Digestive system infections
This presentation is the property of its rightful owner.
Sponsored Links
1 / 17

Digestive system infections: PowerPoint PPT Presentation


  • 51 Views
  • Uploaded on
  • Presentation posted in: General

Digestive system infections:. Barriers to infection: 1-The stomach acid of a pH less than or equal to 4. 2- Shedding of mucosal epithelium lining the alimentary system. 3-A variety of local defense mechanisms; mucus formation and gut motility ( Peristalsis ).

Download Presentation

Digestive system infections:

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -

Presentation Transcript


Digestive system infections

Digestive system infections:

Barriers to infection:

1-The stomach acid of a pH less than or equal to 4.

2-Shedding of mucosal epithelium lining the alimentary

system.

3-A variety of local defense mechanisms; mucus

formation and gut motility( Peristalsis).

4- The normal flora of intestinal tracts.

5-The glycocalyx (mucin-rich layer) of epithelial-cells

surface.

(Clostridium difficileproduces anti-mucin toxins)


Digestive system infections

N

6-The Bile salts detergent action.

7-The secreted antimicrobial peptides.

(EnterotoxigenicE.coliproduces heat-labile toxin that

suppress these peptides.

8-Mcells of Peyer patches have surveillance function.

9-Secretory IgA.


Establishment of infectious diseases in the digestive system

Establishment of infectious diseases in the digestive system:

The defense barriers are changed in favor of the microbe due to:

1-Anatomic alterations:

A-Obstructionsto the flow of intestinal secretions

(gallbladder stones).

B-Surgery may create intestinal “blind loops” that are

isolated from the moving stream of intestinal

contents.

Absence of flushing action of intestinal secretions.

Bacterial overgrowth syndrome; malabsorption.


Digestive system infections

N

2-Changes in stomach acidity; due to proton-pump

inhibitors:

-Decreased pathogenic dose results in colonization of

intestinal mucosa; ExampleSalmonella species.

-Shigella species and E.coliO157:H7 are acid resistance.

3-Alterations to the normal flora; due to broad-spectrum

antibiotics.

Pseudomembrane colitis; Clostridium difficile.

4-Invasion of Gut by virulent microbial strains.


Intestinal invasive diseases inflammation and damage

Intestinal invasive diseases , inflammation and damage:

1-Invasive Enteritis, and dysentery (bloody diarrhea):

A-Shigelladysenteriae infection:

Pathogenic dose: less than 200 CFU.

Reservoir: human colon only (no animal carriers).

Transmission: Fecal-Oral, Person to Person.

Pathogenesis:

- Endotoxin triggers inflammation.

- Shiga toxin type I: Enterotoxic and cytotoxic activities.

It is interfering with 60S ribosomal subunit; necrosis.

-The microbe invades the M cell in the lumen of Gut.


Digestive system infections

N

Multiply inside these cells, using actin polymerization to infect neighboring epithelial cells.

Released , engulfed by intestinal macrophages.

Escape from APC, infects other epithelial cells.

Very Shallow ulceration of intestinal mucosa.


Digestive system infections

N

Enterocolitis, shigellosis (most severe form is dysentery).

Fever , lower abdominal cramps; diarrhea first watery,

then bloody with mucus.

Invasive infection: shallow ulcerative Enterocolitis.

Hemolytic-Uremic syndrome.

B-Entamoebahistolytica(dysentery).

Microbiology:

Gram-negative short bacilli,

Nonmotile, Non-spore formers.

Enterobacteriaceae grow best on XLD.

Facultative anaerobic, non-Lactose fermenters.

Can not produce H2S and identify by API 20E


2 invasive enteritis and hemorrhagic colitis enterohemorrhagic e coli

2-Invasive Enteritis and Hemorrhagic Colitis:Enterohemorrhagic E. coli:

- Transmission: food (hamburger), milk, Fecal-Oral.

- Incubation period: 3-5 days.

- Reservoir: Cattle; bovine feces, pork.

- Pathogenic dose: 10-100 CFU.

- Toxin: Verotoxin : Exotoxin

- Pathogenesis:

- EHEC bind to cells in the large intestinal

mucosa(Caecum,Colon).

- Verotoxin-Epithelial receptor interaction.

- Decrease protein synthesis by interfering with 60 S

ribosomal subunit.


Digestive system infections

N

- Intracellular localization inside lysozyme.

- Cell death; apoptosis.

- Mucosal necrosis; Hemorrhagic Colitis with

bloody diarrhea.

- Shiga like exotoxins; Hemolytic-uremic syndrome.

Microbiology:

-Gram negative short bacilli.

-Lactose fermenters.

- Metallic green sheen on

EMB medium.

- Indole positive.


Digestive system infections

N

3-Invasive Enteritis and Bloody watery diarrhea:

A- Campylobacter jejuni infection:

Reservoir: intestinal tracts of humans, cattle, sheep, dogs, cats, and Poultry.

Transmission:

-Fecal-Oral (direct cont.), Ingestion of contaminated meat

(poultry), contaminate water, or unpasteurized milk.

Incubation period:

3-5 days.

Microbiology:

Gram-negative curved

helical rods

with polar flagella.


Digestive system infections

N

- Microaerophilic ( 10% CO2, 5% O2, and 85% N2) microbe

with an optima of 42˚C temp.

- Humidity should be > 95%.

- Resistance for Cephalothin.

- Sensitive for Nalidixic acid.

- Catalase and oxidase positive.


Pathogenesis of campylobacter jejuni

Pathogenesis of Campylobacter jejuni:

Pathogenicdose: as few as 500 CFU.

The microbe invades the small and large intestinal mucosa.

Colonization of intestinal epithelial layer, engulfed by intestinal dendritic cells(DC).

DC release inflammatory mediators, chemotaxis, cellular

infiltration.

Ulcerative, inflammatory lesions in the jejunum, and ileum.

UlcerativeColitis.

Pus and RBCs in stool; AcuteEnteritis (common cause of

infectious diarrhea worldwide).

- Traveler’s diarrhea and pseudo-appendicitis.


Digestive system infections

N

n


Infective ulcerative colitis and dysentery

Infective Ulcerative Colitis and dysentery:

n


B salmonella enteriditis and salmonella typhimurium

B-Salmonella enteriditisand Salmonella typhimurium :

Reservoir:

-Human: Large intestinal tracts: Carriage state.

-Animals: most important: Chicken.

Transmission:

1-Fecal-Oral from carrier person.

2-Ingestion of contaminated

chicken products

(raw chicken, eggs).

Incubationperiod: 6-48 hours.


Pathogenesis

Pathogenesis:

TheMicrobe invades the ileocecal region lymphoid tissue.

Invasion of Lamina propria; endotoxin activity.

Dendritic cell activation; production of TNF and IL-8.

PMN cells chemotaxis and PG response.

PG stimulate cellular cAMP of epithelial cells.

Release of NaCl from intestinal epithelial cells; dehydration.

PMN cells prevent mesenteric lymph node and RES invasion.

Bloody watery diarrhea.

Diagnosis:

Clinical: abdominal symptoms and fever.

Laboratory: Stool culture: similar to Salmonellatyphi.


C listeria monocytogenes

C- Listeria monocytogenes:

listeriolysin

Associated food and Transmission:

-Unpasteurized milk products, undercooked meat & raw

vegetables

-Fresh soft cheese.

-Ready-to-eat meat.

Incubation period: 8 - 48 hrs.

Pathogenesis:

Invasion of intestinal epithelium.

Intracellular survival: Listeriolysin-O.

Cell-mediated immunity.

Watery bloody diarrhea.

host

actin

Division

Jet formation


  • Login