no

transiently colonizes respiratory & GI tracts of hospitalized patients

*major colonizers of cystic fibrosis & bronchiectasis patients & other chronic lung diseases

Pseudomonas aeruginosa pneumonia

this is the leading cause of VAP (ventilator associated pneumonia)

presentation: fever, chills, & purulent sputum

-similar to bacteremia by other GNB (more common in ICU patients)

-more serious as those infected are already immuno-compromised

-pts develop ecthyma gangrenosum (mostly in neutropenic and AIDS pts): sm/lg painful reddish, maculopapular lesions-->purple-->black/necrotic (not nearly as edematous as anthrax lesions)

Pseudomonas aeruginosa skin infection=ecthyma gangrenosum

(opportunistic infections of existing wounds/burns, hair follicles)

other P. aeruginosa skin infections incl: pyoderma (darker appearance than impetigo from staph aureus/pyogenes) & eye infections (corneal ulcer)

Pseudomonas aeruginosa

infections of the outer ear ("swimmer's ear")

from mild irritation-->destruction of cranial bones

1. endocarditis (common in IV drug abusers; tricuspid valve damaged)

2. osteomyelitis, arthritis, etc.

gram-

slightly curved aerobic rod

polar flagella => motility

mucoid colonies 

encapsulated

produces sweet grape-like odor & green color on nutrient

lactose non-fermenter on MacConkey agar

oxidase+

curved

oxidase+

gram- bacilli

very motile (single polar flagellum)

salt tolerant

non-fastidious 

grow @ wide temp & pH ranges

pathogenic strains are NOT capsulated (and => rapidly cleared from blood => infections are confined to intestines)

human infections accidental

cholera toxin & toxin co-regulated pilus (serotype O1 & O139 produce this toxin)

ALL strains produce LPS

ex. O1 can cause cholera even in absence of cholera toxin (accessory cholera enterotoxin & zonnula occludens toxin)

mediates adherence to intestinal mucosal cell

acts as binding site for phage w/ genes for cholera toxin

[bicomponent toxin: monomeric enzymatic part (A) & pentameric binding moiety (B)]

-B binds to intest epithel cells --> transfers A subunit into cytosol --> transfers ADP-ribose to G-protein --> ADP-ribosylated G-protein activates adenylate cyclase => incr cAMP => inhib reabsorption of Na+ & incr Cl- in intestinal lumen => diarrhea

1. cholera (metabolic acidosis, hypokalemia, hypovolemic shock, painless but severe diarrhea; rice-water stool)

2. gastroenteritis: milder diarrhea caused by toxin- strain

curved facultative non-fastidious rod (salt requirement=halophilic)

transmission: eating contaminated seafood/water

Vibrio parahaemolyticus

Vibrio vulnificus

poorly understood

thermostable direct hemolysin (TDH): incr Cl- secretion via incr [Ca2+] in epithelial cells; => hemolysis in human but NOT sheep RBCs

1. GI infection (range from self-limiting diarrhea-> mild cholera-like illness w/ blood/mucus)

2. wound infection (from exposure to contaminated water)

1. capsule: anti-phagocytic

2. cytolysins/collagenase/protease/siderophores

3. optimum Fe enhances virulence

-infection: most frequent during warm months/exposure to seawater; erythema, pail bullae, tissue necrosis, & septicemia

-sepsis syndrome: esp after eating contaminated raw-oysters; severe sepsis w/ liver disease (Fe availability; very high mortality 50%)

curved bacilli

darting motility (polar flagella)

oxidase+

stool specimen: ID V. cholerae (dark field microscopy)

serum agglutination (O1 serogroup)

TCBS agar: sucrose fermenting Vibrios are yellow

Species growing yellow (+) colonies fermenting sucrose:

Vibrio cholerae O1

Vibrio cholerae non-O1

Vibrio alginolyticus

Non-sucrose fermenters growing dark blue-green colonies:

Vibrio parahaemolyticus

Vibrio vulnificus

transmission: contaminated water, undercooked oysters, shrimp, other seafood

diseases: opportunistic systemic diseases in I/C pts (hepatobiliary issues); diarrheal disease/wound infection in healthy pts

ID: grows on TCBS agar; NOT halophile (growth not expidited w/ excess salt); oxidase+

gram-

spiral

micro-aerophilic rods (grow expedited w/ decr 02 and incr C02 

low G&C content

unable to ferment carbohydrates

Campylobacter jejuni

Campylobacter fetus

Name the genus:

-colonizes chicken GIT (fecal-oral transmission w/in flock)

-human acquisition from contaminated poultry/other meat, water, milk

-# of GI infections in US > Salmonella + Shigella GI infections

S-layer inhib complement mediated killing => bacteremia

infection recurrence <= antigenic variation of the S-layer protein components

gastroenteritis

-#1 cause in US

-affects: jejunum, ileum, & colon

-symptoms: fever, headache, myalgia, and/or malaise (12-48 hrs) --> diarrhea, abdominal px, fever

-complications: causes 20-40% of all Guillain Barre Syndromes

Septicemia:

-carried by monocytes to blood

-bacterium able to resist serum's bactericidal activity

-progression: starts as gastroenteritis --> persistent bacteremia, septic arthritis, meningitis

phase contrast OR dark field microscopy for "darting motility"

difficult to use traditional stains

tell micro lab to look for "vibrioid" species in stool

curve/S-shaped thin/small rod

*consider this infectious agent in all cases of inflammatory diarrhea (fever & fecal leukocytosis)

slow

microaerophilic

requires C02/high temp (42*C)

special Campy-BAP media (inhibit growth of bowel flora)

also grows on Modified Campylobacter Charcoal Differential Agar (MCCDA)

young:spiral / mature:coccoidal w/ polar flagella

motility/ability to adhere to mucosa

urease producer (makes ammonia that incr juxta-mucosal pH to survive)

chronic gastritis

not clinically significant 

[10-20% develop gastric/duodenal ulcers; 1-2% risk of stomach cancer; <1% risk of gastric MALT lymphoma]

translucent growth on enriched nutrient agar

grows w/ moist microaerophilic conditions

test for specific IgG antibodies

*Urea breath test (fasting pt drinks solution 13C/14C urea; exhaled air will show urea has been digested)