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123 Cards in this Set
- Front
- Back
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Organisms most likely to cause acute exacerbation of COPD
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H influenzae
S pneumoniae M. Catarrhalis |
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64 y/o pt presents with, fever, productive cough, with green sputum, and acute exacerbation of his COPD. WBC was slightly elevated but diff was normal, as was the CXR. Most likely organism
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H. influenzae
S, pneumonia is also seen in COPD, but the usually causes pneumonia. M. catarrhalis is also possible and indistinguishable from H pneumoniae |
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Haemophilus species are what type of bacteria. Growth occurs on what agar?
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small, Gram- coccobacillary rods
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Para species of Haemophilus require what for growth? What about the other species?
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V factor:
nicotinamide adenine dinucleotide V and X factor |
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X factor
V factor |
heme
NAD |
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H. influenzae requires what for growth
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X and V factor
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The two different groups of H influenzae are differentiated by?
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The presence or absence of a polysaccharide capsule. Type-1 have a capsule, type-2 do not.
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What do all groups of H. influenzae contain in their cell wall
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LPS
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Pathogen that easily spreads from the nasopharynx into the middle ear to cause otitis media or into the sinuses to cause sinusitis
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NTHi...non-typable(group 2) H influenzae
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Child presents with sudden fever, dyspnea, stridor, tachypnea, and drooling. Organism?
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Epiglottitis:
Virtually the only cause is Hib |
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H. influenzae strain that cannot be serotyped with antisera to the polysaccharide capsules
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Group 2:
Are unencapsulated, thus they do not contain a polysaccharide capsule. |
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Strain of Haemophilus that contains a polyribitol phosphate capsule
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Hib:
major pathogen that causes most invasive damage of group 1 strains. |
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Haemophilus strain that caused majority of meningitis before vaccination
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Hib
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In the past, it was the major pathogen of Haemophilus
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Hib:
Now there is a vaccine |
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H influenzae are normally found where?
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part of the normal flora of respiratory tract
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Cause most H. influenzae in adults? children?
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NTHi (Group2)
Group1 |
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Transmission of H. infleunzae
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Respiratory droplets
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Major cause of lower respiratory infections and CNS infections in children of developing countries
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Hib
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Allows NHti organisms to colonize the respiratory tract
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IgA protease
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Often can spread from the nasopharynx to the bronchi to cause chronic bronchitis, with excessive tracheobronchial mucus production
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NTHi
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Txmt of H influenza
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Macrolides and cephalosporins
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Pneumonia causing pathogen associated with alcoholics
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K. pneumoniae
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67 y/o pt with a hx of COPD presents with abrupt onset of fever, chills, and R sided CP. WBC is elevated as are bands. CXR shows consolidation of the R upper lobe. Most likely organism?
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S. pneumoniae
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Likely organism in postinfluenza pneumonia
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S. aureus
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Pathogenesis of S. pneumoniae
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1. Colonization of upper airway.
2. Aspiration of large bacterial inoculum 3. Failure of host defense to clear bacteria 4. Bacterial proliferation 5. inflammatory response (lung pathology) |
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Gram stain of pt shows numerous PMN's and gram+, lancet shaped diplococci
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S. pneumoniae
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S. pneumoniae are what type of organism
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Gram+ lancet shaped diplococci
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Most common cause of community acquired pneumonia
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S. pneumoniae
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Is S. pneumoniae catalase positive or negative? Optochin sensitive or resistant?
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Negative
Sensitive |
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Outer layer of S. pneumoniae
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Thick capsular polysaccharide
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S. pneumoniae is able to colonize mucosal colonization via? What do they bind to?
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IgA protease:
IgA produced by airway epithelial cells, prevents adherence and colonization. Bind to GlcNac B1,3-Gal dissaccharide groups on epithelial cell glycolipids. |
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How does smoking and alcohol among other toxins increase colonization of bacteria in the lung after aspiration?
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Dysfunction of mucus and cilia functions
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Most common cause of meningitis in adults
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S. pneumoniae
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Loss of the normal intrapulmonary compartementalization of the inflammatory response results in?
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Bacteremia that leads to systemic inflammatory response and cardiac failure
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DOC for susceptible pneumococcal strains? What about suspected S. pneumoniae with empirical evidence only (before cultures known)?
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Penicillin
Ceftriaxone |
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Released during bacterial lysis and is active in pore formation and is cytotoxic to virtually every lung cell
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Hemolysin aka pneumolysin
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Pathology of lobar pneumonia
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1. Congestion:
Earliest stage of lobar pneumonia, is characterized by extensive serous exudation, vascular engorgement, and rapid bacterial proliferation. 2. Red hepatization: Airspaces are filled with PMN's, vascular congestion occurs, and extravasation of rbc's. 3. Grey Hepatization: Accumulation of fibrin, associated with inflammatory WBC's and RBC's in various stages of disintegration; alveolar spaces are packed with inflammatory exudates 4. Resolution: Characterized by resorption of exudate. |
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Characterized by resorption of exudate.
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Resolution
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Earliest stage of lobar pneumonia, is characterized by extensive serous exudation, vascular engorgement, and rapid bacterial proliferation.
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Congestion
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Airspaces are filled with PMN's, vascular congestion occurs, and extravasation of rbc's.
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Red hepatization:
2nd stage in pneumonia |
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Results from an accumulation of fibrin, associated with inflammatory WBC's and RBC's in various stages of disentegration; alveolar spaces packed with inflammatory exudates
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Grey hepatization
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Type of exudate seen in S pneumoniae
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Intra-alveolar exudates spreading rapidly within a lobe and through the pores of kohn, until the entire lobe is consolidation.
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Gives S. pneumoniae antiphagocytic properties
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Polysaccharide capsule
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Bacteria aspirated into the lung first encounter what host defense? What else is important for effective opsonization and phagocytosis?
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Alveolar macrophages
IgG and and complement C3, with clearance via C3b |
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66 y/o Homeless man presents with cough, fever, chills, night sweats, and chest pn. He admits to drinking 2 quarts of vodka a day. He also complains of a frequent cough with blood-tinged sputum. WBC was elevated and CXR showed a R upper lobe cavitated lesion. Most likely cause?
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K. pneumoniae:
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K. pneumoniae is what type of bacteria
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Enterobacter:
Short, plump, Gram- bacilli Lactose fermenting, urease positive, indole negative bacteria that are nonmotile and nonflagellated |
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Is K. pneumoniae motile?
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no
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Major virulence factor for K. pneumoniae
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Polysaccharide capsule...k antigen:
antiphagocytic |
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The outer membrane of K. pneumoniae contains what?
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Its gram-...so it has LPS and thus endotoxin (lipid A).
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Common nosocomial pathogen
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K. pneumoniae
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How does K. pneumoniae gain access to the lung? How does the CPS inhibit phagocytosis?
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Oropharyngeal carriage and aspiration of bacterial pathogens
Inhibits activation of C3b and causes antigenic mimicry by selective deposition of C3b onto LPS. this results in inhibition of of MAC(C5b-C9). |
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Type of pneumoniae present in K. pneumoniae
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Bronchopneumonia:
Acute inflammatory infiltrates from the bronchioles into adjacent alveoli causing patchy distribution of opacity on xray. |
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How may lung abscess from in K. pneumoniae?
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Encapsulated bacteria in the polymicrobic infection results in necrotic destruction of alveolar spaces, cavity formation, and production of blood-tinged sputum due to endothelium damage.
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Txmt of K. pneumoniae
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Extended spectrum penicillins, aminoglycosides, quinolones, and other antibiotics.
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Frequently involved in infections associated with respiratory tract manipulations, such as tracheostomy and mechanical ventilation
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K. pneumoniae:
Common nosocomial pathogen |
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P. Aeruginosa is what type of organism?
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STRICTLY aerobic Gram- rod
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P. aeruginosa is motile by what structure?
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Single polar flagellum
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Pathogen with a fruity odor on blood agar plates and pigmented by pyocyanin
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P. aeruginosa
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Transmission of P. aeruginosa
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Ingestion of or contact with contaminated water, ice; aerosolization of contaminated liquids; penetration of contaminated objects; ingestion of contaminated foods (tomatoes).
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Serves as an adhesin for glycolipids on respiratory epithelial cells in P. Aeruginosa infections. What is the receptor on epi cells?
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Exoenzyme S
Sialic acid (N-acetylneuraminic acid) |
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What type of pt is especially susceptible to P. aeruginosa
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CF
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Major cause of morbidity in CF pts?
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P. aeruginosa infection characterized by LPS activated neutrophilic inflammatory response that interferes with pulmonary function.
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Causes ADP-ribosylation of EF-2, which inhibits protein synthesis
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Exotoxin A:
Seen in P. aeruginosa |
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After colonization, what happens to P. aeruginosa in the lung?
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Phenotypic shift:
Become mucoid by producing an alginate capsule. Lose their flagella, establishing a permanent and localized chronic infection Capsule forms biofilm that protects against phagoctosis |
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Txmt for P. aeruginosa
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Extended spectrum penicillins, cephalosporins, or a carbapenem
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Major organisms associated with post-influenza secondary bacterial pneumonia
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S. aureus
S. pneumoniae |
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What type of bacteria is S aureus? Are they motile? catalase positive?
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Gram + that occur, singly, in pairs, or in grape-like clusters.
Nonmotile catalase positive |
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What is S. aureus resistant to (besides drugs)?
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High salt conc, Temp up to 50C, and drying
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Most widely used and generally acceptable criteria for for the identification of S aureus
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Coagulase+
Ability to clot plasma |
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Reservoir for S aureus
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nose...but may also be present on the skin
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How does S. aureus transmit to the lungs to cause infection?
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Aspiration of bacteria or hematogenously via IVDU
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How does S. aureus lead to pneumonia? What role does influenza virus play?
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Influenza virus destroys the ciliary defense, allowing colonization of opportunistic bacteria. S. aureus adheres to the cell wall via techoic acids
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Hallmark of S. aureus infection
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Abscess:
Fibrin wall surrounded by inflamed tissues enclosing a central core of pus...consistent with opacity of lung in CXR. |
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Pyogenic inflammation causing acute mucopurulent conjuctivitis is associated with what infection?
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S. aureus. breakdown of epi lining from rubbing and wiping. The bacteria spread from the nares of the nasal cavity during influenza, and into the eye.
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Pt presents with 3 week hx of cough, fever, and weight loss. Cough is productive, with foul smelling sputum. There is draining lesion from the chest wall containing yellow granules. WBC was not elevated. CXR showed left lung infiltrates with upper lobe cavity. Most likely organism? Txmt?
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Actinomyces israelii (thoracic actinomycosis
Penicillin G or in penicillin allergic pts, clindamycin |
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What type of organism is Actinomyces?
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Filamentous gram+, non-acid fast, anaerobic (hence foul smelling abscess) bacteria.
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Foul smelling bacteria sputum is associated with what type of organism
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anaerobes that form abscesses, such as Actinomyces.
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Draining abscesses with yellow granules are diagnostic for?
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actinomyces
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Where is actinomyces normally found? How is actinomyces transmitted? who is at risk?
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Normal part of human oral and GI flora.
Transmission is endogenous: Aspiration of oropharyngeal secretions containing pathogen. Persons with poor dental hygiene are at risk |
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In infected tissue, the organism forms dense masses known as sulfur granules. What do the colonies look like?
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Actinomyces:
"Molar tooth" colonies |
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Pathogenesis requires synergistic presence of other anaerbic commensals, such as Fusobacterium
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Actinomyces:
Forms a polymicrobial infection, with suppurative and granulomatous response. |
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Forms a chronic suppurative abscess that spreads mainly be direct extension to other tissues of the chest wall, and ultimately forming a draining sinus that discharges sulfur granules
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Actinomyces
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38 y/o male presents with 2 weeks of fever, productive cough, R-sided CP, and a painful lesion on his arm. He is a landscaper that has worked outside for most of his life. WBC was very elevated, with 79% PMN's. CXR revealed multiple nodular lesions, some of which were cavitating in the L upper lobe. Biopsy obtained from bronchoscopy showed a budding yeast. Most likely organism?
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Blastomyces dermatitidis:
Itraconazole in immunocompetent pts, unless CNS lesions are present, then use amphotocerin B. |
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Growht conditions and agar used for blastomyces? characteristics?
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Grows slowly at 25C on Sabouraud agar as a White Fluffy mold
At 37C on blood agar, the fungus grows as brown, wrinkled colonies |
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Large yeast with broad based budding in biopsies is diagnostic for?
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B. dermatitidis
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Infection of B. dermatitidis results from? Where is it endemic?
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inhalation of microconidia and conversion to the yeast forms in the lungs. This switch occurs at body temp. Incubation is 4-6 wks.
Southeast US and is found in heavily wooded, swampy areas |
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Incubation period for B. dermatitidis
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4-6 wks
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Focal micro-abscesses in the papillary dermis that presents as verrucous skin lesions with pustular features. This is common in what respiratory infection?
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B. dermatitidis:
organ spread is due to lymphohematogenous spread. |
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What type of fungus is B. dermatitidis?
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dimorphic
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Filamentous, weakly gram+ and acid-fast bacteria. Are they anaerobes? slow or fast growers?
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Nocardia asteroides:
they are aerobic, slow growers, that use fungal media. They must be cultured for several weeks. |
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What type of pts are at high risk for developing Nocardiosis?
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Pts receiving cytotoxic or immunosuppresive drugs(steroids) and pts with AIDS.
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Txmt of N. asteroides
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SFX/TMP
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Major mode of acquisition of N. asteroides
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Inhalation of contaminated dust
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Chronic, subcutaneous infection, characterized by slow extension along lymphatics and destruction of deeper tissues
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Madura foot:
N. asteroides |
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Lung pathology in uncontrolled infection includes inflammatory endobronchial masses or diffuse pneumonitis, and abscess
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N. asteroides
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Chronic symtpoms of fever, cough, night sweats, and weight loss should prompt you to what disease?
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TB...although all the fungi (H. capsulatum or Blastomycoses) may also present this way.
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Within what lung region does TB normally populate
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Upper lobe
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What type of bacteria are mycobacteria?
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acid-fast bacilli:
red rods |
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Cell wall contains mostly lipids in the form of mycolic acids
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mycobacterium
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Major mode of transmission for TB
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airborne
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Agar media for mycobacterium
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Lowenstein:
grows slowly |
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Why is TB found more in thte upper lobe of the lungs?
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Obligate aerobes:
cause disease only in highly oxygenated tissues |
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Where do mycobacteria live and proliferate? How do they avoid phagocyte killing? receptor?
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Macrophages:
LAM is recognized by the macrophage mannose receptor. They express C3 convertase activity, forming C3b on its surface for recognition by CR4, this initiates phagocytosis. However, they inhibit phagolysosome fusion within the cytoplasm of the macrophage. They proliferate within the phagosome and eventually burst the macrophages. |
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Toxic virulence factor of M. tuberculosis that kills PMN's, causing irreversible damage to the mitochondria. What else does it do?
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Cord factor:
Also, stimulates the formation of granulomas, a hallmark of TB. Granulomase are collections of macrophages that have taken on properties of epithelial cells. These epitheloid cells coalesce within the granuloma to form giant cells. When fully developed, a chronic granuloma encapsulated within fibrin consists of a central core of large, multinucleated giant cells containing TB, a midzone of epitheloid cells, and a peripheral zone of fibroblasts, monocytes, and lymphocytes. |
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Collections of macrophages that have taken on epithelial cells(epithelioid). If the macrophages coalesce, what does this form? Hallmark of what disease? When fully formed, what is it encapsulated by? Core?
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Granuloma
Giant cells TB When the chronic granuloma is fully formed, it contains a central core of large, multinucleated giant cells and tubercule bacilli, a midzone of epithelioid cells, and an outer layer of fibroblasts, monocytes, and lymphocytes. |
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TB granulomas may be visualized on CXR as?
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Lobar(Ghon focus) and perihilar lymph node involvement.
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Key CD4+ TH1 subset effector molecule for efficient killing of M. tuberculosis? What does this cause?
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Nitric Oxide of marophages. Controlling of infection, which causes a +PPD skin test.
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During TB infection, cell mediated immunity is primarily through what?
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CD4+ TH1 subset T cells that activates IFN-gamma to stimulate macrophages
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The majority of TB infections are active or latent? What reactivates the infection?
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Latent:
Bacterial replication is balanced by killing via macrophages, so it remains at a low level, and pts are asymptomatic. However, waning of cell-mediated immunity (age, stress, illness) leads to reactivation. |
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At what pt may a person transmit TB
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At some pt. after reactivation, the central core of the chronic granulomas becomes caseuous and necrosis, which may disrupt a bronchus and cause exhaling of tubercule bacillus.
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Dissemination of TB to the midthoracic vertebraal bodies, causing osteomyelitis
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Potts disease
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In HIV pts, spread of TB through the CNS typically involves what areas? Complications?
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TB meningitis:
Basilar meninges Hydrocephalus and CN palsies. |
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Endemic in the SW united States (San Joaquin valley). Common reservoir?
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C. immitis:
Arid soil around rodent burrows. |
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Infection of C. immitides results from?
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Inhalation of arthroconidia
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Deposition of arthroconidium is where within the lung? Pathogenesis?
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Terminole bronchiole:
Arthrospore develops into into a thick-walled spherule filled with endospores. This encites inflammation with neutrophils, and cell-mediated immunity causes chronic granulomatous inflammation. Caseation w/o calcification occurs, resulting in pulmonary lesions. |
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Dissemination of C. immitis is seen as what characteristic?
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erythema nodosum of the skin
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30 y/o male presents with 3 week hx of fever, night sweats, dry cough, and severe fatigue. He had recently visited Pheonix, AZ on vacation. WBC was normal. Erythema nodosum lesions were found on his back, and there was a large cavity in his R upper lobe on XRAY. Organism? Txmt?
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C. immitis:
Fluconazole or itraconazole |
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Dimorphic fungus that once within the pulmonary alveoli, form thick-walled non budding spherules, that can produce thousands of endospores
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C. immitis:
Arthroconidia are inhaled and the arthrospores transform. |
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5 workers present to the ER following a 1-week hx of fever, chills, night sweats, cough, and fatigue. They had been working in an abandoned building where they observed a colony of pigeons and pigeon droppings were noted throughout. WBC was slightly elevated. CXR showed multiple nodular infiltrates in both lungs and popcorn calcification. Organism? Txmt?
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H. capsulatum:
Itraconazole |
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Endemic to regions along the Ohio and Mississippi River valleys. Reservoir?Infection?
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H. capsulatum
Soil contaminated with bird and bat droppings. Respiration of conidia after soil is disturbed. |
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Grows as a mold form within soil, but is transformed into a yeast once within the host (due to temp increase)
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H. capsulatum
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Once within thte alveoli, this organism is engulfed by neutrophils and macrophages, where microconidia transform into budding yeast, and are able to grow intracellulary within the macrophages.
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H. capsulatum:
Causes granulomatous inflammation and calcified fibrinous granulomas and caseous necrosis. |
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Agar mycelial growth produces characteristic macroconidia, with a thick wall and finger-like projections, and microconidia
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H. capsulatum
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