Micro: Enteric Bacteria

Front 1

Which diarrheal diseases are primarliy toxin mediated?

Back 1

Cholera

ETEC (EHEC)


Yersinia enterocolitis

Front 2

Enterotoxigenic E. Coli: Symptoms

Back 2

watery diarrhea, nausea, abdominal cramps, low grade fever

travelers diarrhea and infantile diarrhea

Front 3

Describe the virulence of ETEC?

Back 3

Enterotoxin (Cholera like)

LT: heat labile; similar to cholera toxin but milder

ST: heat stabile; causes increase in cGMP

has fimbriae and CFAs for colonization in the Small Intestine

Front 4

ETEC: What common disease does it cause?

Back 4

Traveller's diarrhea

Front 5

Enteroinvasive E. Coli(EIEC): Describe its mode of infection and symptoms.

Back 5

INVASION of Large intestine epithelium similar to Shigella

causes dysentery w/ fever, abd. cramping, blood and pus in stool

Front 6

Enteropathogenic E. Coli: What common disease state does it cause?

Back 6

Infant diarrhea

Front 7

EPEC: Describe its mode of pathogenecity?

Back 7

ADHERENCE to enterocytes (Small intestine)

effacement of microvilli

expresses intimin- mediates entry in to cell

bundle forming pilli for attachment

Front 8

EPEC: Describe pathogenesis

Back 8

ADHERENCE to sm. intestine enterocytes

EFFACEMENT of microvilli

*inflammatory response may cause ulceration

Front 9

What strain of EHEC causes disease?

Where is it typically found?

Back 9

the O157:H7 serotype

it is found in cattle, beef products, and fruit and veggies that have been fertilized with tainted manure

Front 10

What characteristic differentiates EHEC from other strains of E. coli?

Back 10

Its inability to ferment sorbitol.

Front 11

Describe the symptoms caused by EHEC.

What is its primary pathogenic mehcanism?

Back 11

hemorrhagic colitis, bloody diarrhea, abd. cramping

HUS - possibly because of specific LPS

Front 12

What is the pathogenic mechanism of EHEC?

Back 12

Shiga like TOXIN

Attachment and Effacing of microvilli leading to their death

Large Intestine

Front 13

Yersinia enterocolitica: clinical presentations?

Back 13

enterocolitis involving fever, diarrhea, and abdominal pain

nonenteric lymphadenitis may lead to septicemia

Front 14

Yersinia enterocolitica: pathogenesis?

Back 14

INVASION of M cells in small intestine

secretion of a toxin similar to E. Coli Heat stable toxin

* resevior is farm animals

Front 15

T/F: S. typhii has no animal reservoir while S. enteritidis does.

Back 15

True.

Front 16

How is E. Coli Diagnosed and treated?

Back 16

detection is difficult, some labs may serotype

treated with fluid replacement, antibiotics

EHEC strains grow on Sorbitol agar

Front 17

What are the steps involved in the pathogenesis of S. typhii?

Back 17

*binds M cells of GI epithelia *endocytosed and transferred to Peyer's patch *replicates intracellularly *passes through basal lamina *taken up by macrophage and spread thru RES

Front 18

A chronic carrier state is possible with S. typhii. What organ is notorious for sequestering the bacteria?

Back 18

Gall bladder

Front 19

EAEC: what is its primary pathogenic mechanism?

Back 19

ADHERENCE to enterocytes

Heat stabile toxin called EAST that eleveates cGMP

attaching and effacing lesions

Front 20

What are general characteristics of Enterobacteriaceae?

Back 20

Gram(-) bacteria that are part of the normal intestinal flora

non spore formers

ferment glucose

Facultive anearobes

Front 21

What are the 4 genus' of enterics?

Back 21

enterobacteriaceae, vibrionaceae, pseudomonadaceae, bacteroidaceae

Front 22

What are general characteristics of Enterobacteriaceae?

Back 22

Gram(-) bacteria that are part of the normal intestinal flora

non spore formers

ferment glucose

Facultive anearobes

Front 23

Vibrio Cholera: clinical manifestations?

Back 23

Classic "rice water" stool diarrhea w/ high fluid output

infxn may be asymptomatic, cause mild diarrhea, or result in a carrier state

Front 24

Vibrio Cholera: pathogenesis?

Back 24

polar flagellum (H-ag) - motility

pili- adherance

cholera toxin

*mucinase to digest mucous layers
*NON INVASIVE!

Front 25

Describe the Cholera toxin?

Back 25

two A subunits bridged by disulfide bonds and 5 identical B subunits

A1 is active subunits-enters cell upregulates adenyl cyclase --> increased cAMP leading to cause massive efflux of Na= and H20

*regulon family of genes

Front 26

Vibrio Cholera: Diagnosis?

Back 26

darkfeild microscope

isolation on thiosulfate-citrate-bile-sucrose(TCBS) agar

agglutination in specific antisera

Front 27

Vibrio Cholera: Rx?

Back 27

Rehydration orally

IV Tetracycline

Front 28

Vibrio Cholera: Immunity?

Back 28

post infection Abs

gastric acidity

vaccines are KILLED WHOLE CELLS

Front 29

Vibrio parahemolyticus

Back 29

marine org, infects shellfish

major cause of FP in Japan and in US from eating raw shellfish

explosive diarrhea (w/o blood or mucous), cramps, nausea, vomiting

*produces a toxin

Front 30

Vibrio vulnificus

Back 30

found in salt h2o, infects sun bathers and those ingesting raw shellfish

can cause a fatal bacteremia

immunocompromised, liver diseased and thalassemia increase risk

Front 31

Campylobacter jejuni: transmission?

Back 31

transmitted by contaminated milk, H20, poultry

Front 32

Camplylobacter jejuni: clinical manifestations?

Back 32

bloody, pus-filled diarrhea, severe ab pain, fever

high pediatric incidence

no1 cause of gastroenteritis in developed world

*assoc. w/Guillan-Barre syndrome

Front 33

Camplylobacter jejuni: bacterial characteristics?

Back 33

G- curved rod

microaerophilic

motile

INVASIVE

Front 34

Helicobacter pylori: clinical manisfestations?

Back 34

cause of gastritis, PEPTIC and DUODENAL ULCERS

makes a urease theat produces NH3 from urea

cured with Antibiotics

Front 35

Shigella species: clinical manifestations?

Back 35

shigellosis- fever, chills, abdominal cramps, tenesmus

blood/ pus/ mucous in stool

can cause convulsions and meningitis in infants

S. dysenteriae cause most severe infections; S.sonnei and S.flexneri most common in US

Front 36

Shigella species: transmission?

Back 36

man is primary host

P to P: fecal-oral transmission or by vectors(food, fingers, feces, flies)

associated w/ overcrowding and poor sanitation

Front 37

Shigella species: Pathogenesis?

Back 37

invades/ damages mucosa of large intestine, ulceration, and appearance of PMNS --> scarring

invasion genes are on plasmid, involves actin polymerization

non motile

Shiga toxin, INVASION

Front 38

Shigella species: Describe the Shiga toxin?

Back 38

A+B toxin (similar to Cholera)

inhibits protein synthesis by inactivating the 60s ribosome

also behaves as neurotoxin

*not essential for virulence
*associated w/HUS

Front 39

Shigella species: diagnosis?

Back 39

rectal swab
stool culture

*Shigella IS NOT Normal Flora

Front 40

Shigella species: Rx and immunity?

Back 40

rehydration

antibiotic resistance emerging

previous infection only gives short lived immunity, no vaccine

Front 41

Salmonella gastroenteritis: clinical manifestations?

Back 41

diarrhea, fever, cramping, nausea, vomiting, headache

onset 24-48 hrs after ingestion

diarrhea has rotten egg smell

blood stream invasion may occur, but disease is usually self limiting

Front 42

Salmonella gastroenteritis: organisms

Back 42

S.typhi --> typhoid fever

S.typhimurium - most common causitive org in US

S. enterica

Front 43

What are the 3 clinical sydromes that can result from infection with Salmonella species?

Back 43

1. enteric fever

2. septicemic syndrome

3. gastroenteritis

Front 44

Salmonella gastroenteritis: transmission?

Back 44

fecal-oral route

pet turtles

chicken, raw eggs, mayonaise

unpasteurized OJ, apple cider

Front 45

Salmonella gastroenteritis: pathogenesis?

Back 45

attachment and invasion of mucosal (M cells) of SMALL INTESTINE, damages tissue

may produce a toxin but not major virulence factor

*INVASIONS

Front 46

Salmonella gastroenteritis: diagnosis?

Back 46

fecal culture on selctive/differential agar (Salm are lac-)

slide agglutination for serogroups

Front 47

Salmonella gastroenteritis: Rx and immunity?

Back 47

flouroquinolones (ciprofloxacin)

antimotility drugs

no vaccine

Front 48

Enteric Fevers: causitive agents?

Back 48

S. typhi - typhoid fever, Vi antigen (capsular polysacchride)

S. paratyphi and S.schotmulleri cause milder fevers

Front 49

Enteric Fevers: clinical manifestations?

Back 49

intially malaise, headache, anorexia

wk1: gradual stepwise rise in fever, constipation or diarrhea

wk2: rose spots, hi fever, septecemia

wk3: fever remits, may have ulceration and gut perforation --> bloody diarrhea

Front 50

Enteric Fevers: pathogenesis?

Back 50

ingested and multiply in small intestine

penetrate mucosa at distal end ileum through M cells at Peyers Patches, move through blood stream --> bacteremia

infection of gall bladder can lead to chronic carrier state or reinfection

Front 51

Enteric Fevers: Transmission?

Back 51

S.typhi only infects humans by direct contact or ingesting food contaminated by orgs shed by carrier (Typhoid Mary)

Front 52

Enteric Fevers: Diagnosis?

Back 52

isolation of org on agar or serotyping

blood is positive in wk1 of infection

stool is positive after wk1

Widal test

Front 53

Enteric Fevers: Rx and immunity?

Back 53

Short course, fluoroquinolones

Abs protects, infection stimulates cellular immunity

Vaccines: killed whole cells, live attenuated, IV injected capsular polysacchride

Front 54

Septicemic Syndrome: organism and clinical manifestations?

Back 54

S. cholraesuis

causing spiking fevers w/ frequent seeding to various organs --> abscesses, meningitis, pneumonia, osteomyelitis, endocarditis

Front 55

General characteristics of Enteric Bacteria

Back 55

Gram - bacilli