enteric bacteria Flashcards by Caleb Houghton

enteric bacteria
gram?
shape?
common in what flora?

Gram−
bacilli
Some are common members of human and animal flora

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pathogenic enteric bacteria

Some are members of commensal groups that have become pathogenic due to acquired virulence factors like toxins from plasmids, bacteriophages or“pathogenicity islands”

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motility of enteric bacteria

Most can be motile with peritrichous flagella (H-antigen)

Some are non-motile (Shigella, Klebsiella, Yersinia)

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pili of enteric bacteria

Most have surface pili: fimbriae for adherence and sex pili for
plasmid conjugation

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capsules of enteric bacteria
named antigen?
which species

Some species have capsules (K or Vi antigen)

most Klebsiella species, some Enterobacter and E.coli species

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enteric bacteria LPS

all strains with outer-membrane LPS (heat-stable endotoxin) with enterobacterial common antigen and serotype-specific O- antigen

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When bacteria have a toxin like cholera toxin:

get watery diarrhea

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When also have a toxin like

Shiga toxin:

get blood in diarrhea

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When also have inflammation

and neutrophils:

get pus in diarrhea =dysentery

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Characterization of various
pathogenic E. coli strains is
based on

toxins produced and pattern of cell invasion and destruction

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transmission modes of enteric bacteria

Transmission: • person-to-person • “seven F’s” = feces, food,
fluids, fingers, flies, fomites, and fornication

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other virulence factors of gram- enteric bac could cause?

bacteremia

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LPS of enteric bac common antigen? variable portion?

Outer- and inner-core sugars are the enterobacterial common antigen
O antigen is the variable portion

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LPS also known as

heat stable enterotoxin

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LPS shedding

LPS gets shed from bacteria and is bound by plasma protein LBP (LPS-binding protein).
This facilitates binding to macrophages and enhances inflammatory response

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lipid A of LPS activates?

inflammatory response of macrophages

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“pathogenicity island”

= chromosomal location with multiple virulence factors and toxin genes, readily transferable together by conjugation.
Example: uro-pathogenic E.coli

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cholera-like AB-exotoxin mechanism

B component binds the membrane of the host cell and A component penetrates
A component will act as an ADP ribotrasferylase and activate a G pro
G pro causes adenylate cyclase to increase cAMP leading to increased electrolyte and water secretion= severe watery diarhea

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cholera-like AB-exotoxin known as

heat liable enterotoxin

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Type III secretion system
found in what strains?
mechanism?

present in: Yersinia, Salmonella, Shigella, enteropathogenic EPEC (E.coli), Pseudomonas and Chlamydia (all gram-)

20-protein system that looks like a short, hollow flagellum (“needle”) to inject a variety of species specific toxins into host cells; often affects actin filaments/ rearranges them to allow bacteria to adhere (EPEC)

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intimin/ TIR
strains seen in?
how is TIR delivered?

seen in both EPEC and EHEC

TIR delivered to host cell mem via type III secretion, allows both e coli strain to bind

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Escherichia coli transmission

person-to-person
contaminated food
human and animal feces (no hand washing; insect vectors)

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additonal pathogenic e coli strains

Uro-Pathogenic E.coli

• Meningitis-associated E.coli

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e coli gram?

negative

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e coli virulence factors

``` heat-labile enterotoxin “LT" (cholera-like AB-exotoxin) shiga toxin (AB-exotoxin cytotoxin) ```

Ø heat-labile enterotoxin “LT" of E coli

(cholera-like AB-exotoxin): ADP-ribosylation of G protein ► cAMP ► loss of water + electrolytes ► watery diarrhea (e.g. foodborne enterotoxigenic ETEC E.coli) cause of travellers diarhea

Shiga toxin of E coli mechanism? strain? additonal complication?

(AB-exotoxin cytotoxin): inactivation of 60S ribosome subunit by removal of a specific adenine base from a nucleotide of 28S rRNA ► stop translation ► cell death ►bloody diarrhea (e.g. foodborne enterohemorrhagic EHEC E.coli O157:H7) In addition: ► hemolytic uremic syndrome ► kidney damage

Shigella dysenteriae

In Shigella dysenteriae this set of symptoms “diarrhea with blood” is combined with intestinal cell invasion, apoptosis and neutrophilia (► “pus”) to define “dysentery

treatment of mild forms of diarhea

oral rehydration | mixture of water with salts and sugars

seasonal occurance of GI diseases

more common when warm= spoiled food

EHEC EnteroHemorrhagic (typically O157:H7) clinical presentation

bloody diarrhea hemorrhagic colitis hemolytic uremic syndrome

EHEC EnteroHemorrhagic (typically O157:H7) treatment

replenish fluids (antibiotics are contraindicated)

UroPathogenic presentation | casuative strains %?

cystitis/ bladder infections | 70-90% caused by E coli, 5-10 by klebsiella/proteus amd 5-10 by s. saprophyticus

Shigella dysenteriae cell entry/infection

Shigella dysenteriae epidemiology

oral-fecal route, contaminated food/ water, humans the only source

Shigella dysenteriae virulence factors | lead to?

Shiga toxin: bloody and watery diarrhea cell invasion: neutrophils/ pus both lead to dysentery

``` Salmonella strain causes what fevers? reservoir? mortality? ```

S.enterica • enteric fever, typhoid fever • human reservoir • high mortality

Many Salmonella species cause? | from what source outside humans?

* gastroenteritis | * poultry reservoir= foodborne illness

Virulence Factors of salmonella

type III secretion | growth within macrophages

type III secretion in salmonella induces?

Type III secretion induces enteric epithelial uptake via M cells

endosomal growth in macrophages by salmonella allows for? how can it not be destroyed in macrophages? destruction of what gut structure?

intracellular endosome growth in macrophages: secretes protein that prevents phagosome-lysosome fusion in S.typhi serovars: Ø through macrophages: invasive into different tissues and organs (bacteremia) Ø destruction of Peyer’s Patches ► intestinal rupture

``` Salmonella invasion of intestinal epithelia which cells? causes? release of? transport to? ```

* M cell uptake through ruffles: transport through epithelial layer. * Electrolyte release to lumen (diarrhea/gastroenteritis). * Release of inflammatory exudate. * Transport to lymph nodes / transient bacteremia, can lead to further disease

Typhoid Fever diagram how can it lead to speticemia? carrier state?

Enterobacteriaceae gram shape respiration

Gram- rods, aerobic / facultatively anaerobic

Vibrio cholerae gram shape found where?

Gram− vibrio (curved rods) (salt tolerant) found in estuaries and marine environments

Virulence Factors of vibro cholarae

``` toxin co-regulated pilus cholera toxin additional toxin “ST” Neuraminidase other toxins ```

virulence factors of Vibro cholera delivered how (to the bac)?

toxin is phage CTXφ-encoded and regulated by pilin-regulating chromosomal gene

Ø toxin co-regulated pilus (tcp) of Vibro cholera allows for?

adhesion to small intestinal epithelia

cholera toxin/ ST toxin of Vibro Cholera

``` cholera toxin (heat-labile exotoxin “LT”): protein A causes cAMP rise + watery diarrhea an additional toxin “ST” can raise cGMP levels with a similar effect ```

Neuraminidase of vibro cholera

-increase cholera toxin binding

CTXφ (a bacteriophage) and Vibrio cholerae

TCP = Toxin coregulated pilus, TCP production is induced within the intestine, while production in other environments appears to be minimal, allows the phage to deliver genes to the bacteria for replication, expression and secretion (contains the genes for various virulence factors)

which genes of CTXφ (a bacteriophage) encode the cholera toxin for Vibrio cholerae

ctxA and ctxB encode the proteins that comprise cholera toxin

cholera vax

formalinized whole-cell vaccine (inactivated cell) : several doses; partial protection for 2-3 yrs

epidemic strains of cholera | common one/ new one?

Common epidemic strain: serovar O1 | New strain: serovar O139 with capsule as new virulence factor (O1 vaccine does not protect)

clincal features vibro cholera | limited?

severe watery diarrhea | self-limiting: intestinal surface cells with bacteria are shed

treatment vibro cholera

rehydration

epidemiolgy of vibro cholera

fecal transmission | under cooked coastal crabs

Campylobacter jejune | gram and shape

Gram− | vibrio (short S- or comma-shaped rods)

Campylobacter jejune virulence factors

Ø LPS Ø capsule Ø cytolethal distending toxin Ø Growth in intestinal tract:

Campylobacter jejune growth in intestinal tract where? can lead to?

§ invade intestinal epithelial cells or grow below epithelial layer. § inflammatory response

Campylobacter jejune disease resolution

resolves without treatment in 1 week, creates protective immunity

Campylobacter jejune often from? transmission? diseases caused?

Zoonosis: animal reservoir (intestinal) Transmission: contaminated food Disease: gastroenteritis, diarrhea, dysentery

bacteremia of Campylobacter jejune:

rarely causes bacteremia