BVI, WVIII

Start Studying!

Terms

undefined, object

copy deck

which bacteria is the most common cause of hospital acquired infection and causes clinical disease in 2% of all patient admissions?: Staph aureus
what is the habitat/reservoir of S. aureus?: normal human flora
hospital environments
in general: diseases S. aureus can cause?: can infect any tissue - a very good opportunist
skin infections
food poisoning
endocarditis
toxic shock syndrome
haemolytic pneumonia
four virulence factors posessed by Staph aureus?: 1. techoic acid in cell wall
2. coagulase
3. capsule
4. protein A
regarding S. aurues virulence factors: function of techoic acid in cell wall?: facilitates adhesion to nasal cells
regarding S. aurues virulence factors: function of coagulase?: clots plasma
antiphagocytic
protects against antibodies
regarding S. aurues virulence factors: function of the capsule?: antiphagocytic
regarding S. aurues virulence factors: function of protein A?: binds and sequesters antibodies by Fc end
Staph aureus can obtain a gene that greatly contributes to it's virulence. what gene is this?: Panton-Valentine leukocidin (PV-leuk)
two diseases caused by the PV-leuk gene?: 1. severe community acquired necrotizing boils and skin infections
2. lethal necrotizing hemolytic pneumonia in children
antibiotic of choice to treat Staph aureus?: penicillin
what do we use to treat MRSA?: vancomycin
what about treating VISA and VRSA?: linezolid
quinupritin/dalfopristin (Synercid)
group A strep is also known as?: Streptococcus pyogenes
hemolysis pattern of group A strep?: Beta hemolytic (clear)
group A strep is found in highest concentration in what population?: school children (up to 90% infected)
group B strep is also known as...?: strep agalactiae
hemolysis pattern of group B strep?: Beta hemolysis (clear)
three major virulence factors of Strep pyogenes?: 1. capsule
2. adhesins
3. prophages
describe the adhesins specific to strep pyogenes: cell wall techoic acid adheres to many membranes
M protein on pili attaches to host cells
strep pyogenes has superantigens. how are they classified?: pyogenic and non-pyogenic
streptolysins belong to which classification of superantigen?: non-pyogenic
why are polyphages considered important virulence factors seen in strep pyogenes?: they are a major source of strain variation
transmission of strep throat?: airborne or direct contact
presentation of strep throat?: pharyngitis (inflammed mucous membranes)
affects tonsils or middle ear
fever
two possible complications of strep throat?: scarlet fever
rheumatic fever
how long after a strep throat infection will rheumatic fever show up?: 1-5 wks
cause of rheumatic fever?: cross reacting antibodies to host directed against heart and neuronal tissue
presentation of scarlet fever: red skin rash
strawberry tongue (red and peeling)
pathogenesis of scarlet fever?: erythrogenic toxin carried by phage: rash is due to hypersensitivity to toxin
what sometimes happens after a strep pyogenes skin infection?: acute glonerulonephritis occurs
cause of acute glomerulonephritis seen ~10-14 days after strep infection?: type III hypersensitivity rxn. (immune complex deposition)
treatment for: 1. regular old strep pyogenes? 2. resistant strep: 1. penicillin
2. erythromycin
which bacteria looks like "Chinese letters?": Corynebacterium diptheriae
Gram status of Corynebacterium diptheriae?: Gram (+)
which stains do we use to see Corynebacterium diptheriae?: methylene blue
Loeffler's medium
Tellurite medium
why does Corynebacterium diptheriae stain irregularly (blotchy)?: it contains "metachromatic granules" (globules of polymetaphosphate)
in Tellurite medium Corynebacterium diptheriae shows up as?: dark brown to black
the toxin released by Corynebacterium diptheriae is a two part toxin. describe the parts and their respective functions: 1. B fragment: binds to cells
2. A fragment: inhibitor of host cell protein synthesis
how does Corynebacterium diptheriae cause systemic effects?: the bacteria itself never infects past the throat
- the toxin it releases causes systemic symptoms/damage
describe a "diptheritic membrane": profuse film in throat
caused by degeneration of epithelial cells
composed of fibrin, dead tissue, WBCs, bacteria
**may interfere with breathing**
in a Corynebacterium diptheriae infection, edema in the neck causes?: "bull neck" symptom
which organs does the toxin of Corynebacterium diptheriae target?: heart
kidneys
nerves
what usually causes death in a diptheria infection?: heart failure or respiratory obstruction
treatment for Corynebacterium diptheriae infection?: ANTITOXIN
(preformed antibodies)
*antibiotics do not help cells already exposed to toxin**
what is the name of the immunization available for Corynebacterium diptheriae?: DTaP
DTaP is reccommended at what ages?: 2, 4, and 6 months

then a booster every 4-6 yrs
which organism causes whooping cough?: Bordatella pertussis
characteristics of B. pertussis?: Gram (-) rod
capsule present in vivo
habitat/reservoir of B. pertussis?: humans are the only known reservoir
is Bordatella pertussis easy to grow?: NO! it is very sensitive to the environment (and drying kills it easily)
what is difficult about specimen collection when it comes to Bordatella pertussis?: it is killed by the fatty acids in cotton swabs
(therefore must use calcium alginate throat swabs)
which medium is used to culture Bordatella pertussis?: Regan-Lowe agar
(charcoal+serum overcome fatty acid toxicities in the media)
virulence factors seen in Bordatella pertussis (5)?: 1. endotoxin
2. pertussis toxin (most harmful)
3. heat-labile toxin
4. peptidoglycan cell wall fragment
5. adhesins
exactly which endotoxin does Bordatella pertussis have?: LPS
what does pertussis toxin do?: *increases susceptibility to histamine, seratonin, endotoxin
*increases lymphocyte response
when in heat-labile toxin released and what does it do?: released at cell death
necrotic and lethal
general pathogenesis of Bordatella pertussis?: bacteria slip between epithelial cells in URT
-pertussis toxins secreted
-creates hypersensitivity to histamine
-produces fits of coughing
why does the whooping occur in a Bordatella pertussis infection?: whooping comes from the need to breathe quickly and deeply between extended fits of coughing
what are the 4 stages of whooping cough?: 1. catarrhal
2. paroxysmal
3. convalescent
4. relapse
which stage of whooping cough actually has the "whoop?": paroxysmal
(this stage is characterized by an inappropriate response to a small stimulus)
a Bordatella pertussis infection in adults is called?: 100 day cough
treatment for Bordatella pertussis infections?: mostly symptomatic relief
antibiotics not very effective (once again the toxin is responsible for the disease)
which type of Bordatella pertussis vacacine is currently being used: cellular or acellular?: acellular
(contains proteins only needed to stimulate immunity)
when can a Haemophilus influenzae infection become a medical emergency?: when it causes epiglottitis
(can expand and obstruct airway)
describe the disease progression seen in pneumonia: 1. organism enters lungs
2. alveoli fill with pus and liquid (edema/inflammation)
3. results in reduced air exchange
4. systemic spread via the bloodstream
which type of bacteria is likely to cause: 1. typical pneumonia 2. atypical pneumonia 3. chronic pneumonia 4. pneumonia in newborns?: 1. Strep pneumoniae
2. Mycoplasma pneumoniae
3. Mycobacterium tuberculosis
4. group B strep
which type of bacteria is likely to cause: 1. pneumonia in the immunocompromised? 2. community acquired pneumonia?: 1. pneumocystis jirovecii
2. Strep pneumoniae, H. influenzae, K. pneumoniae
which type of bacteria is likely to cause primary atypical pneumonia? (2): 1. Mycoplasma pneumoniae
2. Chlamydia pneumoniae
which type of bacteria is likely to cause nosocomial pneumonias? (2): GRAM NEGATIVE RODS
Klebsiella
Pseudomonas
which type of bacteria is likely to cause opportunistic pneumonia?: Nocarida (plus community acquired bacteria)
which type of bacteria is likely to cause aspiration pneumonia?: anaerobes
Staph aureus
gram negative aerobic rods
which type of bacteria is likely to cause pneumonia in the neonate? (2): E. coli
group B strep
which organism is likely to cause pneumonia in infants? (2): Chlamydia trachomatis
RSV
which organism is likely to cause pneumonia in children (1/2-5 yrs)? (2): RSV
Parainfluenza virus
which organism is likely to cause pneumonia in children (5-15 yrs)?: Mycoplasma pneumoniae
Influenza Type A virus
which organism is likely to cause pneumonia in adults <30? (2): mycoplasma pneumoniae
strep pneumo
which organism is likely to cause pneumonia in adults >65 yrs?: strep pneumo
H. influenzae
which three bacteria cause rust colored sputum?: Streptococcus pneumoniae
Klebsiella pneumoniae
Legionella pneumophila
which organism is the leading cause of pneumonia in children <3 yrs old?: strep pneumo
characteristics of strep pneumo?: gram (+) diplococcus
large capsule
alpha hemolytic
colonies autolyse in late growth
optichin sensitive
habitat of streptococcus pneumoniae?: strict human parasite
which two tests, when used together, detect 98% of streptococcus pneumoniae cases?: Gram stain
urinary antigen
lcan s. pneumoniae live in a phagolysosome?: NO!
this is the major host defense!
what is the most important virulence factor of strep pneumo and what are its functions?: capsule
- anti phagocytic
- prevents opsonization in absence of an antibody
- antibody against capsule opsonizes bacteria
three important toxins released by strep pneumo?: 1. pneumolysin
2. hemolysin
3. adhesin
function of pneumolysin released by Streptococcus pneumoniae?: slows ciliary beating in URT
kills pulmonary epithelial cells
which virulence factor causes alpha-hemolysis on blood agar plates?: hemolysin
function of adhesin released by Streptococcus pneumoniae?: choline binding protein helps bacteria stick to respiratory epithelium.
classic treatment for Streptococcus pneumoniae?: penicillin
treatment for Streptococcus pneumoniae if resistance is seen?: erythromycin
fluoroquinolones
Streptococcus pneumoniae also causes what other diseases? (3): 1. Bacteremia
2. Meningitis
3. Otitis media
characteristics of group B Streptococcus?: gram (+)
chain forming
fastidious
very tiny colonies
hemolytic pattern of group B Streptococcus?: Beta hemolytic
catalase status of group B Streptococcus?: catalase negative
habitat/reservoir of group B Streptococcus?: GU tract
group B Streptococcus causes what diseases? (2): 1. pneumonia in newborns (~50% fatality)
2. meningitis in newborns
in relation to group B Streptococcus: describe the mode of transmission and the time frame in early and late onset disease.: transmitted perinatally
early onset disease - within 24 hrs
late onset disease - 7-10 days
when does the CDC recommend that we screen for group B Streptococcus in pregnant mothers?: between 35th and 37th wk
(then give prophylactic antibiotics - penicillin)
what two test are available to detect group B Streptococcus?: 1. Rapid GBS testing
2. IDI-strep assay
characteristics of Klebsiella pneumoniae? - gram stain - ferments lactose?: Gram (-) rod
enteric bacterium (related to E.coli)
ferments lactose
habitat/reservoir of Klebsiella pneumoniae?: free-living in soil and water
human intestines
sometimes URT
two major diseases caused by Klebsiella pneumoniae?: 1. Pneumonia
2. Urinary tract infections (nosocomial)
describe the pneumonia caused by Klebsiella pneumoniae: includes necrosis of the lungs
when left untreated - 90% fatal!
hard to treat (resistance is increasing)
two virulence factors used by Klebsiella pneumoniae?: 1. Pili (adhesins on end of pili adhere to mucosal surfaces - "grappling hooks")
2. capsule (inhibits phagocytosis and intracellular killing)
mechanism of antibiotic resistance seen in Klebsiella pneumoniae?: plasmid-mediated
characteristics of Pseudomonas aeruginosa? -gram stain - ferments lactose?: Gram (-) rod
does NOT ferment lactose
why is Pseudomonas aeruginosa blue?: blue due to polycyanin excretion
(polycyanin also gives off "grape juice" smell)
when is Pseudomonas aeruginosa pneumonia most often seen?: in CF patients
characteristics of Legionella pneumophila? gram? structure? Abx. resistance?: Gram (-) rod
single polar flagellum
Beta lactamase positive
does Legionella pneumophila grow easily on medium?: NO - it is fastidious and will not grow on blood agar.
- requires charcoal yeast extract agar, then tiny colonies appear in 3-5 days
habitat/reservoir of Legionella pneumophila?: free living in soil and water
may survive in amoebas
commonly found in stagnant water...
spread by environmental aerosols
three s/s of Legionnaire's pneumonia?: 1. high non-remitting fever (103-105 degrees F)
2. shaking chills
3. rigor and severe prostration
Besides pneumonia, Legionella also causes what disease?: Pontiac fever
(mild flu-like illness)
virulence factors of Legionella pneumophila?: 1. intracellular parasite
2. MIP
3. Dot/ICM
4. Pore-forming toxins
when we say Legionella pneumophila is an intracellular parasite, what do we mean?: it enters fibroblasts and alveolar phagocytes: it wants to be phagocytosed!
what is MIP?: macrophage infectivity potentiator
helps organism survive initial phagocytosis
what is Dot/Icm?: Type IV secretion system that inhibits phagosome maturation
function of pore forming toxins?: one inserts so bacterium can enter host cell
other inserts so bacterium can exit host cell
three ways to diagnose Legionella pneumophila in the lab?: 1. fluorescent antibody
2. increase in antibody titers
3. isolation of organsim via lung biosy
treatment for Legionella pneumophila pneumonia?: erythromycin drug of choice
*should be continued for at least 3 wks. to prevent relapse
characteristics of Mycoplasma pneumoniae?: NO CELL WALL!
very small cell and colony size
what makes Mycoplasma pneumoniae unique among prokaryotes?: cholesterol is required for the membrane
habitat/reservoir of Mycoplasma pneumoniae?: mucous membranes of URT and GU tract
*humans are only known reservoir*
what type of disease does Mycoplasma pneumoniae cause?: primary atypical "walking" pneumonia
describe the disease progression of pneumonia caused by Mycoplasma pneumoniae: -begins as upper respiratory "cold" symptoms
-notorious for sore throat and headache
-chills and fever early on
-violent coughing attacks
-produces only sparse whitish mucous
-bradycardia
age group where Mycoplasma pneumoniae pneumonia is most commonly seen?: ages 5-19
prevalent in concentrated populations (students, army barracks etc)
two virulence factors produced by Mycoplasma pneumoniae?: 1. adherence factor
2. toxic metabolites
describe the adherence factor seen in Mycoplasma pneumoniae: -terminal structure at one end of cell
-specifically binds to RBCs, epithelial cells, macrophages
-bacteria hang on to cell
- irritate airways and cause cough
describe the toxic metabolites released by Mycoplasma pneumoniae: -locally produced waste products
-harm host cells
treatment for Mycoplasma pneumoniae pneumonia?: tetracycline and erythromycin
(NOT cell wall inhibitors - remember there is no cell wall!)
characteristics of Mycobacterium tuberculosis?: -gram +
-acid-fast
-slender rods
-aerobic
-catalase (+)
why doesn't Mycobacterium tuberculosis stain well?: it has mycolic acids in cell envelope - these stain well with acid fast stains
is Mycobacterium tuberculosis "hardy"?: YES
very resistant to dehydration
is Mycobacterium tuberculosis fastidious?: YES
hard to grow - must grow on glycerol medium (Lowenstein-Jensen medium)
-grows very slow (weeks)
habitat/reservoir for Mycobacterium tuberculosis?: humans and cattle
describe the pathogenesis of a tuberculosis infection: -one organism can cause disease!
-phagocytosed by an alveolar macrophage
-grows in macrophage, kills it, repeats process
-body reacts and forms a tubercle around infection to "wall it off"
-forms a caseated tubercle
-may remain dormant for years - then - tubercle ruptures and infection begins all over again
of the people that get infected with Mycobacterium tuberculosis - how many of them progress to TB?: only 10%
how is TB diagnosed?: *acid fast organisms in sputum
*auramine-O stain - fluorescent detection, easier to see cells
four virulence factors of Mycobacterium tuberculosis?: 1. glycan rich surface
2. cord factor
3. proteasomes
4. mycolic acids
function of glycan-rich surface of Mycobacterium tuberculosis?: inhibits phagocytosis by macrophages BUT ALLOWS PHAGOCYTOSIS by alveolar macrophages
function of cord factor in Mycobacterium tuberculosis?: (rope like growth)
*stimulates macrophage phagocytosis
*induces granuloma formation
*inhibits oxidative phosphorylation
*mitochondria degenerate
function of proteasomes secreted by Mycobacterium tuberculosis?: *degrade cytosolic proteins
*protect against NO
function of mycolic acids found on Mycobacterium tuberculosis?: makes bacteria hard to digest and resistant to drying
(allows cells to remain viable in the sputum for weeks to months)
four drug therapy for TB involves?: isoniazid
rifampin
pyrazinamide
ethambutol
*4 drugs for 2 months OR 2 drugs for 4+ months
vaccine for TB?: YES, but not used in US
called BCG vaccine
describe defense mechanisms used by the lungs according to particle size: 1. nasal clearance - large particles
2. tracheobronchial clearance via mucociliary action (3-10 micron particles)
3. alveolar clearance (1-5 micron particles = SMALL)
describe alveolar clearance: dust cells phagocytose
carry it to ciliated epithelium or lymph nodes
bronchopneumonia is also called?: lobar pneumonia
describe bronchopneumonia: -patchy consolidation
-often an extension of pre-existing bronchitis
-frequently basally located
in what age group is bronchopneumonia MC seen in?: the extremes of life
(infancy/old age)
describe lobar pneumonia: acute bacterial infection of a large portion of a lobe or an entire lobe
how are organisms spread in lobar pneumonia?: through pores of Kohn
what organism causes >90% of all lobar pneumonias?: Streptococcus pneumoniae
which organism is #2 in causing lobar pneumonias?: Klebsiella pneumoniae
what are the four stages recognized in untreated lobar pneumonia?: 1. congestion
2. red hepatization
3. gray hepatization
4. resolution
what is going on during the congestion stage of lobar pneumonia?: lots of intra-alveolar fluid
few neutrophils
what is going on during the red hepatization stage of lobar pneumonia?: -exudate rich in red cells, fibrin, neutrophils
-lung is firm and liver like
what is going on during the gray hepatization stage of lobar pneumonia?: -disintegration of RBCs
-persistance of fibrin/WBCs
what is the resolution stage of lobar pneumonia characterized by?: resolution and reorganization
clinical s/s of lobar pneumonia?: malaise
fever/chills
productive cough by day 3
rusty sputum
pleuritic chest pain/friction rub
what is the difference between treated and untreated lobar pneumonia?: treated - afebrile within 48 hrs
untreated - sick 10 days, then resolves by lysis or gradual lysis
what three tests are used to diagnose lobar pneumonia?: 1. sputum gram stain
2. sputum culture (more accurate)
3. blood culture (also accurate)
what is empyema?: spread of pneumonia infection to the pleural cavity (complication of pneumonia)
abcesses are common with which two bacteria causing pneumonia?: 1. Klebsiella
2. Pneumococci
besides pneumonia, what else can cause lung abcesses?: -aspiration of infective material
-antecedent primary bacterial infection
-septic emboli
-neoplasia
by what mechanism does a lung abcess heal?: by secondary intention
aspirations are more common in which bronchi?: right
clinical s/s of a lung abcess: cough
fever
productive sputum
weight loss
clubbing
what are four complications of lung abcesses?: 1. extension into pleural cavity
2. hemorrhage
3. septic emboli
4. secondary amyloidosis
where in the lung is viral and micoplasmal pneumonia located?: in the alveolar walls
(small particles)
clinical course of primary atypical pneumonia? (caused by viruses or mycoplasma): -begins as URI
-extends to lower respiratory tract
-low mortality
are the pleura usually involved in atypical pneumonia?: NO
s/s of atypical pneumonia?: fever
headache
myalgia
cough
alveolar capillary block
are most cases of pharygitis bacterial or viral?: viral
(Rhino, Adeno, Corona)
most common cause of bacterial pharyngitis?: GABHS
s/s of classic strep throat: winter-spring
children
abrupt onet
fever
headache
tonsil exidate
No URI s/s
treatment goals for strep throat?: prevent rheumatic fever complications
prevent suppurative complications
what does treatment of GABHS NOT prevent?: post-strep glomerulonephritis
first choice antibiotic for GABHS?: penicillin (10d)
if strep throat and allergic to penicillin?: cephalosporin
clindamycin
macrolides (erythromycin, clarithromycin, azithromycin)
which group of antibiotics should not be used to treat GABHS due to resistance?: Tetracyclines (TMP/SMX)
acute otitis media is most often caused by? (3): 1. S. pneumoniae
2. H. influenzae
3. M. catarrhalis
if we choose to treat acute otitis media - what antibiotic do we use?: Amoxicillin
sinusitis is most often caused by a bacteria of virus?: virus
which two bacteria commonly are a cause of sinusitis?: S. pneumoniae
H. influenzae
general clues to tell us if a sinusitis/cold is bacterial?: -symptoms last longer than 7 days
-purulent nasal discharge
-unilateral maxillary/tooth pain
-worsening after initial improvement
treatment strategies for sinusitis?: *all viral/most bacterial: don't treat
*persistent/severe: narrow spectrum antibiotic first
drug of choice in acute otitis media that is resistant to amoxycillin?: augmentin
cefuroxime
what are some symptoms not to ignore in a patient with a URI and/or sinusitis?: -fever longer than 10d
-increasing pain
-eye symptoms
-headache
-stiff neck
Top 3 bacteria causing typical community-aquired pneumonias?: 1. Streptococcus pneumoniae
2. Haemophilus influenzae
3. Staphylococcus aureus
Top 3 bacteria that cause atypical pneumonia?: 1. Mycoplasma pneumoniae
2. Legionella pneumophilia
3. Chlamydia pneumoniae
in what type of patients are atypical agents (esp. Legionoella) associated with increased mortality?: the elderly
treatment strategy for CAP -outpatient -previously healthy -no recent abx. therapy: Macrolide (Erythromycin, Azythromycin, Clarithromycin)
-or-
Doxycycline
treatment strategy for CAP -outpatient - previously healthy -recent abx therapy in last 3 months: *respiratory FQ
*advanced macrolide + high dose amoxycillin
*advanced macrolide + high dose amoxycillin/claulanate
treatment strategy for CAP -outpatient -comorbidity(COPD,CHF,DM,etc) -no recent abx therapy: *advanced macrolide
*respiratory FQ
treatment strategy for CAP -outpatient -comorbidity(COPD,CHF,DM,etc) -recent abx activity: *respiratory FQ
*advanced macrolide + a Beta-lactam
treatment strategy for CAP -suspected aspiration with infection: *amoxicillin-clavulanate
*clindamycin
treatment strategy for CAP -influenza with bacterial superinfection: *Beta-lactam (high dose amox, amox/clav, cefpodoxime, cefprozil, cefuroxime)
*respiratory FQ
treatment strategy for CAP -inpatient - medical ward -no recent abx therapy: *respiratory FQ
*advanced macrolide + Betal lactam
treatment strategy for CAP -inpatient-medical ward -recent abx activity: *advanced macrolide + beta-lactam
which bug should we worry about in an ICU patient?: Pseudomonas
treatment strategy for CAP -inpatient/ICU -recent abx therapy -Pseudomonas not an issue: *Beta-lactam + advanced macrolide or respiratory FQ
treatment strategy for CAP -inpatient/ICU -pseudomonas not an issue -allergic to b-lactams: *respiratory FQ w or w/o clindamycin
treatment strategy for CAP -inpatient/ICU -pseudomonas is an issue: *antipseudonal agent + ciprofloxacin
* antipseudomonal + aminoglycoside + respiratory FQ or macrolide
what are the antipseudomonal agents?(5): piperacillin
pip/tazo
imipinem
meropenen
defepime
treatment strategy for CAP -inpatient/ICU -pseudomonas in an issue -allergic to beta lactams: *aztreonam + levoflaxacin
*aztreonam + moxifloxacin w/or w/o aminoglycoside
treatment strategy for CAP -nursing home: *respiratory FQ
*amox-clav + advanced macrolide
an acute cough illness in otherwise healthy adults is known as?: acute bronchitis
how long should acute bronchitis last?: 1-3 wks
is acute bronchitis more oftenly caused by a bacteria or a virus?: virus (>90%)
viruses causing acute bronchitis? (6): 1. influenza A/B
2. Parainfluenza
3. RSV
4. coronavirus
5. adenovirus
6. rhinovirus
three bacterial causes of acute bronchitis?: 1. Bordatella pertussis
2. Mycoplasma pneumoniae
3. Chlamydia pneumoniae
how is acute bronchitis managed?: Antibiotics are of NO BENEFIT if there is no pneumonia present
in acute bronchitis: when would we consider therapy?: 1. pneumonia present
2. outbreaks of M.pneumoniae, C.pneumoniae, B.pertussis
antibiotic regimen to treat B. pertussis?: Macrolide
(except in infants <2wks - treat with erythromycin)
do we treat AECB?: Yes
what do we use to treat AECB?: narrow spectrum antibiotic (doxycycline, amox, TMP/SMX)
what is the most important cause of death in the world?: TB
two virulence factors seen in TB?: 1. cord factor
2. LAM (Lipoarabinomannan)
what is cord factor?: secreted by TB cells - causes "serpentine" growth in vitro
what is LAM?: *similar to endotoxin
*inhibits IFN-gamma activation of macrophages
*stimulates macrophage to secrete IL-10 (IL-10 inhibits TB induced T-cell proliferation)
why is compliment activation found on the surface of mycobacteria?: -facilitates phagocytosis without the respiration burst needed for killing
where in the lung does the primary TB infection occur?: usually subpleural between upper and lower lobe
which cells phagocytose mycobacteria?: alveolar macrophages
what happens in the primary TB infection?: *bacteria are transported to the regional (subpleural and hilar) lymph nodes
* T cell immunity usually results in 2-3 wks
*results in calcified scars in the lung and lymph nodes
the calcified scars in the lung and lymph nodes are known as?: Ghon complexes
in the primary TB infection: where do the mycoplasma proliferate?: inside the macrophages and lymph nodes
a minority of primary TB cases don't resolve: instead they?: become progressive pulmonary TB
what occurs to cause a secondary TB infection?: reactivation of the primary TB infection
what percentage of primary TB infections reactivate to form secondary TB infections?: 5-10%
where does the secondary TB infection most often occur?: apices
what are the three forms of progressive pulmonary TB?: 1. Cavitary fibrocaseous TB
2. Miliary TB
3. TB bronchopneumonia
describe the morphology of cavitary fibrocaseous TB: *erosion of bronchioloes causing cavity formation
*usually remains localized to apex
*may spread to other areas of the lung, or via lymphatics and blood
besides the apices, what other part of the lung is involved in cavitary fibrocaseous TB?: the pleura
(see fibrous pleuritis, empyema, serous effusion)
what are some possible complications of TB infections in the air passages?: 1. endobronchial and endotracheal TB
2. laryngeal seeding
3. intestinal TB
Miliary TB is primarily caused via what type of spread?: lymphohematogenous spread
involved organs in miliary TB?: bone marrow
spleen
retina
kidneys
adrenals
testes
Name four organs that are resistant to miliary TB involvement: 1. heart
2. striated muscle
3. thyroid
4. pancreas
what are scrofula?: infection of the cervical lymph nodes (in this case due to miliary TB)
what is Pott's disease?: TB infection of the Vertebrae
(fistulas along psoas drain to groin)
name of miliary TB complication in bones?: tuberculous osteomyelitis
which type of progressive pulmonary fibrosis used to be called "galloping consumption," and spreads rapidly through the lung?: tuberculous bronchopneumonia
does tuberculous bronchopneumonia form tubercles?: not really
a Ghon complex is indicative of?: primary TB
what cell type is often found within a caseating granuloma?: Langhan's cells
what would TB look like on an acid fast stain?: small, positive staining bacilli

Start Studying!

Deck Info

Number of cards 247