Bacterial Causes of Bacterial Causes of GastroenteritisGastroenteritis

P. Omayma MohammadP. Omayma Mohammad

Bacteria causing gastroenteritisBacteria causing gastroenteritisThe main sources of infection in gastroenteritis is the The main sources of infection in gastroenteritis is the

ingestion of contaminated food, water or drinks, or consumption ingestion of contaminated food, water or drinks, or consumption of improperly cooked meat of infected animals.of improperly cooked meat of infected animals.

1.1. Salmonella gastroenteritis.Salmonella gastroenteritis.

2.2. Shigella, bacillary dysentery.Shigella, bacillary dysentery.

3.3. Vibrio cholera, V. parahemolyticus.Vibrio cholera, V. parahemolyticus.

4.4. Diarrheagenic E coli; EPEC, ETEC, EHEC, EIEC, EAEC.Diarrheagenic E coli; EPEC, ETEC, EHEC, EIEC, EAEC.

5.5. Campylobacter.Campylobacter.

6.6. Clostridium deficil: antibiotic associated diarrhea, Clostridium deficil: antibiotic associated diarrhea, pseudomembranous gastroenteritis.pseudomembranous gastroenteritis.

7.7. Yersinia enterocolitis.Yersinia enterocolitis.

8.8. Listeria monocytogenes.Listeria monocytogenes.

Small intestine infectionsSmall intestine infections

BacterialBacterial:: E. coliE. coli (ETEC, EPEC), (ETEC, EPEC), Clostridium Clostridium perfringens, Vibrio choleraperfringens, Vibrio cholera sp., sp., Vibrio Vibrio parahemolyticus.parahemolyticus.ViralViral:: Rotavirus, Adenovirus, Astroviruses, Norwalk Rotavirus, Adenovirus, Astroviruses, Norwalk virus, Noroviruses (Norwalk-like viruses)virus, Noroviruses (Norwalk-like viruses)

Large intestine infections:Large intestine infections:Bacterial:Bacterial: E. coli E. coli (EHEC, EIEC, EAEC)(EHEC, EIEC, EAEC), Shigella, Shigella sp., sp., SalmonellaSalmonella sp., sp., CampylobacterCampylobacter sp., sp., YersiniaYersinia sp., sp., Clostridium difficileClostridium difficile

Salmonella OrganismSalmonella Organism- members of the family Enterobacteriaceae.- members of the family Enterobacteriaceae.

Classification:Classification:

Salmonella are classified according to DNA-DNA hybridization Salmonella are classified according to DNA-DNA hybridization

into 7 groups; I-VII. Nearly all of the salmonella that infect man into 7 groups; I-VII. Nearly all of the salmonella that infect man

are in group I, which includes more than 1400 serotypes.are in group I, which includes more than 1400 serotypes.

The most important salmonellae are:The most important salmonellae are:

S.typhiS.typhi and and S.paratyphiS.paratyphi,, which cause typhoid (enteric) fever which cause typhoid (enteric) fever

(enteritis + systemic disease).(enteritis + systemic disease).

S.typhimureum S.typhimureum and and S. enteritidisS. enteritidis, which cause food poisoning , which cause food poisoning

and enterocolitis.and enterocolitis.

S.cholera suisS.cholera suis, which causes septicemia. , which causes septicemia.

MorphologyMorphology- Gram negative bacilli, motile with peritrichous - Gram negative bacilli, motile with peritrichous

flagellae, capsulated.flagellae, capsulated.

Cultural characters:Cultural characters:

Facultative anaerobes, grow on simple media, on Facultative anaerobes, grow on simple media, on MacConkey and DCA agar they produce pale non-MacConkey and DCA agar they produce pale non-lactose fermenting colonies.lactose fermenting colonies.

Serological classification:Serological classification:

Salmonella posses somatic (O), flagellar (H), and Salmonella posses somatic (O), flagellar (H), and some as S. typhi, posses capsular (Vi) antigens.some as S. typhi, posses capsular (Vi) antigens.

According to O antigen, salmonella are classified According to O antigen, salmonella are classified into O serogroups; A, B, C1, C2, D and E.into O serogroups; A, B, C1, C2, D and E.

Morphology of SalmonellaMorphology of Salmonella

Typhoid Fever, Enteric FeverTyphoid Fever, Enteric FeverCausative organismCausative organism:: S.typhi and paratyphi A, B, C. S.typhi and paratyphi A, B, C.Source of infection:Source of infection: S. typhi and paratyphi A and B S. typhi and paratyphi A and B

are primarily infective for man, so the source of are primarily infective for man, so the source of infection is human, a case or a carrier.infection is human, a case or a carrier.

Route of infectionRoute of infection:: oral through contaminated food, oral through contaminated food, drinks, raw vegetables, fruits, milk and milk products.drinks, raw vegetables, fruits, milk and milk products.

Role of chronic carriers as source of infectionRole of chronic carriers as source of infection: : the organism chronically colonize the gallbladder the organism chronically colonize the gallbladder serving as a reservoir to infect other people. They can serving as a reservoir to infect other people. They can colonize for up to a year following resolution of colonize for up to a year following resolution of symptoms in 1-5% of those infected. In very few case symptoms in 1-5% of those infected. In very few case the organism may colonize the urinary tract.the organism may colonize the urinary tract.

Pathogenesis and ClinicalPathogenesis and Clinical PicturesPictures

- Salmonella cause disease by Salmonella cause disease by invasioninvasion, they do not , they do not produce toxins.produce toxins.

- Virulence factors:Virulence factors:

1- capsule1- capsule

2- Motility through flagellae.2- Motility through flagellae.

3- the ability to live intracellularly. 3- the ability to live intracellularly. - The lesion site is in the ileum & large intestineThe lesion site is in the ileum & large intestine

- The ingested organisms reach the intestine, enter the- The ingested organisms reach the intestine, enter the

lymphatic, then the blood stream causing bacteremia lymphatic, then the blood stream causing bacteremia

for one week.for one week.

- Through blood, the organism is carried to many - Through blood, the organism is carried to many

organs; intestine where they multiply in Peyer,s organs; intestine where they multiply in Peyer,s

patches, kidney and excreted in urine, liver causing patches, kidney and excreted in urine, liver causing

focal necrosis and inflammation of gall bladder and focal necrosis and inflammation of gall bladder and

excreted in bile to reach the intestine.excreted in bile to reach the intestine.

- The organism may reach the periosteum and lungs.- The organism may reach the periosteum and lungs.

Clinical Picture:Clinical Picture:

I.P.:I.P.: 10-14 days. 10-14 days.

- Fever, headache, malaise, constipation, - Fever, headache, malaise, constipation, bradychardia and myalgia.bradychardia and myalgia.

- The liver and spleen are enlarged.- The liver and spleen are enlarged.

Lab Diagnosis of Typhoid FeverLab Diagnosis of Typhoid Fever

A-Isolation of the organism:A-Isolation of the organism:1-During the first week:1-During the first week: isolation from isolation from bloodblood by blood by blood

culture:culture:- Subculture on selective media as MacConkey agar, Subculture on selective media as MacConkey agar,

SS agarSS agar- Pale colonies (non-lactose fermenting colonies) are Pale colonies (non-lactose fermenting colonies) are

identified by:identified by:

1-gram stain.1-gram stain.

2-biochemical reactions.2-biochemical reactions.

3-serological typing by slide agglutination with anti-3-serological typing by slide agglutination with anti-

salmonella sera.salmonella sera.

2-During the second week:2-During the second week:A- Isolation from stool:A- Isolation from stool:The organism is most readily isolated in the second The organism is most readily isolated in the second

and third week.and third week.Stool samples are cultured on:Stool samples are cultured on:• MacConkey agar DCA agar or SS agar.MacConkey agar DCA agar or SS agar.• Tubes of selenite F broth for enrichment, incubated Tubes of selenite F broth for enrichment, incubated

for 24 hours and then subcultured on MacConkey for 24 hours and then subcultured on MacConkey and DCA agar.and DCA agar.

B- Isolation from urine:B- Isolation from urine:The organism appears in urine from second week The organism appears in urine from second week

onward, but its excretion in urine may be onward, but its excretion in urine may be intermittent, hence isolation needs repeated intermittent, hence isolation needs repeated subcultures. subcultures.

Antibodies to salmonella appear in the serum of the patient Antibodies to salmonella appear in the serum of the patient

during the second weekduring the second week and reach maximum during the 4and reach maximum during the 4thth week. They are detected by Widal test, which is a tube week. They are detected by Widal test, which is a tube agglutination test.agglutination test.

• At least 2 samples are obtained at interval of 7-10 days to At least 2 samples are obtained at interval of 7-10 days to detect rising titer.detect rising titer.

• A single O antigen suspension is used for S. typhi and A single O antigen suspension is used for S. typhi and paratyphi A & B (due to antigen sharing), but an H antigen paratyphi A & B (due to antigen sharing), but an H antigen suspension is used for each type.suspension is used for each type.

• Serial dilutions of the patient serum are prepared; 1/20, 1/40, Serial dilutions of the patient serum are prepared; 1/20, 1/40, 1/80, 1/160, 1/320--------1/80, 1/160, 1/320--------

• High or rising titer of O antibodies (equal or more than 1/160) High or rising titer of O antibodies (equal or more than 1/160) indicates active infection because anti-O antibodies appear indicates active infection because anti-O antibodies appear early and disappear faster than anti-H antibodies. early and disappear faster than anti-H antibodies.

B B - - Serological diagnosisSerological diagnosis (Widal test)(Widal test)

PreventionPrevention

1 - Sanitary measures must be taken to avoid contamination of food and water.2- Carriers must not be allowed to work as food

handlers.3- Vaccination: are partially effective a) TAB vaccine which is a heat killed vaccine

given by s.c.i., 0.5-1cc, at 2 doses with one month interval.

b) Oral administration of live avirulent mutant strain of S.typhi has given significant protection in areas of high endemicity.

c)c) Vi capsular polysaccharideVi capsular polysaccharide of S. typhi given of S. typhi given intramuscularly.intramuscularly.

Salmonella enterocolitisSalmonella enterocolitis

- S. typhimureum and S. enteritidis (salmonellosis).- S. typhimureum and S. enteritidis (salmonellosis).

PathogenesisPathogenesis:: Invasive GastroenteritisInvasive Gastroenteritis (large intestine) (large intestine)

- The organisms are mainly pathogens to animals and poultry - The organisms are mainly pathogens to animals and poultry and is transmitted to man through improperly cocked meat of and is transmitted to man through improperly cocked meat of infected animals, eggs, dairy products, contaminated water infected animals, eggs, dairy products, contaminated water and from food contaminated with rat excreta.and from food contaminated with rat excreta.

Clinically:Clinically: IP is 24-48 h, the organism multiply in the intestine IP is 24-48 h, the organism multiply in the intestine causing infective and not toxic poisoning, that is why the IP is causing infective and not toxic poisoning, that is why the IP is long.long.

- There will be nausea, vomiting, headache, diarrhea and low - There will be nausea, vomiting, headache, diarrhea and low grade fever, abdominal cramps. The condition resolves within grade fever, abdominal cramps. The condition resolves within 2-3 days2-3 days

- The organism can be isolated from stool.- The organism can be isolated from stool.

Shigella and Bacillary DysenteryShigella and Bacillary Dysentery

Morphology, Cultural characters and Morphology, Cultural characters and Serological ClassificationSerological Classification

- Gram –ve rods, non-motile, non-capsulated.- Gram –ve rods, non-motile, non-capsulated.

- Facultative anaerobes, pale non-lactose fermenting - Facultative anaerobes, pale non-lactose fermenting colonies on MacConkey and DCA.colonies on MacConkey and DCA.

- According to O antigen, shigella are classified into 4 - According to O antigen, shigella are classified into 4 groups:groups:

1- group A, Sh. dysenteriae, including 13 serotypes.1- group A, Sh. dysenteriae, including 13 serotypes.

2- group B, Sh. flexneri, including 8 serotypes.2- group B, Sh. flexneri, including 8 serotypes.

3- group C, Sh. boydii, including 18 serotypes.3- group C, Sh. boydii, including 18 serotypes.

4- group D, Sh. sonnei, including one serotype.4- group D, Sh. sonnei, including one serotype.

PathogenesisPathogenesisShigellae are highly communicable, transmitted from person Shigellae are highly communicable, transmitted from person to person through fecal-oral route. Food and water outbreaks to person through fecal-oral route. Food and water outbreaks may occur.may occur.

Infection is limited to GIT without blood invasion.Infection is limited to GIT without blood invasion.

The main pathogenic process is the The main pathogenic process is the invasioninvasion of the of the mucosal epithelial cells, where the organism multiply, infect mucosal epithelial cells, where the organism multiply, infect adjacent cells of the large intestine and terminal ileum.adjacent cells of the large intestine and terminal ileum.

Microabscesses are formed with necrosis of the mucous Microabscesses are formed with necrosis of the mucous membrane, superficial ulceration, bleeding and formation of membrane, superficial ulceration, bleeding and formation of pseudomembrane, which consists of leucocytes, fibrin and pseudomembrane, which consists of leucocytes, fibrin and cell debris.cell debris.

As the process subsides, granulation tissue fill the ulcerated As the process subsides, granulation tissue fill the ulcerated areas with formation of scars. areas with formation of scars.

- Shigella dysenteriae produce an exotoxin - Shigella dysenteriae produce an exotoxin (Shiga(Shiga toxin),toxin), which adds to the pathogenesis. which adds to the pathogenesis.

- Shiga toxin acts as an enterotoxin, a cytotoxin and a - Shiga toxin acts as an enterotoxin, a cytotoxin and a neurotoxin affecting the CNS causing meningismus neurotoxin affecting the CNS causing meningismus and coma. and coma.

- The toxic activity and the invasive property act in - The toxic activity and the invasive property act in sequence; the toxin produces an early non-bloody sequence; the toxin produces an early non-bloody voluminous diarrhea and invasion results in later voluminous diarrhea and invasion results in later dysentery with blood and bus in stool and dysentery with blood and bus in stool and tenesmus.tenesmus.

Clinical PictureClinical Picture- - Shigellosis is mainly a disease of children, but adult Shigellosis is mainly a disease of children, but adult

may be affected.may be affected.

- IP: 1-2 days- IP: 1-2 days

- sudden onset of fever, tenesmus, diarrhea. Stool - sudden onset of fever, tenesmus, diarrhea. Stool contains contains blood and mucous.blood and mucous.

- In case of - In case of Sh. dysenteriaeSh. dysenteriae, early non-bloody diarrhea , early non-bloody diarrhea due to the exotoxin. Convulsion may also occur.due to the exotoxin. Convulsion may also occur.

- Recovery occurs in most cases, however, in children - Recovery occurs in most cases, however, in children and elderly dehydration, acidosis and even death and elderly dehydration, acidosis and even death may occur.may occur.

- Very few remain as chronic carriers.- Very few remain as chronic carriers.

- Man is the only reservoir.- Man is the only reservoir.

Laboratory DiagnosisLaboratory Diagnosis

1.1. Specimens:Specimens: fresh stool, mucous flecks and rectal fresh stool, mucous flecks and rectal

swabs.swabs.

2.2. Macroscopic examination for blood and mucus.Macroscopic examination for blood and mucus.

3.3. Microscopic examination for Microscopic examination for pus cells and RBCs.pus cells and RBCs.

4.4. Culture: on MacConkey, DCA or Salmonella, Culture: on MacConkey, DCA or Salmonella,

Shigella (SS) agar, XLD agar.Shigella (SS) agar, XLD agar.

5.5. Pale non-lactose fermenting colonies are identified Pale non-lactose fermenting colonies are identified

by: gram stain, biochemical reactions and specific by: gram stain, biochemical reactions and specific

antisera. antisera.

Vibrio CholeraVibrio Cholera

Morphology, Cultural CharactersMorphology, Cultural Characters

- Vibrios are among the most common bacteria in - Vibrios are among the most common bacteria in surface water worldwide.surface water worldwide.

- Gram-ve curved comma-shaped bacilli, motile with - Gram-ve curved comma-shaped bacilli, motile with one polar flagellum.one polar flagellum.

- Highly aerobic, growth is favored by alkaline pH (8-- Highly aerobic, growth is favored by alkaline pH (8-9).9).

- On alkaline peptone water, they grow forming a - On alkaline peptone water, they grow forming a surface pellicle within 8 hours.surface pellicle within 8 hours.

- On TCBS (thiosulfate citrate bile sucrose), which is - On TCBS (thiosulfate citrate bile sucrose), which is the specific medium for V.cholera, they give yellow the specific medium for V.cholera, they give yellow colonies because they ferment sucrose.colonies because they ferment sucrose.

Biochemical ReactionsBiochemical Reactions

- Oxidase positive.- Oxidase positive.

- Ferment sucrose and mannose.- Ferment sucrose and mannose.

- They give positive - They give positive cholera-red reactioncholera-red reaction:--:--→→

on nitrate peptone water, they produce indole on nitrate peptone water, they produce indole from peptone and reduce nitrate to nitritefrom peptone and reduce nitrate to nitrite

Nitrite +indole ----→ nitrose indole, which on Nitrite +indole ----→ nitrose indole, which on addition of sulfuric acid (H2SO4) ----→addition of sulfuric acid (H2SO4) ----→

red color.red color.

Antigenic Structure & Biologic Antigenic Structure & Biologic ClassificationClassification

►According to O antigen (LPS)According to O antigen (LPS)

Classic Cholera

Cholera like illnessNon-O1/nonO139

Group O1 Group O139

CholeraCholera- - an acute infectious disease characterized by sever vomiting an acute infectious disease characterized by sever vomiting

and watery diarrhea and watery diarrhea (rice-water stool).(rice-water stool).- endemic in Indian subcontinent and world-wide epidemics may - endemic in Indian subcontinent and world-wide epidemics may

occur.occur.Pathogenesis:-Pathogenesis:- • V.choleraV.cholera is pathogenic only for man. is pathogenic only for man.• Route of infection: fecal-oral route through contaminated Route of infection: fecal-oral route through contaminated

water, other drinks and food.water, other drinks and food.• Infection is restricted to the small intestine with no invasion of Infection is restricted to the small intestine with no invasion of

blood.blood.• The organism attach to the brush border of the microvilli of The organism attach to the brush border of the microvilli of

epithelial cells epithelial cells without invasionwithout invasion and produce the and produce the enterotoxinenterotoxin, which is the main virulence. , which is the main virulence. Mucinase enzymeMucinase enzyme dissolve the protective glycoprotein coating the intestinal cells dissolve the protective glycoprotein coating the intestinal cells helping adherence. helping adherence.

The Vibrio cholera EnterotoxinThe Vibrio cholera Enterotoxin- A heat-labile toxin which consists of 2 subunits; A & B.- A heat-labile toxin which consists of 2 subunits; A & B.

- Subunit B attaches to certain receptors on the epithelial - Subunit B attaches to certain receptors on the epithelial

surface of the intestine, promoting entry of subunit A into the surface of the intestine, promoting entry of subunit A into the

cells.cells.

- Activated subunit A leads to activation of adenylate cyclase - Activated subunit A leads to activation of adenylate cyclase

enzyme with the result of increase in intracellular cyclic AMP enzyme with the result of increase in intracellular cyclic AMP

(adenosine monophosphate) that leads to prolonged (adenosine monophosphate) that leads to prolonged

hypersecretion of water and electrolytes.hypersecretion of water and electrolytes.

- There is increased Na-dependent Cl secretion and absorption - There is increased Na-dependent Cl secretion and absorption

of Na and Cl is inhibited.of Na and Cl is inhibited.

- Sever diarrhea results (osmotic diarrhea), more than 20L/day, - Sever diarrhea results (osmotic diarrhea), more than 20L/day,

resulting in dehydration, acidosis, shock and death.resulting in dehydration, acidosis, shock and death.

Laboratory DiagnosisLaboratory Diagnosis

A- First case in a non-endemic area:-A- First case in a non-endemic area:-This may be a start of an epidemic, so needs rapid This may be a start of an epidemic, so needs rapid diagnosis.diagnosis.- Stool is inoculated on alkaline peptone water.- Stool is inoculated on alkaline peptone water.- After incubation for 6-8 hours, the surface pellicle - After incubation for 6-8 hours, the surface pellicle growth is examined as follow:-growth is examined as follow:-1.1. A wet mount smear to observe darting movement.A wet mount smear to observe darting movement.2.2. Gram stain.Gram stain.3.3. B.R. ,oxidase +ve, cholera red reaction +veB.R. ,oxidase +ve, cholera red reaction +ve4.4. Subculture on TCBS.Subculture on TCBS.5.5. Serological identification with specific anti-O1 and Serological identification with specific anti-O1 and O139 antibodies.O139 antibodies.

B- B- secondary case in an epidemic:secondary case in an epidemic:- In an established epidemic, and also in endemic - In an established epidemic, and also in endemic

areas, cases are diagnosed by microscopic areas, cases are diagnosed by microscopic

examination of fresh stool for comma-shaped bacilli examination of fresh stool for comma-shaped bacilli

with characteristic motility, which can be immobilized with characteristic motility, which can be immobilized

by adding specific O antis era.by adding specific O antis era.

Direct methods for detection of Direct methods for detection of V. choleraV. cholera in stool in stool

include fluorescent antibody staining, agglutination include fluorescent antibody staining, agglutination

and PCR.and PCR.

Treatment and ProphylaxisTreatment and ProphylaxisTreatmentTreatment

mainly by I.V. fluid and electrolytes.mainly by I.V. fluid and electrolytes.

ProphylaxisProphylaxis by 2 types of vaccines: by 2 types of vaccines: A heat-killed vaccine, or a LPS vaccine extracted A heat-killed vaccine, or a LPS vaccine extracted

from V.cholera, is given by s.c.i in repeated doses from V.cholera, is given by s.c.i in repeated doses can confirm limited protection.can confirm limited protection.

A live oral vaccine which protects against the A live oral vaccine which protects against the cholera toxin, prepared by recombinant DNA cholera toxin, prepared by recombinant DNA technique, is recently available.technique, is recently available.

Diarrheagenic E.coliDiarrheagenic E.coli

Morphology & cultural characters:Morphology & cultural characters:

- Gm –Ve rods, motile, facultative anaerobes.- Gm –Ve rods, motile, facultative anaerobes.

- Lactose fermenting colonies.- Lactose fermenting colonies.

E.coliE.coli that cause diarrhea are classified into 5 that cause diarrhea are classified into 5

Classes according to pathogenesis:Classes according to pathogenesis:

1.1. Enteropathogenic E.coli (EPEC).Enteropathogenic E.coli (EPEC).

2.2. Enterotoxigenic E.coli (ETEC).Enterotoxigenic E.coli (ETEC).

3.3. Enteroinvasive E.coli (EIEC).Enteroinvasive E.coli (EIEC).

4.4. Enterohemorrhagic E.coli (EHEC). Enterohemorrhagic E.coli (EHEC).

5.5. Enteroaggregative E.coli (EAEC).Enteroaggregative E.coli (EAEC).

EPEC:EPEC:- Certain serotypes of E.coli were proved to cause - Certain serotypes of E.coli were proved to cause

infantile diarrhea; O55, O111 etc, in infants less than infantile diarrhea; O55, O111 etc, in infants less than 6 months.6 months.

Enteropathogenic mechanism:Enteropathogenic mechanism:- Small intestine infection.- Small intestine infection.● ● some strains possess a plasmid that code for an some strains possess a plasmid that code for an adherence factor (EAF) that mediate adherence of adherence factor (EAF) that mediate adherence of EPEC to microvillus cells which leads to increases in EPEC to microvillus cells which leads to increases in Ca levels and then rearrangements in actin, needed Ca levels and then rearrangements in actin, needed for intimate contact of human cells, and final stages for intimate contact of human cells, and final stages of cell destruction of cell destruction L.D.:L.D.: serotyping. serotyping.

ETEC:ETEC:One of the most important causes of diarrheaOne of the most important causes of diarrheaespecially in infants and traveler diarrhea.especially in infants and traveler diarrhea.Pathogenesis:Pathogenesis:- Small intestine infection- Small intestine infection..Produce 2 types of Produce 2 types of enterotoxinenterotoxin; LT and ST.; LT and ST.

LTLT is functionally related to cholera toxin, activates adenyl is functionally related to cholera toxin, activates adenylcyclase with increased cAMP in the intestinal mucosa.cyclase with increased cAMP in the intestinal mucosa.ST ST acts by activation of guanyl cyclase with increase ofacts by activation of guanyl cyclase with increase of intracellular cGMP.intracellular cGMP.LD of ETEC:LD of ETEC:1.1. DNA probe to detect the plasmids coding for LT or ST.DNA probe to detect the plasmids coding for LT or ST.2.2. Effect of LT on Y-1 adrenal cell culture.Effect of LT on Y-1 adrenal cell culture.3.3. ELISA to detect toxin in stool.ELISA to detect toxin in stool.

EIEC:EIEC:Enteropathogesis:Enteropathogesis:- Large intestine infection.- Large intestine infection.- similar to that of Shigella i.e., enteroinvasiveness - similar to that of Shigella i.e., enteroinvasiveness through Plasmid mediated invasion of epithelial cells. through Plasmid mediated invasion of epithelial cells. The plasmid code for an outer protein which mediate The plasmid code for an outer protein which mediate

invasion. invasion. LDLD: : 1-Sereny test 1-Sereny test 2- DNA probe to identify the 2- DNA probe to identify the plasmid.plasmid.3- ELISA to detect the outer 3- ELISA to detect the outer membrane protein.membrane protein.

EHEC: EHEC: E coli O157 H7E coli O157 H7Route of infectionRoute of infection:: Ingestion of contaminated food Ingestion of contaminated food(undercooked hamburgers)(undercooked hamburgers) and waterand waterPathogenesis:Pathogenesis: elaborate elaborate phagephage encoded potent cytotoxin encoded potent cytotoxin which affect vero cell culture, hence the name which affect vero cell culture, hence the name VerotoxinVerotoxinthat is similar to that is similar to Shiga toxinShiga toxin. Verotoxin blocks protein. Verotoxin blocks proteinsynthesis. The majority of the pathology occurs in thesynthesis. The majority of the pathology occurs in the ascending and transverse colon lamina propria. Damageascending and transverse colon lamina propria. Damage to the kidneys is due to swollen glomerular epithelial cells,to the kidneys is due to swollen glomerular epithelial cells, fibrin deposition and infiltrates of inflammatory cells.fibrin deposition and infiltrates of inflammatory cells.CP:CP: bloody diarrhea and in severe cases can lead tobloody diarrhea and in severe cases can lead tohemolytic uremic syndrome (HUS), which may occur inhemolytic uremic syndrome (HUS), which may occur insporadic cases or in outbreaks.sporadic cases or in outbreaks.Lab Diagnosis:Lab Diagnosis: - Serotyping - Serotyping - DNA probe to detect the DNA phage coding for the Verotoxin.- DNA probe to detect the DNA phage coding for the Verotoxin.

EaggEC:EaggEC:- a major cause of traveler diarrhea and more persistent - a major cause of traveler diarrhea and more persistent

diarrheadiarrhea

- Identified by their mannose resistant adherence to HEP-2- Identified by their mannose resistant adherence to HEP-2

cells. cells.

Pathogenesis:Pathogenesis: infection of large intestine. Aggregative pattern infection of large intestine. Aggregative pattern due to certain thin pili due to certain thin pili

CP:CP: watery watery diarrheadiarrhea with vomiting and dehydration in infants. with vomiting and dehydration in infants. EAEC is a common cause of more persistent diarrhea seen EAEC is a common cause of more persistent diarrhea seen in adults and children. in adults and children.

LD:LD: adherence to HEP2 cells. adherence to HEP2 cells.

Campylobacter jejuniCampylobacter jejuni

C. jejuni and C. coli are common cause of enteritisC. jejuni and C. coli are common cause of enteritis

especially in children. C. jejuni causes about 95% of especially in children. C. jejuni causes about 95% of campylobacter enterocolitis. campylobacter enterocolitis.

Morphology:Morphology: gm-ve comma or s-shaped rods, motile gm-ve comma or s-shaped rods, motile with one polar flagellum.with one polar flagellum.

Cultural charactersCultural characters: microaerophilic (5%O2) and needs : microaerophilic (5%O2) and needs 10%CO2. Growth is better at 42°C.10%CO2. Growth is better at 42°C.

Skirrow’s medium, which is a blood agar supplemented Skirrow’s medium, which is a blood agar supplemented with vancomycin, polymyxin B and Trimethoprim is with vancomycin, polymyxin B and Trimethoprim is the selective medium.the selective medium.

BR:BR: oxidase positive and catalase positive. oxidase positive and catalase positive.

Pathogenesis:Pathogenesis:- Water, food as raw milk, meat, poultry contaminated Water, food as raw milk, meat, poultry contaminated

with domestic animal and puppies excreta are the with domestic animal and puppies excreta are the major sources of infection.major sources of infection.

- Localized tissue invasion and toxic activity of some Localized tissue invasion and toxic activity of some strains (enterotoxin and cytotoxin) are responsible strains (enterotoxin and cytotoxin) are responsible for the enteritis.for the enteritis.

LD:LD:

1- gm stained smears of stool.1- gm stained smears of stool.

2- wet preparation to observe the motility2- wet preparation to observe the motility

3- Culture on Skirrow blood agar and identification of 3- Culture on Skirrow blood agar and identification of the growth by gm stain and BR.the growth by gm stain and BR.

ComplicationsComplications::- Some cases of C. jejuni may be complicated by - Some cases of C. jejuni may be complicated by

Guillian-Barré syndrome, which is an autoimmune Guillian-Barré syndrome, which is an autoimmune disease due to formation of antibodies against the disease due to formation of antibodies against the organism that cross react with antigen on the organism that cross react with antigen on the neurons.neurons.

Clostridium deficilClostridium deficil- Cause pseudomembranous colitis which may complicate - Cause pseudomembranous colitis which may complicate

antibiotic therapy.antibiotic therapy.

Morphology:Morphology: gm +ve anaerobic bacilli which are part of normal gm +ve anaerobic bacilli which are part of normal flora of colon.flora of colon.

Pathogenesis:Pathogenesis: as a complication of antibiotic therapy, the drug- as a complication of antibiotic therapy, the drug-sensitive flora are suppressed allowing Cl.dificile to multiply sensitive flora are suppressed allowing Cl.dificile to multiply and produce exotoxin A which is an enterotoxin that cause and produce exotoxin A which is an enterotoxin that cause watery diarrhea and B toxin which is a cytotoxin that cause watery diarrhea and B toxin which is a cytotoxin that cause damage to the colon mucosa with pseudomembranous damage to the colon mucosa with pseudomembranous formation.formation.

Drugs most commonly cause this condition are ampicillin, Drugs most commonly cause this condition are ampicillin, clindamycin and at present the most common drugs are 2clindamycin and at present the most common drugs are 2ndnd and 3and 3rdrd generation cephalosporin as they are being most generation cephalosporin as they are being most commonly used. commonly used.

Lab diagnosis:Lab diagnosis:

1- detection of toxin A and B in stool supernatant by 1- detection of toxin A and B in stool supernatant by ELISA.ELISA.

2- isolation of the organism on anaerobic media.2- isolation of the organism on anaerobic media.

Treatment:Treatment:

1- withdrawal of the causative drug.1- withdrawal of the causative drug.

2- metronidazole or vancomycin.2- metronidazole or vancomycin.

Listeria monocytogenes:Listeria monocytogenes:• Gm+ short bacilli, motile.Gm+ short bacilli, motile.• Aerobic, on blood agar produce a narrow zone of Aerobic, on blood agar produce a narrow zone of ββ

hemolysis.hemolysis.• Catalase positive.Catalase positive.

Pathogenesis:Pathogenesis:- depend on the ability of Listeria to invade and grow depend on the ability of Listeria to invade and grow

inside phagocytic cells, so CMI is more effective inside phagocytic cells, so CMI is more effective than humoral immunity.than humoral immunity.

- The organism is primarily an animal pathogen, man The organism is primarily an animal pathogen, man gets infection through contact with animals, their gets infection through contact with animals, their feces, but mainly through ingestion of unpasteurized feces, but mainly through ingestion of unpasteurized milk or cheese and contaminated vegetables.milk or cheese and contaminated vegetables.

The disease is called The disease is called listeriosislisteriosis and its forms are: and its forms are:- Infection of pregnant women leads to abortion, still-Infection of pregnant women leads to abortion, still-

birth and premature labor.birth and premature labor.- Infection of the neonates during delivery or Infection of the neonates during delivery or

transplacentally may cause meningitis transplacentally may cause meningitis 1-4 weeks 1-4 weeks later.later.

- Infection in immunosuppressed causes bacteremia Infection in immunosuppressed causes bacteremia and meningitis especially in renal transplant and meningitis especially in renal transplant patients.patients.

- Gastroenteritis. Gastroenteritis.