Micro -- LRT Flashcards

1
Q

Chest pain, hacking cough w/ some sputum production, fever, after signs of common cold, no infiltrate on CXR

A

bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

causes bronchitis

A
Usually viral (if >14 days - id bacteria)
rhinovirus, paramyxovirus, adenovirus, influenza c, coxsackievirus, RSV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

bacterial causes for bronchitis

A

mycoplasma pneumoniae, chlamydia pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

bronchiolitis

A

inlammation of bronchial tree as low as bronchioles - usually in infants younger than 1 yr
RSV, paramyxovirus, adenovirs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

pertussis phases

A
incubation period (3-21 days)
catarrhal stage = cold sxs (1-2 weeks)
paroxysmal stage = severe and uncontrollable coughing 
convalescent phase = bacteria decreasings, still coughing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

pertussis toxin

A

AB toxin – results in high levels of cyclic AMP and lots of mucus production. In that way similar to Diptheria. Tracheal cytotoxin kills ciliated cells. Antibiotics primarily effective in catarrhal stage only.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

culture pertussis on

A

bordet-gengou agar, regan-lowe now

or direct fluorescent ab test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what do flu vaccines target

A

NA cleaving of HA/SA that permits viral spread

multiples strains of A but also against B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

minor changes in antigens occur due to gene mutation in influenza virus.

A

antigenic drift (a and B)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

major changes in antigens occur due to gene reassortment in influenza virus.

A

antigenic shift (A)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

flu strains named after

A

HA protein (16) and NA proteins (9) – A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

influenza can predispose to

A

pneumonia!

s. aureus, H. influ, S. pneumo, S. pyo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

most common cause of pneumonia

A

S. pneumo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

S. pneumo characteristics

A

Bacteria - gram + - diplococci - catalase negative – alpha hem (green) - bile-eschulin neg - optochin susceptible = s. pneumo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bacteria - gram + - diplococci - catalase negative – alpha hem (green) - bile-eschulin neg - optochin susceptible

A

S. pneumo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Common causes of pneumonia in 18-40

A

Mycoplasma
C. pneumoniae
S. pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Common causes of pneumonia in 40-65

A
S. pneumoniae
     H. influenzae
     Legionella
Anaerobic bacteria
viruses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Common causes of pneumonia >65

A
S. pneumoniae
     Gram (-) rods
     H. influenzae
viruses
anaerobic bac
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pneumonia in kids

A

RSV

parainfluenza virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

S. agalactiae characteristics

A
bacteria
gram +
cocci
catalase - 
beta hemo
bacitracin resistant
S. ag (Group B strep)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
bacteria
gram +
cocci
catalase - 
beta hemo
bacitracin resistant
A

S. agalactiae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Nocardia asteroides characteristics

A

Gram +
Beaded filaments
Weakly acid fast
obligate aerobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Gram +
Beaded filaments
Weakly acid fast
obligate aerobe

A

N. asteroides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

sputum color - s. pneumo

A

rust colored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

sputum color - pseudomonas, haemophilus, pneumococcal

A

green

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

klebsiella sputum

A

red currant jelly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

abaerobic sputum

A

foul-smelling, bad tasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

characteristics TB

A

acid fast
aerobic
bacilli
fastidious (3-8 weeks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

pneumonia neonates

A

S. agalactiae (group B)

E. coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

children pneumonia

A

viruses (RSV)
M. pneumoniae
C. pneumoniae
S. pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

nosocomial pneumonia

A
Gram - rods
staph aureus (drug resistant)
32
Q

Immunocompromised

A
Gram (-) rods
Streptococcus pneumoniae
Fungi
Filamentous bacteria
Pneumocystis jiroveci (CD4<200)
Viruses
33
Q

Aspiration pneumonia

A

anaerobes

34
Q

alcholics pneumonia

A

Streptococcus pneumoniae
Klebsiella pneumoniae
Anaerobes

35
Q

IV drug use pneumonia

A

s. aureus

36
Q

Post viral secondary infection pneumonia

A

s. aureus

37
Q

chronic steroids pneumonia

A

nocardia spp.

38
Q

clinical presentation influ A/B

A

common cold, flu (leads to primary viral or secondary bacterial pneumonia)

39
Q

Influ A and B pathology

A

Inhaled through aerosols. Infects the larynx mucosa via contact of the viral hemagglutinin (HA) envelope protein with sialic acid on cell surfaces (leads to endocytosis). The viral neurominidase (NA) envelope protein is important for cleaving HA bound to sialic acid, this permits viral spread. Virus replication in host cells can lead to death of the host cell leading to tissue damage and disease. The immune response to infection also contributes to disease via production of IL-1 and IFN-γ.

40
Q

S. agalactiae clinical presentation

A

neonatal meningitis, neonatal pneumonia, neonatal sepsis

41
Q

pathology s. aga

A

bacteria is carried in the maternal genital tract. Can colonize the neonate following obstetric complications. Causes meningitis (develops weeks after birth) or pneumonia (develops within a day after birth).

42
Q

dx s. aga

A

Gram stain of CSF, urine, blood. Gram (+), β-hemolytic, bacitracin resistant.

43
Q

tx s. aga

A

penicillin g

44
Q

m. pneumo has no

A

cell wall (no gram stain)

45
Q

m pneumo most commonly affects

A

people in close quarters (dorms)

46
Q

clinical presentation m. pneumiae

A

tracheobronchitis, atypical pneumonia (walking pneumonia)

47
Q

pathology m. pneumoniae

A

Only infects humans. Transmitted by respiratory droplets. Adheres to respiratory epithelium, inhibits ciliary motion and destroys mucosa. Infection leads to localized inflammation. B-cell response can generate antibodies that may autoreact with erythrocytes (IgM cold agglutinins), brain, and heart. Can lead to arthritis.

48
Q

dx m. pneumoniae

A

Presence of cold hemagglutinin, no cell wall, fried egg appearance, serology.

49
Q

tx m. pneumoniae

A

Erythromycin or tetracycline.

50
Q

tetracycline mechanism

A

Bind 30S to prevent attachment of aminoacyl-tRNA (elongation)

51
Q

Clamydia pneumoniae most often infects

A

young adults

52
Q

clincial presentation chlamydiae pneumo

A

atypical pneumo

53
Q

c. pneumoniae pathology

A

community-acquired. Microorganism is an obligate intracellular parasite and enters the upper respiratory tract epithelium and becomes phagocytosed by macrophages. Lymphocytes infiltrate site of infection leading to local pulmonary edema, necrosis, and hemorrhage. Two life-forms: extracellular (EB), and intracellular (RB). EB is the infective form.

54
Q

dx c. pneumo

A

Giemsa stain to visualize intracytoplasmic inclusions. Serology.

55
Q

tx c. pneumo

A

doxycycline

56
Q

S. aureus clinical presentaiton

A

Local = skin/subcutaneous: impetigo, cellulitis, folliculitis, furuncles, carbuncles. Respiratory: pneumonia with cavitations. Systemic = acute endocarditis, meningitis, osteomyelitis, septic arthritis.

57
Q

pathology s. aureus

A

Bacteria colonize skin (following breach) or nasopharynx (following intubation or viral infection) → overgrow and evade host defenses using protein A, coagulase, hemolysins, and leukocidins. Neutrophils localize to site of infection → purulent abscesses form → skin/subcutaneous infections or pneumonia results. Deeper invasion into the bloodstream relies on the hyaluronidase, staphylokinase, and lipase virulence factors.

58
Q

dx s. aureus

A

Gram + clusters, catalase +, coagulase +

59
Q

tx s. aureus

A

antibiotic treatment is with either penicillinase-resistant penicillins or vancomycin

60
Q

vancomycin moa

A

Bind D-al-D-al of cell wall precursor inhibit release from bactoprenol carrier, inhibiting peptidoglycan cell wall synthesis – translgycosylase

61
Q

penicillinase-resistant penicillins

A

Nafcillin, Dicloxacillin

62
Q

legionella pneumophila clinical presentation

A

pontiac fever

Legionnaire’s disease (atypical pneumonia)

63
Q

pathology legionella

A

Naturally inhabits water reservoirs. Inhaled through aerosols from respiratory devices, air conditioners. Adheres to respiratory epithelium via pili. Phagocytosed by alveolar macrophages. Survives and proliferates inside the macrophage. Infected macrophages secrete neutrophil chemoattractants which can lead to Pontiac fever (acute illness lasting 2-5 days) or Legionnaire’s disease (neutrophils arrive from microabscesses which can be seen on x-ray which leads to sever atypical pneumonia).

64
Q

dx legionella

A

Gram stains poorly, best visualized with silver stain.
Culture on charcoal yeast extract with iron and cysteine.
Urinary antigen detected by radioimmunoassay.
Serology.

65
Q

tx legionella

A

erythromycin

66
Q

erythromycin moa

A

Bind 23S of 50S to prevent translocation - Binds to 50S ribosomal RNA near the peptidyltransferase center blocking peptide chain elongation.

67
Q

begin prophylaxis for PCP when

A

CD4 < 200

68
Q

pathology PCP

A

cyst inhaled by most in childhood leading to asymptomatic or mild pneumonia. Stays latent in the lungs. In immunocompromised hosts it exhibits uncontrolled growth leading to an inflammation response that then leads to pneumonia.

69
Q

dx pcp

A

silver stain of induce sputum. Bronchoalveolar lavage or lung biopsy. Cysts forming dark oval bodies.

70
Q

tx pcp

A

TMP-SMX or pentamidine

71
Q

mechanism TMP-SMX

A

PABA analog - acts as comp inh for dihydropteraste sythetase
inhibits bacterial hihydrofolate reductase

run out of purines

72
Q

mycobacterium tuberculosis clinical presentation

A

hemoptysis, fever, weight loss, fatigue

73
Q

Nocardia asteroides clinical presentation

A

pneumonia, abscesses in the kidney and the brain

74
Q

pathology n. asteroides

A

Found in the soil and inhaled followed by phagocytosis. Mycolic acid in the cell wall allows for intracellular survival and proliferation. Caseous granulomas wall off infectious particles. Pneumonia and cavatations form. May spread via the blood to adjacent tissue to form abscesses in the kidney and brain.

75
Q

dx n. asteroides

A

Gram (+), aerobic, beaded filaments, weakly acid-fast.

76
Q

tx n. asteroides

A

TMP-SMX, surgical drainage of abscesses.