Unit 4 - Bacterial Pneumonia: Pseudomonas/Burkholderia and Chlamydia

Question 1

what are the Pseudomonad bacteria?

Answer 1

also called Burkholderia

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

Question 2

explain P. aeuroginosa bacteriology?

• growth?
• use of Ab?

Answer 2

• 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

Question 3

explain P. aeruginosa pathogenesis?

-growth requirements?

Answer 3

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)

Question 4

who are “vulnerable” patients to P. aeruginosa?

Answer 4

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

Question 5

explain P. aeruginosa community-acquired pathogenesis?

Answer 5

• 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

Question 6

what are P. aeruginosa virulence factors?

Answer 6

• 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

Question 7

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

Answer 7

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

Question 8

what is ecthyma gangrenosum?

Answer 8

patch of destroyed tissue in immunocompromised due to P. aeruginosa

Question 9

what does nonbacteremic pneumonia show on CXR?

Answer 9

resembles S. aureus

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

Question 10

what does bacteremic pneumonia show on CXR?

Answer 10

progresses rapidly

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

Question 11

what does P. aeruginosa lab show?

Answer 11

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

Question 12

what is P. aeruginosa treatment?

Answer 12

• 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

Question 13

what is prevention of P. aeruginosa

Answer 13

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

Question 14

what is the bacteriology of B. cepacia?

Answer 14

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

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

Question 15

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

Answer 15

• 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

Question 16

what is the pathogenesis of B. cepacia?

Answer 16

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

Question 17

what is treatment of B. cepacia?

Answer 17

• 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

Question 18

what is bacteriology of B. pseudomallei?

Answer 18

motile G- rod (similar to P. aeruginosa)

-developing nation veterinary disease (Melioidosis)

Question 19

how is B. pseudomallei transmitted?

Answer 19

direct contact with contaminated water or soil

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

Question 20

what is the pathogenesis of B. pseudomallei?

Answer 20

• 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)

Question 21

what are risk factors for B. pseudomallei?

Answer 21

• diabetes
• renal dysfunction
• chronic pulmonary disease

Question 22

how does one diagnose B. pseudomallei?

Answer 22

• 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

Question 23

how does one treat B. pseudomallei?

Answer 23

long-term ceftazidime

Question 24

what is the bacteriology of P. mallei?

Answer 24

(AKA glanders; developing world veterinary disease)

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

Question 25

explain the pathogenesis of B. mallei

Answer 25

- 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

Question 26

what is the septicemia associated with B. mallei?

Answer 26

similar to B. pseudomallei - flushing - cyanosis - disseminated pustular eruption - fatal in 7-10 days

Question 27

how to diagnose B. mallei?

Answer 27

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

Question 28

what is treatment for B. mallei?

Answer 28

long-term amoxicillin and clavulanate | -reportable to FBI and CDC (as weaponizable)

Question 29

what is the bacteriology for Chlamydia pneumoniae?

Answer 29

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

Question 30

what is the bacteriology for Chlamydia psittaci?

Answer 30

bird-borne rare airborne zoonosis - infected birds transmit via respiratory route through direct contact or aerosolization - rare but serious

Question 31

what is the bacteriology for Chlamydia trachomatis?

Answer 31

infant is infected at birth | -transmitted when infant passes through infected birth canal --> conjunctivitis and pneumonia

Question 32

explain the history/exam of C. pneumoniae

Answer 32

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

Question 33

explain the history/exam of C. psittaci

Answer 33

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

Question 34

explain the history/exam of C. trachomatis

Answer 34

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

Question 35

explain lab results for C. pneumoniae

Answer 35

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

Question 36

explain lab results for C. psittaci

Answer 36

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

Question 37

explain lab results for C. trachomatis

Answer 37

- culture or hybridization like genital chlamydia | - radiograph: bilateral interstitial infiltrates with hyperinflation

Question 38

explain treatment for C. pneumoniae

Answer 38

- doxycycline - alt: erythromycin, azithromycin, clarithromycin, telithromycin - most cases are mild and respond to outpatient treatment

Question 39

explain treatment for C. psittaci

Answer 39

- tetracycline or doxycycline | - curable in 7-14 days with early diagnosis and treatment

Question 40

explain treatment for C. trachomatis

Answer 40

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