Bacterial Pneumonia 1 Flashcards
P. aeruginosa
Gram?
Aerobe?
Fermenter?
Oxidase?
What does it produce?
Where is it found?
What are its growth requirements?
Detergents and disinfectants?
Antibiotics?
What makes it a good nosocomial pathogen?
Gram(-) rods
Strict aerobes
Nonfermenters
Oxidase(+)
1 - Produces pyocyanin GREEN (exotoxin) & pyoverdin (siderophore)
2 - Glycocalyx (slime layer) (anti-phagocytic)
Usually free-living environmental
Can be normal flora
Minimal growth requirements
Resistant to detergents & disinfectants
Extremely Ab resistant
Fairly common saprophyte (eats dead material); Opportunistic pathogen
Ability to grow in water + Ab resistance + vulnerable patients = nosocomial pathogen
Grows easily in IV fluid, irrigation solutions
“Vulnerable:” extensive burns, chronic respiratory disease (CF), immunosuppression, long-term catheterization, IVs, neonates
P. aeruginosa Nosocomial Pathogenesis by the Numbers
1 cause of osteocondritis
Causes 10% of all nosocomial infections, #2 cause of nosocomial pneumonia, #1 for ICU pneumonia
Most common Gram(-) isolate from corneal ulcerations and endocarditis
Second most common cause of brain abscess in cancer patients
P. aeruginosa Community-Acquired Pathogenesis
What are 4 different manifestations of the bacteria?
Endocarditis in IV drug users
Otitis externa / folliculitis in underchlorinated hot tubs
Osteochondritis in puncture wounds through sneaker soles (most common in children)
Corneal infection in contact lens wearers
P. aeruginosa pathogenesis - VIRULENCE FACTORS
Endotoxin: cell wall component; when bloodborne -> sepsis
Exotoxins: can be released into tissue (ExoA, similar to diphtheria tox) or injected into host cells (type III secretion sys, ExoS, damages cytoskeleton)
Enzymes: elastase, protease: histotoxic, facilitate invasion of bloodstream
Pyocyanin interferes with the terminal electron transfer system (toxic to aerobes)
Glycocalyx is antiphagocytic
Efflux pumps: toss antibiotics back out of cytoplasm
-Outer membrane is 10-100X less permeable to antibiotics than E. coli ‘s
P. aeruginosa diagnosis:
Where can it infect?
What happens if immunocompromised or neonate?
Can infect anywhere, but predominantly nosocomial UTI, CF pneumonia, burns: local infections in previously-healthy hosts
If immunocompromised or neonate, progression to sepsis, >50% mortality
Pneumonia
Endocarditis
Meningitis
Ecthyma gangrenosum
LESION BEGAN ON THE INSIDE – BAD PROGNOSIS
P. aeruginosa diagnosis: exam
CHEST XRAY and Lab
What does nonbacteremic pneumonia look like?
What does bacteremic look like/
Nonbacteremic pneumonia resembles S. aureus: diffuse bronchopneumonia (usually bilateral with distinctive nodular infiltrates with small areas of radiolucency) and pleural effusions
Bacteremic progresses rapidly, note (1) poorly-defined, hemorrhagic, often subpleural, nodular areas with a small central area of necrosis and (2) multiple, 2-mm to 15-mm, necrotic, umbilicated nodules with hemorrhagic parenchyma – starts with sepsis
2 sets of cultures: aerobic & anaerobic (2nd will fail)
Culture from relevant fluids: sputum for lungs, biopsy / aspirate for joints, CSF for CNS, blood for sepsis
Nonfermenting, oxidase(+)
Metallic sheen on triple-sugar-iron (TSI) agar
Green color on nutrient agar (pyocyanin)
Fruity aroma
Biochemical tests available
P. aeruginosa treatment
Remove/change catheters/IVs
Begin Abs without delay
Ab sensitivity testing
Continue testing during treatment
For uncomplicated UTIs, ciprofloxacin
Everything else: Antipsuedomonal penicillin: piperacillin/tazobactam or ticarcillin/clavulanate plus gentamicin or amikacin
P. aeruginosa prevention
Keep neutrophil counts up
Remove/change catheters/IVs
Burn unit precautions
Handwashing
Experimental vaccines are available to CF patients
Burkholderia cepacia
What is a similarity to P. aeruginosa?
Who does it infect?
Like P. aeruginosa, Grows easily in IV fluid, irrigation solutions
Like pseudomonas but not as successful bacteria. A previously healthy patient will not get infected
Unlike P. aeruginosa, very limited ability to infect otherwise-healthy patients, may be considered “colonizing” rather than “infecting”
CF pneumonia, pneumonia in other preexisting diseases with neutropenia, catheter-assoc UTIs, IV-assoc septicemia, wound infections, foot rot in swamp-deployed military
CF / cepacia pneumonia experience has become more common as CF longevity has improved
Cepacia pneumonia in CF centers forms outbreaks
Cepacia Syndrome: accelerated pulmonary course with rapidly-fatal bacteremia
B. cepacia diagnosis and treatment
No pyocyanin
No treatment required in otherwise-healthy patient
If CF, cancer, HIV, etc: Treat with trimethoprin-sulfamethoxazole, alternates third-generation cephalosporins, ciprofloxacin, ampicillin-sulbactam, chloramphenicol, or meropenem
Experimental vaccines are available to CF patients
B. pseudomallei
Where is it found?
How is it transmitted?
Gram? Motility?
Primarily developing-nation veterinary: melioidosis (mel-lee-oy-DO-sis)
Transmission by direct contact with contaminated water, soil
Motile Gram(-) rod
Human-to-human transmission can rarely occur; standard precautions, mask on patient
US has a few cases per year: travelers, immigrants, IV drug users
B. pseudomallei pathogenesis
What does the disease look like?
what are risk factors?
what happens with a milder infection?
Initial Symptoms flulike (fever, sweats, rigors, headache) + muscle tightness, light sensitivity
Range of severity: acute local to septicemia with abscesses in all organs
Septicemia Flushing Cyanosis Disseminated pustular eruption High fevers Rigor Bloody, purulent sputum Untreated fatal in 7-10d
Risk factors for severe infection include diabetes, renal dysfunction, chronic pulmonary disease
Milder infections may “resolve” and then reactivate years later; reactivation from lung abscess resembles TB
Reactivation seen in Vietnam veterans
B. pseudomallei diagnosis and treatment
Diagnose by patient history, culture & Gram stain from blood, urine, skin lesions
PCR and immunofluorescence assays exist
Imaging studies may also be helpful: abnormal chest X ray plus multiple small abscesses in liver & spleen on sonogram
Treat with several weeks of Ceftazidime alone or in combination with either trimethoprim-sulfamethoxazole or amoxicillin clavulanate
Reportable
Burkholderia mallei
Primarily developing-nation veterinary: Glanders
Bacterium is nonmotile
Both melioidosis and glanders have been used as biowarfare agents: during WWI, used to infect Russian horses&donkeys.
Both could theoretically be used against humans in aerosolized form.
Rare zoonosis, assumed infected discharge passes through broken skin
Maintained in animal reservoirs, not soil or water – cleared from US livestock in 1945
Human-to-human transmission can rarely occur; standard precautions, mask on patient
Symptoms flulike (fever, sweats, rigors, headache)
Severity varies
- Acute localized: nodule at infection site
- Acute pulmonary: bronchitis -> pneumonia
- Acute septicemic: fulminant, multiorgan involvement
Septicemia: flushing, cyanosis, and a disseminated pustular eruption untreated fatal 7-10 days
Milder infection may establish a chronic form called “Farcy”
B. mallei diagnosis and treatment
Diagnose by patient history, culture & Gram stain from blood, urine, skin lesions
PCR and immunofluorescence assays exist
Long-term Ab treatment with amoxicillin and clavulanate, doxycycline, or trimethoprim and sulfamethoxazole
Reportable
If no evidence of animal attack or occupational exposure, inform CDC and FBI as well as local health authorities.
