Unit 4 - Bacterial Pneumonia: Atypicals Flashcards
describe the bacteriology of Legionella
poorly staining G- rods (need silver or IF)
- faculative intracellular parasites
- -free-living motile w/ flagella (infectious phase)
- -intracellular nonmotile (replicative phase)
when has the accidental opportunistic lifestyle of legionaires arisen?
recently (1970s)
- natural: form biofilms in stagnant freshwater, parasite protozoa (waterborne), full life cycle
- unnatural: biofilms in HVAC systems, enter human lungs (aspirated), parasitize alveolar MP as dead end host (hard to remove once established)
how do simultaneously-exposed cases of legionella occur?
form in an outbreak, but are not contagious
-most common source is contaminated water supply
how do legionella replicate within phagocytic cells
- begin living in biofilm on warm water or in soil
- taken up by phagocytes
- “contained” in altered phagosome (not merged to lysosome)
- becomes motile and escapes the phagosome
- lyses the cells and spreads to another
what are Legionella virulence factors
- mip - unknown, required to invade monocytes
- Dot/Icm locus - T4SS (involved in altering endosome)
- pilE/pilD - pilus formation (attachment)
- Mak/Mil/pmi - unknown
- Pep/pro - Zn metalloprotease (escape)
what are the 3 outcomes of Legionella infection in humans
- asymptomatic seroconversion
- Pontiac fever
- flulike in previously healthy patient
- incubates hours to 2 days
- symptoms immunogenic as immune system kills live and/or clears dead bacteria
- resolves w/o complication - Legionnaires disease
- pneumonia in previously ill or immunosuppressed
- suppression of kidney function; diarrhea
- incubates 2-10 days
- usually resolves w/ hospitalization and treatment
- can be fatal
what do the different outcomes of Legionella depend on?
- all 3 caused by same bacteria
- differences are in the hosts, possibly also dosage
what are risk factors for Legionnaire’s disease?
- increasing age
- immunosuppression
- smoking
- chronic heart/lung disease
- chronic swallowing disorder
- male
why is mortality of Legionnaire’s disease decreasing?
- prompt diagnosis
- early use of appropriate antibiotics
how do nosocomial LD outbreaks occur?
hospitals are hot spots for LD outbreaks
- large numbers of at-risk individuals
- old complex plumbing
- hot water tanks at reduced temperature to prevent scalding
- -fix with thermal mixing valves
what does the presentation of LD look like?
- altered mental status
- headache
- high fever/chills
- pneumonia/cough/chest pain (not clinically distinct from other pneumonias, so need lab to differentiate LD)
- pancreatitis
- acute renal failure
- diarrhea
what lab do you use to diagnose LD?
urine antigen test (commercial ELISA test)
- fast
- cell wall component excreted starting 3 days after symptom onset
- test complete in hours
- reiiably detects LP1 strain of L. pneumophila
- -doesn’t detect other strains/species
- causes 90% of LD in US
- testing significantly associated w/ reduced mortality
how does the urine Ag test work?
Ag capture ELISA
- petri dish coated with Ab for LD
- patient sample is added; if Ag is present, Ab binds it
- patient sample is removed
- tagged secondary Ab binds other side of Ag
- unbound Ab is removed and TAg is assayed
how do you culture Legionella?
respiratory secretions
- much slower; fastidious, requires special nutrients
- technically demanding
- detects many strains and species of Legionella
- 27% fatality rate among culture+, urine-test- patients
- needed to trace outbreaks
what is treatment for Legionella?
- Pontiac fever: often resolves w/o treatment
- LD: needs antibiotic that penetrates infected cells
- -Levofloaxin (M. pneumoniae and S. pneumoniae)
- -Azithromycin
- -Old-school erythromycin
what is the best way to diagnose LD?
both urine Ag test and culture
- biopsy not necessary, but may show bacteria if silver-stained
- G stain will fail
what is post-acute care for LD?
many patients who recovery from LD experience following for up to 17 mo, but most recover w/in one year
- fatigue
- neurological symptoms
- neuromuscular symptoms
- cough
what is the bacteriology of C. burnetti?
proteobacteria (related to LD)
- zoonosis of asymptomatic infection of ruminants
- transmitted to humans by inhalation of aerosols of infected ruminant urine, feces, birthing matter (no vector)
- extremely infectious <10 IUs can cause disease; dried samples remain infectious for months
what are virulence factors of C. burnetti?
- acid phosphatase
- superoxide dismutase
- both help bacteria survive in fused lysosome-endosomem
how are humans sickened with C. burnetti?
bacteria multiply within alveolar monocytes and macrophages
- travel to liver, spleen, BM
- creates complications with pregnancy
- common in Netherlands, France, Spain, Iraq
what is the pathogenesis of C. burnetti?
- fever, chills, sweats
- severe headache
- dry cough
- pneumonia and hepatitis (most common)
- complications of pregnancy
- rarely fatal, but is reportable
- rare: rash, endocarditis
how do you diagnose C. burnetti?
same as Rickettsia
- immunohistological methods
- ELISA
- immunofluorescence
how do you treat C. burnetti?
same as Rickettsia
- doxycycline
- fluoroquinolones
how do you prevent C. burnetti?
vaccine is available to farm and veterinary personnel and military stationed in Middle East
explain mycoplasma bacteriology
-what is unique about it
smallest free-living organisms (0.3 um diameter)
- strictly aerobic
- no cell wall; little Gran staining, but penicillins and cephalosporins are ineffective
- only prokaryotic cell membrane that contains cholesterol
- difficult to grow on media, require special nutrients
- colonies have a “fried egg” shape
- only one serotype, but immunity is incomplete (can recur)
- bacterial metabolism produces H2O2 (tissue damage)
how does mycoplasma infect?
pathogenic only to humans
- reside on mucosal surfaces of respiratory and genital tracts (assume rod shape, attachment proteins at tip)
- transmitted by inhalation of respiratory aerosols
- causes tracheobronchitis, bronchiolitis, 5-10% progress to atypical “walking pneumonia” due to epithelial necrosis
- Ab against mycoplasma (cold-agglutinins) X-react with RBC membranes so patients may become anemic
- -resolves spontaneously with disease
what does mycoplasma cause during infection?
P1 adhesin binds respiratory epithelial cells
- causes ciliostasis –> dry cough, exacerbates chronic bronchitis, asthma
- local inflammation from bacterial wastes
- tissue destruction by CARDS exotoxin
- -related to pertussis toxin
what does mycoplasma show on exam?
non-specific upper or lower airway
- more prevalent in winter
- fever, aches/pains, oropharyngeal inflammation
- erythematous tympanic membranes
- conjunctivitis
- rash
- moderate rhonchi and rales
- CXR looks worse than patient
when does mycoplasma resolve?
in 10-14 days, very low mortality even without treatment
what does Mycoplasma diagnosis show on lab?
self-limited and antibiotic-responsive
- culture and molecular labs available
- patient may be anemic
what is Mycoplasma treatment?
- fluoroquinolones cover mycoplasma and all similarly-presenting bacterial infections
- erythromycin, azithromycin, clarithromycin, tetracycline all work slightly better against mycoplasma
- longer treatment courses (14-21 days) needed b/c of M’s slow growth, intracellular penetration
- macrolide resistance is emerging in Japan and China
