. However, the duration of

diarrhea in patients infected with atypical EPEC was significantly longer than that caused by

other species or where no pathogens were identified. Infection with atypical EPEC is associated

with prolonged diarrhea.(6)

6. Diagnosis

SOURCES / SPECIMENS: Stools and fecally contaminated material

Stool culture is a common method used to identify E. coli . DNA probes and techniques such as

PCR can be applied directly to clinical samples and food. Both typical and atypical EPEC are

most frequently identified by detection of the eae gene encoding the intimin protein. The

presence of the eae gene and demonstration of the absence of the verotoxin (enterotoxin)

gene are absolutely required for the molecular identification of EPEC .(7)

Serotyping of atypical strains is insufficient to assess the pathogenic properties of such strains,

because such organisms are quite variable in their repertoire of virulence determinants. We

have applied genetic and phenotypic analysis to a collection of 118 typical and atypical strains

of EPEC and non-EPEC serogroups, to identify common and unique virulence loci and traits inthese organisms. We determined the presence of and some characteristics of the LEE region,

and we searched for the occurrence of virulence-associated markers within the E. coli species.

Furthermore, we also determined their adherence patterns and serotypes. These data can be

used to detect atypical EPEC in clinical specimens and to elucidate the role of specific virulence

factors.(5)

7. Special treatment and vaccine

Treatment with trimethoprim/sulfamethoxazole (TMP-SMX) or quinolones reduces the

duration of diarrhea.

Treatment of fluid and electrolyte loss is usually achieved through oralrehydration. The use of the World Health Organization Oral Rehydration Salts (ORS) solution

has been recommended. Intravenous rehydration may be necessary for infants, individuals with

excessive vomiting, or those with severe dehydration. Bismuth subsalicylate may decrease the

amount of diarrhea and the duration of disease. Antimicrobial therapy is generally not

indicated, because of the self-limited nature of most of these diseases.



IMMUNIZATION: There are currently no vaccines approved for human use against

diarrheagenic E. coli.

NUR ‘ ADILAH FAISAL SABRI (10-3-273)

ENTEROINVASIVE ESCHERICHIA COLI

(EIEC)

Escherichia coli is a gram negative bacteria that normally inhabit the intestine of humans and

animals. There are strains that are harmless and some are pathogenic to humans.

For instance, EIEC. These organisms are pathogenically so closely related to Shigella species.This bacterium is classified as one of the diarrheogenic E.Coli.

The picture above showing Enteroinvasive E.coli

Source : blog.naver.com

1. DEFINITION

The strains of Escherichia Coli that invade or penetrates the gut mucosa and multiplies in the

colon epithelial cells, resulting Shigellosis like changes of the mucosa. This strain will produce

severe diarrhea illness that can resemble shigellosis expect for the absence of vomit, shorter

duration of illness and number of bowel movements.



2. SEROTYPES

There are about 243 serotypes that were studied and isolated in different regions of the

country over the period 1954-1988 and at least 106 organisms can cause illness.

The strain that are known as enteroinvasive E.Coli (EIEC) belong to the following O serotypes:

O28ac:NM; O29:NM; O112ac:NM; O121:NM; O124:NM; O124:H30; O164:NM; O167:NM.

EIEC 0124 is the most frequently isolated and is associated with sporadic cases in travellers.

Occasional outbreaks related to ingestion of contaminated water or food and from person to

person transmission of the disease.

EIEC 0164 is the most prevalent serotype that is isolated in Bulgaria.

3. PREVALENCE

Enteroinvasive Escherichia Coli was first isolated in Italy during the World War II.

This bacterium can cause dysentery but it is less reported than other etiological agents that can

cause diarrhoea all over the world.

Any age of people all over the world are susceptible to be infected by this bacterium, but can

cause severe manifestations in very young and very old persons.

It is most commonly isolated in developing countries and in rural and slum areas. This is due to

poor sanitation and low socioeconomic status. It is fewer in developed countries and in cities.

Outbreaks of food-borne infections due to EIEC have also been reported elsewhere, mostly

from unpasteurized milk and uncooked hamburger.

4. RESERVOIR

There is no specific known animal reservoir of EIEC. The primary source for EIEC is human.

Evidence suggested that illness is transmitted by contamination of food and water and from

person to person especially by food handlers.



Diagram above showing uncooked burger is a source of E.coli

Source : www.doctortipster.com

5. VIRULENCE FACTORS:

Virulence literally means the degree of pathogenicity of a group organisms indicated by the

ability of the organisms to invade tissues. Some of the methods are by adhesions, invasions and

produce toxins.

- Similarly to Shigella, EIEC has the ability to invade colonic epithelium and multiplies in the

cell causing destruction but it is apparently lack of fimbrial adhesins but do possesses adhesins

(an outer membrane protein) to interact with the epithelial mucosa. Unlike Shigella, they do

not produce LT or ST toxins.

- EIEC also secretes Ipas (Invasion plasmid antigens) A-D into a host cell and trigger several

events that will lead to membrane ruffling, phagocytosis and bacterial engulfment. Once

internalized, bacteria is surrounded by an inclusion membrane in the cytoplasm of the host cell.

-A system of Type III secretion genes are important to modify the host cell signalling and

membrane lysis are encoded in their plasmid. They possesses a plasmid that encodes an outer

membrane protein called IcsA that is located at one pole of the bacterial cell which propels

through the bacterial cytoplasm like head of ‘comet tail’. This will trigger actin polymerization



that is necessary for spread of the bacteria to another host cell by propelling outward and

pushing into the adjacent cell but not to the bloodstream therefore avoiding extracellular

response.

- The conclusion is, this bacteria can interact with the host cell invade by endocytosis lysis

of the endocytotic vacuole bacterial multiplication spread to adjacent cells.

The virulence factors for these steps are encoded on a 140 MDA plasmid. Defect of this plasmid

make it non-pathogenic.

SERENY Test is used to test the invasiveness of an organism including EIEC. This test is done by

inoculating the bacteria into pig’s eye and is positive if it results in mucopurulent and

keratoconjunctivitis.



Diagram above showing the mechanism of invasion of Enteroinvasive Escherichia Coli.

Source : www.nature.com

NUR ATHIFAH BINTI MOHAMMAD BASRI (10-3-272)

6. PATHOGENESIS

EIEC closely resemble Shigella in their pathogenic mechanisms. Although the infectivedose of Shigella is low (in the range of 10 to few hundred cells), volunteer feeding studies

showed that at least 106 EIEC organisms are required to cause illness in healthy adults. EIEC

penetrate and multiply within epithelial cells of the colon causing widespread cell destruction.

EIEC invade the epithelium from the intestinal lumen through M-cells. After reaching

the epithelium, they invade epithelial cells and are phagocytosed by resident macrophages.

EIEC escape the phagosome of both cells but while EIEC replicate within epithelial cells, they

induce apoptosis in macrophages. Bacteria are released and can invade the epithelial cells from

the basolateral side, move into the cytoplasm by triggering actin polymerization, and spread to

adjacent cells.

http://www.nature.com/






Figure 1: EIEC infection of colonic epithelial cells

Reference:http://www.hindawi.com/journals/bmri/2013/374395/fig1/

7. DIAGNOSIS

During the early (acute) phase of infection, large numbers of EIEC are excreted in the faeces.Contaminated feces samples can be examined in the laboratory for diagnosis. These EIEC

strains of E. coli can be distinguished from the many other E. coli in the feces by a number of

special tests (including immunochemical, tissue culture, and gene probe tests). The lab

diagnosis of EIEC takes about 3 days. Below are several tests that can be done to diagnose:

1. PCR :

Scientist has developed multiplex PCR assays that detect EIEC isolates. The targets selected

for EIEC isolates (and also Shigella spp) are ipaH. The ipaH sequences are present at multiple

sites on both the large invasive plasmid and the chromosomes in EIEC strains and also inShigella spp. These PCR were specific and sensitive for rapid detection of target isolates in

stools.

2. Serotype marker:

To correctly identify diarrheagenic E.coli strains, these organisms must be differentiated

from non-pathogenic members of the normal flora. Serotype markers correlate, sometimes

http://www.hindawi.com/journals/bmri/2013/374395/fig1/






very closely, with specific categories of E.coli ; however, these marker are rarely sufficient in

and of themselves to reliably identify a strain as diarrheagenic.

3. HEp-2 cell adherence and DNA hybridization:

Due to insufficiency of serotype marker to identify diarrheagenic strain of E.coli, thedetection of it has focus increasingly on the identification of certain characteristics which

themselves determine the virulence of these organisms which include Hep-2 cell adherence and

DNA hybridization.

8. TREATMENT

Treatment of EIEC infection is dependent on the severity of the symptoms, the age of the

patients, and coo morbidities (such as diabetes etc). Treatments include:

1. Avoidance of dehydration and rehydration

i. Oral therapy - if vomiting and dehydration are not severe. Small amounts and often, ideally

with and balanced electrolyte solutions, but other fluids can be used. Avoid high sugar drinks

as this may worsen diarrhea and dehydration.

ii. Nasogastric therapy - in a hospital setting may be used to avoid intravenous therapy.

iii. Intravenous therapy - where vomiting and/or dehydration are severe, or there is an

altered level of consciousness or other coo morbidities.

2. Treatment of other symptoms

i. Pain and fever can be treated with paracetamol or ibuprofen

ii. Anti-emetics - can be useful where vomiting is a predominant feature, but generally not

recommended in children.

iii. Antidiarrheals - should be avoided because of the risk of bacteremia.

3. Antibiotics such as TMP-SMX ( trimethoprim-sulfamethoxazole)

It helps to eradicate susceptible strains of EIEC (that are not resistant) from intestines.

4. Hospitalisation.

Recommended for:

i. The very young (<6 months) and the very elderly

ii. Moderate to severe dehydration and ongoing losses

iii. Those with other significant medical conditions

iv. Altered level of consciousness

http://www.rightdiagnosis.com/treat/antidiarrheals.htm

http://www.rightdiagnosis.com/treat/antibiotics.htm

http://www.rightdiagnosis.com/treat/antibiotics.htm

http://www.rightdiagnosis.com/treat/antidiarrheals.htm



5. Refeeding

i. Early age appropriate refeeding is now recommended once vomiting is controlled and

rehydration is complete

ii. Use complex carbohydrates such as rice, potatoes, and bread; and lean meatsiii. Delay in reintroduction of non-human milk has previously been recommended due to the

risk of lactose intolerance, but there is an increasing body of evidence that suggests

reintroduction of milk once tolerated, or even continuing milk during an acute illness, is not

associated with increased adverse outcomes

iv. Breastfeeding should continue as tolerated

6. Public Health measures and good hygiene

i. To avoid spread of disease

ii. To identify the source of the disease

References

NUR EZZATI AIZA BINTI MAHAT

1. http://europepmc.org/articles/PMC2732489/reload=0;jsessionid=fTdeHFIpbnfQFAgbC

VNK.4

2. http://wwwnc.cdc.gov/eid/article/8/5/01-0385_article.htm

3. http://wwwnc.cdc.gov/eid/article/8/5/01-0385-f3.htm

4. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC150271/

5. http://europepmc.org/wicket/bookmarkable/uk.bl.ukpmc.web.utilities.redirect.Redir

ectPage?table=T1/&articles=PMC2732489


7. http://textbookofbacteriology.net/e.coli_4.html

NUR AQILAH TAJUDEEN

1. “Infectious Diseases” journal by Sherwold L. Gorbash ( published by Lipincott,

Willsons & William) 3rd

edition.

2. Texas University, USA portal by Dr. Alfredo G. Torres.

3. Principle of Bacterial Pathogenesesis by Eduardo A. Groisman – published by Elsevier

4. E.Coli Infections journal by Shannon D Manning; consulting editor Hillary Babcock,

foreword by David L Heymann 2nd

Edition.

http://europepmc.org/articles/PMC2732489/reload=0;jsessionid=fTdeHFIpbnfQFAgbCVNK.4




http://wwwnc.cdc.gov/eid/article/8/5/01-0385_article.htm

http://wwwnc.cdc.gov/eid/article/8/5/01-0385-f3.htm

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC150271/

http://europepmc.org/wicket/bookmarkable/uk.bl.ukpmc.web.utilities.redirect.RedirectPage?table=T1/&articles=PMC2732489





http://textbookofbacteriology.net/e.coli_4.html

http://textbookofbacteriology.net/e.coli_4.html





http://wwwnc.cdc.gov/eid/article/8/5/01-0385-f3.htm






5. http://jcm.asm.org/content/45/11/3620.full

6. http://wwwnc.cdc.gov/eid/article/8/5/01-0385_article.htm#virulencecharacteristics

7. www.pubmed.com

8. www.cdc.gov.com

NOR SALEHAH SAZLI

1. http://wwwnc.cdc.gov/eid/article/8/5/01-0385-t1.htm

2. http://europepmc.org/wicket/bookmarkable/uk.bl.ukpmc.web.utilities.redirect.Redir

ectPage?table=T1/&articles=PMC2732489

3. http://www0.nih.go.jp/JJID/62/318.pdf

4. http://jcm.asm.org/content/48/4/1452.full

5. http://jid.oxfordjournals.org/content/188/11/1685.full

6. http://wwwnc.cdc.gov/eid/article/12/4/05-1112_article.htm


8. http://www.scielo.br/scielo.php?pid=S0074-02762005000400004&script=sci_arttext

NUR ‘ADILAH FAISAL SABRI

1) Steddman’s Medical Dictionary

2) www.pubmed.gov – US National Library of Medicine National Institute

of Health.

3) Edited by Barbara Lund, Microbiological Safety and Quality of Food

(book)

4) Edited by Eduardo A. Groisman, Principles of Bacterial Pathogenesis (book)

5) Edited by Maxx Sussman, Escheria Coli (Mechanism of Virulence) (book)

6) www.textbookofbacteriology.net

7) www.ehagroup.com

8) Edited by Martin Dwarkin, The Prokaryotes – Vol 6 Protobacteria Gamma Classes (book)

9) Brazilian Journal of Microbiology vol. 35 Jan./June 2004

10) www.flep.org

http://jcm.asm.org/content/45/11/3620.full

http://wwwnc.cdc.gov/eid/article/8/5/01-0385_article.htm#virulencecharacteristics

http://www.pubmed.com/

http://www.cdc.gov.com/

http://wwwnc.cdc.gov/eid/article/8/5/01-0385-t1.htm





http://www0.nih.go.jp/JJID/62/318.pdf


http://jid.oxfordjournals.org/content/188/11/1685.full



http://www.scielo.br/scielo.php?pid=S0074-02762005000400004&script=sci_arttext

http://www.pubmed.gov/

http://www.textbookofbacteriology.net/

http://www.ehagroup.com/

http://www.flep.org/

http://www.flep.org/

http://www.ehagroup.com/

http://www.textbookofbacteriology.net/

http://www.pubmed.gov/

http://www.scielo.br/scielo.php?pid=S0074-02762005000400004&script=sci_arttext



http://jid.oxfordjournals.org/content/188/11/1685.full


http://www0.nih.go.jp/JJID/62/318.pdf



http://wwwnc.cdc.gov/eid/article/8/5/01-0385-t1.htm

http://www.cdc.gov.com/

http://www.pubmed.com/

http://wwwnc.cdc.gov/eid/article/8/5/01-0385_article.htm#virulencecharacteristics




NUR ATHIFAH MOHAMMAD BASRI 1. http://www.textbookofbacteriology.net/e.coli_4.html

2. http://www.hindawi.com/journals/bmri/2013/374395/fig1/


4. http://www.rightdiagnosis.com/e/enteroinvasive_e_coli_infection/treatments.htm

5. http://www.affordablerx.com/php/articles.php?ArticleID=6681

http://www.textbookofbacteriology.net/e.coli_4.html



http://www.rightdiagnosis.com/e/enteroinvasive_e_coli_infection/treatments.htm

http://www.affordablerx.com/php/articles.php?ArticleID=6681

http://www.affordablerx.com/php/articles.php?ArticleID=6681

http://www.rightdiagnosis.com/e/enteroinvasive_e_coli_infection/treatments.htm



http://www.textbookofbacteriology.net/e.coli_4.html

Diarrheagenic e. Coli Official

Documents

Transcript of Diarrheagenic e. Coli Official