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Bacteriology (mine) > Streptococci > Flashcards

Streptococci Flashcards

1
Q

What happens in alpha hemolysis?

A

erythocytes NOT destroyed; greenish discoloration

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2
Q

What happens in beta hemolysis?

A

erythrocytes ARE destroyed; clearing underneath growth

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3
Q

What happens in gamma hemolysis?

A

non-hemolytic; anything that’s not alpha or beta

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4
Q

What’s the basis of lancefield classification?

A

C-carbohydrates and glycerol teichoic acid

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5
Q

What are the classifcations of Strep?

A

Group A = S. pyogenes

Group B = S. agalactiae

Group D = E. faecalis

*strep pneumoniae and viridans= NONE

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6
Q

What hemoylitic pattern is seen in Strep Pneuomoniae and Strep Viridans?

A

Pneumoniae = alpha/beta/none

Viridans=alpha

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7
Q

What are some characteristics of Strep Pyogenes?

A
  1. transient flora
  2. not always symptomatic
  3. not common to culture
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8
Q

What is the mode of transmission for Strep Pyogenes?

A
  1. from asymptomatic carriers via respiratory droplets and skin-to-skin
  2. via fomites and insect vectors
  3. for soft tissue infections, breakage in skin
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9
Q

What are GAS virulence factors?

A
  1. fibronectin binding proteins
  2. M protein: binds fibronectin and fibrinogen -> antiphagocytic
  3. toxins: Streptococcal Shock Syndrome
  4. capsule: antiphagocytic and anti-Ig
  5. DNAases: pus that’s less viscous than Staph Aureus
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10
Q

What’s the difference between the pus of Staph Aureus vs Strep Pyogenes?

A

GAS has a more liquefying pus

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11
Q

When do we do a rapid strep test?

A

need 2, 3, or 4 criteria of: tonsilar exudates, tender cervical adenopathy, absence of cough, fever

if positive: treat with antibiotics

if negative: back to square one

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12
Q

When do we not do rapid strep test?

A

patients with history of RF, vascular heart disease, immunosuppression, recurrent/chronic pharyngitis

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13
Q

Define cellulitis.

A

diffuse inflammation of CT that spread along the fascial planes

often occuring where skin has previously broken

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14
Q

What layers do erysipelas infect?

A

superficial infections of dermis and upper subcutaneous layer (have well defined edge)

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15
Q

How do we treat the skin infections related to Strep Pyogenes? (impetigo, cellulitis, erysipelas)

A

antibiotics!

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16
Q

What are the streptococcal pyrogenic exotoxins?

A

superantigens (cytokine storm)= interacting with macrophages & helper T cells to release IL-1, IL-2, IL-6, TNF-alpha, TNK-beta, and gamma-IFN

SpeA and SpeC = encoded by lysogenic phages

SpeB = located in bacterial chromosome (found in all GAS)

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17
Q

What’s the treatment for necrotizing fascititis?

A

surgical removal of all the affected areas + empiric antibiotics like vancomycin

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18
Q

What is special about the M protein?

A

shares same epitopes as heart muscles (molecular mimcry) -> so when make Abs to M protein, may make Abs to heart muscles too

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19
Q

What are the theories for post-streptococcal glomerulonephritis?

A
  1. IgG-streptococcal antigen complexes depositing on glomerular tissue
  2. cross-reactivity between unidentified streptococcal Ags and glomerular membrane components
  3. deposition of nephrostreptokinase-plasmin complexes on glomerular basement membrane and subsequent damage by host plasmin
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20
Q

What should be done to prevent spread from S. Agalactiae positive mother to neonate?

A

prophylactic antibiotics for positive MOM to decrease colony size and reduce risk of transmisson

21
Q

What is virulence factor for S. Agalactiae that’s important for preventing phagocytosis?

A

capsule

Type II: adult disease

Type III: infant disease

22
Q

What’s the clinical presentations for early onset GBS?

A

symptoms within day 0-1

respiratory distress, apnea, sepsis (bacteremia is most common form), pneumonia, meningitis

23
Q

What treatment can be utilized for the severe cases of early onset GBS?

A

extracorporeal membrane oxygenation (ECMO): temporizing, supportive treatment to effectively bypass severely diseased lungs while they’re given time to heal from infection

24
Q

What group have a higher proportion of maternal colonization?

A

African Americans and nonsmokers

25
Q

What’s significant of maternal GBS colonization?

A
  1. colonized asymptomatically that comes and goes over months
  2. NOT STDs!! develops over time
  3. bacteria actually live in GI tract but can spread to genital tract
  4. colonization is not altered by or dependent on pregnancy
26
Q

What are some risk factors for early-onset GBS?

A
  1. obstetric: preterm delivery (<37weeks), prolonged rupture of membanes, infection of placental tissues or amniotic fluid (fever during labor)
  2. detectable GBS in mother’s urine (marker for heavy colonization)
  3. previous infant with GBS
  4. low maternal levels of anti-GBS Abs
  5. AA, young maternal age
27
Q

What test follows hemolysis test for GBS?

A

latex agglutination test for confirmation

28
Q

What’s the main virulence factor that prevents phagocytosis of Strep Pneumoniae?

A

capsule (forms halo on culture)

29
Q

What is another important virulence factor for Strep Pneumoniae?

A

pneumolysin (exo-enzyme)- leads to rusty sputum

30
Q

How is Strep Pneumoniae transmitted?

A

respiratory

31
Q

What’s the pathogenesis of Strep Pneumoniae?

A
  1. bacteria colonize epithelial cells and pumps out toxins
  2. capsule facilitates invasiveness
32
Q

What are some predisposing factors for Strep Pneumoniae infection not covered on sketchy?

A

alcoholism, anesthesia, and previous infection

33
Q

What antibiotics is used for treatment of strep pneumo?

A

levofloxacin (quinolone) and ceftriaxone

34
Q

Is there a vaccine for Strep Pneumo?

A

yes, two carbohydrate capsule (use on at risk individuals)

  1. pneumococcal polysaccharide vaccines, PPSV14/PPSV23/Pneumovax (Merck) Pnu-Imune 23 (Wyeth)
  2. pneumococcal conjugate (diphtheria CRM107 protein) vaccines, Prevnar PCV7/PCV13
35
Q

What’s the pathogenesis for S. pneumococcal meningitis?

A
  1. adheres and colonizes nasopharynx
  2. IgA1 protease protects from host Ab
  3. once in bloodstream, capsule helps evade opsonization
  4. enters CSF through receptors on endothelial surface of BBB
36
Q

What’s phase variation?

A

S. pneumoniae being able to change constituition of its capsule

37
Q

How do we treat otitis media from Strep Pneumoniae?

A

antibiotics and myringotomy (drains pus from the middle ear by making small incision) with tympanostomy tubes

38
Q

What is characteristicall seen in S. Pneumonaie culture?

A

autolysis of colonies - as organism die, the colonies fall apart leaving characteristic dimple (donut shaped)

39
Q

What strep pneumo treatment is used on children?

A

penicillin or fluoroquinolone

40
Q

What does enterococcus look like when cultured?

A

cocci in chains or lighter color diplococci

41
Q

What test can be used to differentiate enterococcus from other bacteria?

A

bile esculin agar test (positive = dark color)

42
Q

What are some characteristics of enterococcus that show its tough? (not from sketchy)

A
  1. can grow in pH 4-10
  2. refractory in metal salts
  3. live in temp rage from 5-50oC and survive 30min at 60oC
43
Q

Where can enterococcus be naturally found?

A

part of normal flora-> lives in GI tract

44
Q

What is the treatment of choice for E. faecalis?

A

ampicillin-sulbactam and aminoglycosides (gentamicin or streptomycin) synergistic therapy

*sulbactam = inhibitor of beta-lactamase allowing ampicillin to be effective

45
Q

What is E. faecium resistant to?

A

vancomycin, ampicillin, and gentamicin (aminoglycoside)

46
Q

What is the treatment of choice for E. faecium?

A

nitrofurantoin or linezolid or synercid

47
Q

What are the different Strep Viridans?

A

S. Mutans, S. Sanguinis (cavities and endocarditis), S. milleri (endocarditis)

*all are part of normal flora

48
Q

What’s the treatment of choice for mild infection of Strep (like impetigo)?

A

penicillin or tetracycline (if penicillin allergy)

Bacteriology (mine) (6 decks)

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