Gram Negative Curved Rods – Flashcards
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Unlock answers| organism common in nosocomial infections (esp those associated w/ respirators/indwelling catheters) |
| Pseudomonas aeruginosa |
| characteristics of Pseudomonas aeruginosa |
| *oxidase+ (use this to differentiate bt/w Pseudomonas & Enterobacteriaceae) |
| is Pseudomonas aeruginosa found in normal flora? |
no transiently colonizes respiratory & GI tracts of hospitalized patients *major colonizers of cystic fibrosis & bronchiectasis patients & other chronic lung diseases |
| Pseudomonas aeruginosa strongly adheres to mucus --> |
| decr mucociliary clearance => mucus stasis & accumulation --> P. aeruginosa alters virulence & attenuates host immune response => cause slow lung injury over decades |
| most common P. aeruginosa infection |
Pseudomonas aeruginosa pneumonia this is the leading cause of VAP (ventilator associated pneumonia) presentation: fever, chills, & purulent sputum |
| Bacteremia caused by Pseudomonas aeruginosa |
-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) |
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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) |
| #1 cause of otitis externa |
Pseudomonas aeruginosa infections of the outer ear ("swimmer's ear") from mild irritation-->destruction of cranial bones |
| other diseases caused by Pseudomonas aeruginosa: |
1. endocarditis (common in IV drug abusers; tricuspid valve damaged) 2. osteomyelitis, arthritis, etc. |
| identify Pseudomonas aeruginosa |
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+ |
| characteristics of Vibrio cholerae |
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 |
| major Vibrio cholerae serotype in south east asia |
| O1 |
| Vibrio cholerae virulence |
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) |
| function of toxin regulated pilus (Vibrio cholerae) |
mediates adherence to intestinal mucosal cell acts as binding site for phage w/ genes for cholera toxin |
| function of colonization factors (Vibrio cholerae) |
| colonizes mucosal cells (essential to virulence) => bacteria not washed out w/ diarrhea |
| cholera toxin mechanism |
[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 |
| 2 diseases caused by Vibrio cholerae: |
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 |
| virulence factor of Vibrio parahaemolyticus |
poorly understood thermostable direct hemolysin (TDH): incr Cl- secretion via incr [Ca2+] in epithelial cells; => hemolysis in human but NOT sheep RBCs |
| diseases caused by Vibrio parahaemolyticus |
1. GI infection (range from self-limiting diarrhea-> mild cholera-like illness w/ blood/mucus) 2. wound infection (from exposure to contaminated water) |
| virulence of Vibrio vulnificus |
1. capsule: anti-phagocytic 2. cytolysins/collagenase/protease/siderophores 3. optimum Fe enhances virulence |
| diseases caused by Vibrio vulnificus |
-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%)
|
| identifying Vibrio species |
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 |
| Name the species exhibiting fermenting growth on thiosulfate citrate bile salt sucrose (TCBS) agar. What carbohydrate are they fermenting and what color are the colonies? |
Species growing yellow (+) colonies fermenting sucrose: Vibrio cholerae O1 Vibrio cholerae non-O1 Vibrio alginolyticus |
Name the species exhibiting non-fermenting growth on thiosulfate citrate bile salt sucrose (TCBS) agar. What carbohydrate are they not fermenting and what color are the colonies?
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Non-sucrose fermenters growing dark blue-green colonies: Vibrio parahaemolyticus Vibrio vulnificus |
| characteristics, diseases, and identification of Aeromonas hydrophila |
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+ |
| general characteristics of Campylobacter & Helicobacter |
gram- spiral micro-aerophilic rods (grow expedited w/ decr 02 and incr C02 low G&C content unable to ferment carbohydrates |
| this genus grows best at 42*C, name 2 important species & associated diseases |
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 |
| Campylobacter |
| #1 cause of bacterial gastroenteritis in US |
| Campylobacter (esp C. jejuni) |
| Pathogenesis: Campylobacter jejuni is endocytosed by monocytes, intestinal epithelial & M cells--> |
| infection => host cell death/bowel ulceration/intense inflammation-->PMNs, monocytes, & eosinophils infiltrate the lamina propria |
| Pathogenesis: Campylobacter fetus has proteinaceous capsule-like layer (S-layer)=> |
S-layer inhib complement mediated killing => bacteremia infection recurrence <= antigenic variation of the S-layer protein components |
| Describe the disease caused by Campylobacter jejuni/coli/upsaliensis: |
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 |
| Describe the disease caused by Campylobacter fetus: |
Septicemia: -carried by monocytes to blood -bacterium able to resist serum's bactericidal activity -progression: starts as gastroenteritis --> persistent bacteremia, septic arthritis, meningitis
|
| identify Campylobacter jejuni |
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) |
| growth of Campylobacter jejuni |
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) |
| visual characteristics of Helicobacter pylori |
young:spiral / mature:coccoidal w/ polar flagella
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| What factors promote stomach colonization of Helicobacter pylori? (colonizes the interface of gastric epith & overlying mucous gel layer) |
motility/ability to adhere to mucosa urease producer (makes ammonia that incr juxta-mucosal pH to survive)
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| 70-100% of pts w/ gastritis & gastric/duodenal ulcers are infected by which pathogen? |
| Helicobacter pylori |
| The majority of Helicobacter pylori infected individuals develop which disease? |
chronic gastritis not clinically significant [10-20% develop gastric/duodenal ulcers; 1-2% risk of stomach cancer; <1% risk of gastric MALT lymphoma] |
| Identify Helicobacter pylori: |
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) |
