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247 Cards in this Set
- Front
- Back
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?
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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
|
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Staph aureus can obtain a gene that greatly contributes to it's virulence. what gene is this?
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Panton-Valentine leukocidin (PV-leuk)
|
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two diseases caused by the PV-leuk gene?
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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
|
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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?
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Beta hemolytic (clear)
|
|
group A strep is found in highest concentration in what population?
|
school children (up to 90% infected)
|
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group B strep is also known as...?
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strep agalactiae
|
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hemolysis pattern of group B strep?
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Beta hemolysis (clear)
|
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three major virulence factors of Strep pyogenes?
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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 |
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strep pyogenes has superantigens. how are they classified?
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pyogenic and non-pyogenic
|
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streptolysins belong to which classification of superantigen?
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non-pyogenic
|
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why are polyphages considered important virulence factors seen in strep pyogenes?
|
they are a major source of strain variation
|
|
transmission of strep throat?
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airborne or direct contact
|
|
presentation of strep throat?
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pharyngitis (inflammed mucous membranes)
affects tonsils or middle ear fever |
|
two possible complications of strep throat?
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scarlet fever
rheumatic fever |
|
how long after a strep throat infection will rheumatic fever show up?
|
1-5 wks
|
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cause of rheumatic fever?
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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?
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erythrogenic toxin carried by phage: rash is due to hypersensitivity to toxin
|
|
what sometimes happens after a strep pyogenes skin infection?
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acute glonerulonephritis occurs
|
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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 |
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which bacteria looks like "Chinese letters?"
|
Corynebacterium diptheriae
|
|
Gram status of Corynebacterium diptheriae?
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Gram (+)
|
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which stains do we use to see Corynebacterium diptheriae?
|
methylene blue
Loeffler's medium Tellurite medium |
|
why does Corynebacterium diptheriae stain irregularly (blotchy)?
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it contains "metachromatic granules" (globules of polymetaphosphate)
|
|
in Tellurite medium Corynebacterium diptheriae shows up as?
|
dark brown to black
|
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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
|
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which organs does the toxin of Corynebacterium diptheriae target?
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heart
kidneys nerves |
|
what usually causes death in a diptheria infection?
|
heart failure or respiratory obstruction
|
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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?
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Bordatella pertussis
|
|
characteristics of B. pertussis?
|
Gram (-) rod
capsule present in vivo |
|
habitat/reservoir of B. pertussis?
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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?
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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 |
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which type of bacteria is likely to cause primary atypical pneumonia? (2)
|
1. Mycoplasma pneumoniae
2. Chlamydia pneumoniae |
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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 |
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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
|
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characteristics of strep pneumo?
|
gram (+) diplococcus
large capsule alpha hemolytic colonies autolyse in late growth optichin sensitive |
|
habitat of streptococcus pneumoniae?
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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?
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1. pneumolysin
2. hemolysin 3. adhesin |
|
function of pneumolysin released by Streptococcus pneumoniae?
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slows ciliary beating in URT
kills pulmonary epithelial cells |
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which virulence factor causes alpha-hemolysis on blood agar plates?
|
hemolysin
|
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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
|
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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 |
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treatment strategy for CAP
-nursing home |
*respiratory FQ
*amox-clav + advanced macrolide |
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an acute cough illness in otherwise healthy adults is known as?
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acute bronchitis
|
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how long should acute bronchitis last?
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1-3 wks
|
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is acute bronchitis more oftenly caused by a bacteria or a virus?
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virus (>90%)
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viruses causing acute bronchitis? (6)
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1. influenza A/B
2. Parainfluenza 3. RSV 4. coronavirus 5. adenovirus 6. rhinovirus |
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three bacterial causes of acute bronchitis?
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1. Bordatella pertussis
2. Mycoplasma pneumoniae 3. Chlamydia pneumoniae |
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how is acute bronchitis managed?
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Antibiotics are of NO BENEFIT if there is no pneumonia present
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in acute bronchitis: when would we consider therapy?
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1. pneumonia present
2. outbreaks of M.pneumoniae, C.pneumoniae, B.pertussis |
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antibiotic regimen to treat B. pertussis?
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Macrolide
(except in infants <2wks - treat with erythromycin) |
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do we treat AECB?
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Yes
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what do we use to treat AECB?
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narrow spectrum antibiotic (doxycycline, amox, TMP/SMX)
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what is the most important cause of death in the world?
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TB
|
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two virulence factors seen in TB?
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1. cord factor
2. LAM (Lipoarabinomannan) |
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what is cord factor?
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secreted by TB cells - causes "serpentine" growth in vitro
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what is LAM?
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*similar to endotoxin
*inhibits IFN-gamma activation of macrophages *stimulates macrophage to secrete IL-10 (IL-10 inhibits TB induced T-cell proliferation) |
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why is compliment activation found on the surface of mycobacteria?
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-facilitates phagocytosis without the respiration burst needed for killing
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where in the lung does the primary TB infection occur?
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usually subpleural between upper and lower lobe
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which cells phagocytose mycobacteria?
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alveolar macrophages
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what happens in the primary TB infection?
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*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 |
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the calcified scars in the lung and lymph nodes are known as?
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Ghon complexes
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in the primary TB infection: where do the mycoplasma proliferate?
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inside the macrophages and lymph nodes
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a minority of primary TB cases don't resolve: instead they?
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become progressive pulmonary TB
|
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what occurs to cause a secondary TB infection?
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reactivation of the primary TB infection
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what percentage of primary TB infections reactivate to form secondary TB infections?
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5-10%
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where does the secondary TB infection most often occur?
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apices
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what are the three forms of progressive pulmonary TB?
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1. Cavitary fibrocaseous TB
2. Miliary TB 3. TB bronchopneumonia |
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describe the morphology of cavitary fibrocaseous TB
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*erosion of bronchioloes causing cavity formation
*usually remains localized to apex *may spread to other areas of the lung, or via lymphatics and blood |
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besides the apices, what other part of the lung is involved in cavitary fibrocaseous TB?
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the pleura
(see fibrous pleuritis, empyema, serous effusion) |
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what are some possible complications of TB infections in the air passages?
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1. endobronchial and endotracheal TB
2. laryngeal seeding 3. intestinal TB |
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Miliary TB is primarily caused via what type of spread?
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lymphohematogenous spread
|
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involved organs in miliary TB?
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bone marrow
spleen retina kidneys adrenals testes |
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Name four organs that are resistant to miliary TB involvement
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1. heart
2. striated muscle 3. thyroid 4. pancreas |
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what are scrofula?
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infection of the cervical lymph nodes (in this case due to miliary TB)
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what is Pott's disease?
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TB infection of the Vertebrae
(fistulas along psoas drain to groin) |
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name of miliary TB complication in bones?
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tuberculous osteomyelitis
|
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which type of progressive pulmonary fibrosis used to be called "galloping consumption," and spreads rapidly through the lung?
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tuberculous bronchopneumonia
|
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does tuberculous bronchopneumonia form tubercles?
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not really
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a Ghon complex is indicative of?
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primary TB
|
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what cell type is often found within a caseating granuloma?
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Langhan's cells
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what would TB look like on an acid fast stain?
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small, positive staining bacilli
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