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40 Cards in this Set

  • Front
  • Back
Enterobacteriaceae
normal gut flora, opportunistic pathogens

primary pathogens
1. salmonella
2. shigella
3. yersinia
4. E. coli (some strains)
E characteristics
gram negative bacilli

facultative

oxidase negative

ferment glucose
E growth media
selective - bile salts & dyes

differential- lactose & pH

coliforms = ferment lactose
pathogens = lactose negative
Coliforms
e. coli and related enteric bacteria (NOT pathogens) that may indicate fecal contamination in drinking water supplies
E antigens
O antigen = lipopolysaccharide

K antigen = capsular polysaccharide

H antigen = flagella
E pathogenesis
colonize epithelial surface and produce toxins

1. ETEC
2. EPEC
3. EHEC

invade mucosal epithelium
1. shigella
2. Enteroinvasive E. coli

invade gut lymphoid tissue, systemic dissemination
1. salmonella species
2. yersinia species
Bacterial Type III Secretion

1. salmonella
2. shigella
3. e. coli
4. yersinia
5. pseudomonas
bacterial effector proteins directly into target cells
*evolved from flagella

found in GRAM NEGATIVE

encoded on 'pathogenicity islands'
*present only in PATHOGENS

Pathogenic function

1. disruption of host cell signaling

2. disturbance of inflammatory response

3. disturbance of cytoskeletal dynamics
Enterotoxigenic E. coli

*incubation 1-3 days
*self-limiting 5 days
acute watery diarrhea

colonize small intestine via fimbriae

production of enterotoxins
1. heat labile toxin: like cholera, cAMP increases
2. heat stable toxin:
increases cGMP
ETEC Dx, Tx, Epi
clinical dx

maintain hydration, give antisecretory agents, antibiotics

human are source

can give prophylaxic antibiotics for travellers
Enteropathogenic E. coli
persistent inflammatory non-bloody diarrhea

colonization of epithelial cells

actin polymerization- via type III secretion

sporadic disease and outbreaks in infants under 2 years of age
Enterohemorrhagic E. coli
evolved from EPEC

bloody diarrhea and Hemolytic Uremic Syndrome (death, hemolytic anemia, thrombocytopenia, kidney failure-thrombus in glomeruli)

colonization of colon and production of SHIGA toxin
(AB structure with N glycosidase activity)

inhibition of protein synthesis in target cells
EHEC dx, tx
culture of SORBITOL non-fermenting

NO antibiotics (will increase risk of HUS and shiga release)

supportive therapy for HUS
*transfusions and dialysis

*early aggressive hydration can decrease risk of HUS
EHEC epi
serious disease in children and elderly

foodborne-person to person

CATTLE are reservoir

improperly cooked beef, unpasteurized juice, veggies, other food

resistant to acidity, not many organisms needed to infect (100 bacteria = disease)
Shigella species

1. s. sonnei
2. s. flexneri
3. s. dysenteriae
4. s. boydii
non-lactose fermenter
non-motile
DYSENTERY - acute bloody diarrhea
*severe intestinal cramping and tenesmus and high fever
Shigella pathogenesis
resistant to gastric acidity

invasion of colonic mucosal epithelial cells

extensive tissue damage

cell to cell spread
S dx, tx, epi
stool culture

Ab (very contagious and will shorten duration)

humans are source

very low infective dose (10)
common in US
Salmonella enterica
NON-lactose fermenter
h2s production
SE non-typhi

*uncommon bacteremia
acute gastroenteritis

occasionally becomes systemic

associated with compromised defense and AB use
SE non-typhi Pathogenesis
colonization of small intestine

invasion of epithelial cell

type III secretion
1. inject effector cells
2. actin binding
3. inositol signaling change
SE non-typhi DX & TX
stool culture

blood culture in systemic disease

no AB for healthy, AB for ICZ

infection from animal, second to CJ for diarrhea
SE type Typhi

Enteric Fever- Typhoid Fever
bacteremia
virulence from capsular polysaccharide

10 days incubation, insidious onset

prolonged fever- ROSE SPOT lesions,

complication in 3rd week
1. ulceration
2. hemorrhage
3. perforation of intestine
4. metastatic infection
SE type Typhi Pathogenesis
invasion of intestinal epithelial cells

survives in macrophage and monocyte

seeds in gut lymphoid tissue- becomes metastatic from there
SE type Typhi Dx, Tx, Epi
blood culture, serology, AB

human source, TYphoid Mary

live attenuated vaccine
(multiple doses)
or
purified virulence polysaccharide vaccine
(single intramuscular inj)
Yersinia Entercolitica
gram negative coccobacilli
lactose non-fermenting
slower growth than other enteric

enterocolitis = 1 to 3 week
YE pathogenesis
invasion of peyer's patches

disruption of phagocytic process

heat stable enterotoxin
YE culture, treatment, epi
culture on enteric agar

self-limited

acquired from animal - PORK
E. coli expressing K1 capsular polysaccharide
Antiphagocytic K1 capsular polysaccharide

poorly immunogenic

(capsule allows it to survive intracellularly in human brain microvascular endothelial cells
EColi K1
culture from CSF, blood

AB therapy

most common etiology of neonatal meningitis
UTI
e.coli (80%)
s. saprophyticus (20%)

do leukocyte esterase assay (dipstick)
UTI in women
sexual activity
pregnancy
Klebsiella pneumoniae

(opportunistic enteric pathogen)
lots of capsular polysaccharide production
Enterobacter cloacae

(opportunistic enteric pathogen
IV fluid contamination, pneumonia, surgical wound infection
Serratia marcescens

(opportunistic enteric pathogen
multiple AB resistance

sepsis, pneumonia, UTI
Proteus Mirabilis

(opportunistic enteric pathogen
urease production, swarming motility, UTI
SEPSIS mechanism
GRAM NEGATIVE

1. LPS- Lipid A bound by serum LBP

2. this complex binds to CD14 and TLR4 on monocytes

3. TNF, IL-1 production and secretion via monocytes

GRAM POSITIVE

same, via peptidoglycan, lipoproteins, pyrogenic exotoxins
Noscomial Sepsis
Gram Positive
-staphy and enterococcus

Gram Negative
-e.coli, klebsiella, enterobacter, pseudomonas

Fungi
-candida albicans

TX=
antimicrobial therapy
supportive
recombinant activated protein C
Pseudomonas aerugnosa
GRAM NEGATIVE Bacillus
oxidase positive
green pigments
persists in soil and moist environments
PA disease
opportunistic infections

pneumonia in CF patients
burn wounds/sepsis
nosocomial pneumonia, UTI, sepsis
PA pathogenesis
adherence to mucins, ECM
biofilm formation
antiphagocytic polysaccharide capsule
exotoxin A
ADP ribosyl transferase modifies EF2- inhibits protein translation
PA dx, tx
culture
AB (has innate and acquired resistance)