Unit 4 - Bacterial Pneumonia: Pseudomonas/Burkholderia and Chlamydia Flashcards

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1
Q

what are the Pseudomonad bacteria?

A

also called Burkholderia

  • P. aeuroginosa
  • B. cepacia
  • B. pseudomallei
  • B. mallei
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2
Q

explain P. aeuroginosa bacteriology?

  • growth?
  • use of Ab?
A
  • G- rods, strict aerobes and non-fermenters
  • oxidase+
  • produces pyocyanin (exotoxin, bright green color) and pyoverdin (siderophore)
  • glycocalyx (antiphagocytic slime layer)
  • resistant to detergents and disinfectants (can live in just distilled H2O)
  • extremely Ab resistant
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3
Q

explain P. aeruginosa pathogenesis?

-growth requirements?

A

fairly common saprophyte (opportunistic)

  • usually free-living environmental that can be normal flora (skin surface) or opportunistic pathogen (in lungs)
  • -ability to grow in water + Ab resistance + vulnerable patients = nosocomial pathogen
  • minimal growth requirements (IV fluid, irrigation solutions)
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4
Q

who are “vulnerable” patients to P. aeruginosa?

A
  • extensive burns
  • chronic respiratory disease (CF)
  • immunosuppression
  • long-term catheterization
  • IVs
  • neonates
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5
Q

explain P. aeruginosa community-acquired pathogenesis?

A
  • endocarditis in IV drug users
  • otitis externa/folliculitis in underchloerinated hot tubs
  • osteochondritis in puncture wounds through soles (most common in children)
  • corneal infection in contact lens wearers
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6
Q

what are P. aeruginosa virulence factors?

A
  • endotoxin: cell wall component (when bloodborne –> sepsis)
  • exotoxin: can be released into tissue (ExoA, similar to diptheria) or injected into host cells (T2SS, ExoS, damages cytoskeleton)
  • enzymes: elastase, protease (histotoxic, facilitate invasion of bloodstream)
  • pyocyanin: interferes w/ terminal electron transfer system
  • glycocalyx: antiphagocytic
  • efflux pumps: toss antibiotics back out of cytoplasm
  • outer membrane is 10-100x less permeable to antibiotics than E. coli
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7
Q

where can P. aeruginosa infection be? in healthy VS immunocompromised?

A

anywhere

  • predominantly nosocomial UTI, CF pneumonia, burns
  • local infections in previously healthy hosts
  • if neonate or immunocompromised: sepsis, pneumonia, endocarditis, meningitis, acthyma gangrenosum has >50% mortality
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8
Q

what is ecthyma gangrenosum?

A

patch of destroyed tissue in immunocompromised due to P. aeruginosa

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9
Q

what does nonbacteremic pneumonia show on CXR?

A

resembles S. aureus

  • diffuse bronchopneumonia
  • -usually bilateral with distinctive nodular infiltrates with small areas of radiolucency
  • pleural effusions
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10
Q

what does bacteremic pneumonia show on CXR?

A

progresses rapidly

  • poorly-defined, hemorrhagic, subpleural, nodular areas with small central area of necrosis
  • multiple, 2-15 mm, necrotic, umbilicated nodules with hemorrhagic parenchyma
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11
Q

what does P. aeruginosa lab show?

A

very easy to culture; must make aerobic and anaerobic (2nd will fail)

  • culture relevant fluids (lung sputum, joint biopsy/aspirate, CNS CSF, blood for sepsis)
  • nonfermenting, oxidase+, beta-hemolysis
  • metalic sheen on triple-sugar-iron (TSI) agar
  • green color on nutrient agar (pyocyanin)
  • fruity aroma
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12
Q

what is P. aeruginosa treatment?

A
  • remove/change catheters/IVs
  • begin antibiotics immediately, with sensitivity testing (repeating during treatment; extremely antibiotic resistant)
  • for uncomplicated UTIs, use ciprofloxacin
  • for everything else, must use combo antibiotics
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13
Q

what is prevention of P. aeruginosa

A
  • keep neutrophil count up
  • remove/change catheters/IVs
  • burn unit precautions
  • handwashing
  • experimental vaccines for CF patients
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14
Q

what is the bacteriology of B. cepacia?

A

similar to P. aeruginosa (grows easily in IV, irrigation)

  • unlike P. aeruginosa, limited ability to infect healthy patients (“colonizing” instead of “infecting”)
  • no pyocyanin
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15
Q

what is the relationship between B. cepacia and CF? how is this related to cepacia syndrome?

A
  • CF/cepacia pneumonia is more common as CF survival improves
  • cepacia pneumonia in CF centers forms outbreaks
  • cepacia syndrome: accelerated pulmonary course with rapidly-fatal bacteremia
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16
Q

what is the pathogenesis of B. cepacia?

A
  • CF pneumonia
  • pneumonia if preexisting disease with neutropenia
  • catheter-associated UTIs
  • IV-associated septicemia
  • wound infections (foot rot in swamp-deployed)
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17
Q

what is treatment of B. cepacia?

A
  • no treatment required if otherwise healthy patient
  • pneumonia + CF, cancer, HIV need exotic antibodies
  • -as hard to kill as aeruginosa (same extreme antibiotic resistance)
  • experimental vaccines available for CF
18
Q

what is bacteriology of B. pseudomallei?

A

motile G- rod (similar to P. aeruginosa)

-developing nation veterinary disease (Melioidosis)

19
Q

how is B. pseudomallei transmitted?

A

direct contact with contaminated water or soil

-human-to-human transmission is rare, but take standard precautions with mask on patient

20
Q

what is the pathogenesis of B. pseudomallei?

A
  • initial: flu-like symptoms + muscle tightness and light sensitivity
  • can progress from acute local infection to septicemia in all organs (fatal in 7-10 days if not treated)
  • septecemia involves:
  • -flushing
  • -cyanosis
  • -disseminated pustular erruption
  • -high fevers
  • -rigor
  • -bloody, purulent sputum
  • may resolve and reactivate from lung abscesses years later (Vietnam veterans)
21
Q

what are risk factors for B. pseudomallei?

A
  • diabetes
  • renal dysfunction
  • chronic pulmonary disease
22
Q

how does one diagnose B. pseudomallei?

A
  • look at patient history (travel, work with animals)
  • culture and G-stain from blood, urine, skin lesions
  • -“wrinkled” colony morphology
  • abnormal CXR + multiple small abscesses in liver and spleen on sonogram
23
Q

how does one treat B. pseudomallei?

A

long-term ceftazidime

24
Q

what is the bacteriology of P. mallei?

A

(AKA glanders; developing world veterinary disease)

  • nonmotile G- rod
  • maintained in animal reservoirs (not environment) so may be possible to eradicate
25
Q

explain the pathogenesis of B. mallei

A
  • animal discharge passes through broken skin
  • rare human-human transmission
  • initial symptoms are flulike, but may progress:
  • -acute localized: nodule at infection site
  • -acute pulmonary: bronchitis, pneumonia
  • -acute septicemic: fulminant, multiorgan
  • -chronic infection: farcy
  • if infectious dose is high, bacterial toxins may cause additional symptoms
26
Q

what is the septicemia associated with B. mallei?

A

similar to B. pseudomallei

  • flushing
  • cyanosis
  • disseminated pustular eruption
  • fatal in 7-10 days
27
Q

how to diagnose B. mallei?

A

patient history, culture, G-stain from urine, blood, skin lesions
-PCR and IF assays exist, but must go to CDC

28
Q

what is treatment for B. mallei?

A

long-term amoxicillin and clavulanate

-reportable to FBI and CDC (as weaponizable)

29
Q

what is the bacteriology for Chlamydia pneumoniae?

A

human-borne community-acquired

  • respiratory secretions transmit from human to human
  • causes 3-10% of adult community-acquired pneumonia
  • pear-shaped elementary bodies
30
Q

what is the bacteriology for Chlamydia psittaci?

A

bird-borne rare airborne zoonosis

  • infected birds transmit via respiratory route through direct contact or aerosolization
  • rare but serious
31
Q

what is the bacteriology for Chlamydia trachomatis?

A

infant is infected at birth

-transmitted when infant passes through infected birth canal –> conjunctivitis and pneumonia

32
Q

explain the history/exam of C. pneumoniae

A

3-4 week incubation period

  • infection is common and asymptomatic or mild
  • fever in first few days, likely absent by time of exam
  • rhonchi and rales present in mild disease
  • headache, sinus percussion tenderness
  • symptoms may be prolonged
33
Q

explain the history/exam of C. psittaci

A

exposure to sick birds

  • 5-14 day incubation period, abrupt onset
  • can be asymptomatic to severe pneumonia
  • nonproductive cough, chest pain, splenomegaly
  • fever is most common symptom (103-105)
  • Horder spots: erythematous, blanching, maculopapular rash
  • severe cases –> meningitis, encephalitis, endocarditis
34
Q

explain the history/exam of C. trachomatis

A

birth-infected infant or severely immunocompromised adults

  • nasal obstruction and discharge
  • cough, tachypnea
  • conjunctivitis
  • middle ear abnormality
  • scattered crackles with good breath sounds
  • most patients afebrile, only moderately ill
35
Q

explain lab results for C. pneumoniae

A
  • MIF Ab tests, serology (pear shaped EB)
  • cell culture impractical
  • chest radiograph: single subsegmental infiltrate in lower lobes
36
Q

explain lab results for C. psittaci

A
  • complement fixing or MIF Ab tests, serology
  • cell culture is hazardous (infectious)
  • radiograph: consolidation in single lower lobe
37
Q

explain lab results for C. trachomatis

A
  • culture or hybridization like genital chlamydia

- radiograph: bilateral interstitial infiltrates with hyperinflation

38
Q

explain treatment for C. pneumoniae

A
  • doxycycline
  • alt: erythromycin, azithromycin, clarithromycin, telithromycin
  • most cases are mild and respond to outpatient treatment
39
Q

explain treatment for C. psittaci

A
  • tetracycline or doxycycline

- curable in 7-14 days with early diagnosis and treatment

40
Q

explain treatment for C. trachomatis

A
  • treat infants with oral erythromycin (not just eye ointment)
  • most patients are moderately ill and respond to appropriate antibiotics
  • course is protracted if untreated