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Microbiology Part 1 > Lec3 Streptococci > Flashcards

Lec3 Streptococci Flashcards

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1
Q

Where does strep normally live [3 places]

A
  • skin
  • mucous membranes
  • GI tract
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2
Q

What is name for group A beta hemolytic strep?

A

streptococcus pyogenes

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3
Q

What is name for group B beta hemolytic strep?

A

streptococcus agalactiae

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4
Q

What are the 4 main types of strep?

A
  • streptococcus pyogenes
  • streptococcus agalactiae
  • strep viridans group
  • streptococcus pneumoniae
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5
Q

Are streptococci gram neg or pos? what shape?

A
  • gram positive

- cocci in chains

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6
Q

What distinguishes streptococci from staphylococci biochemically?

A

streptococci are catalase negative

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7
Q

Does strep grow aerobically or anerobically?

A

both!

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8
Q

What are the 4 nomenclature systems?

A
  • lancefield grouping
  • hemolysis pattern on blood agar
  • genus and species
  • traditional term
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9
Q

What are lancefield groups?

A

system of dividing streps by the surface antigens they have

- group A, group B, group C, etc

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10
Q

What are the three types of hemolysis patterns?

A
  • beta [clear zone around colony]
  • alpha [ green zone]
  • gamma [no zone of hemolysis]
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11
Q

How do you distinguish GAS from other beta-hemolytic streptococci?

A

GAS is sensitive to bacitracin

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12
Q

What is the M protein of GAS?

A
  • main virulence factor
  • anchored in cell membrane
  • strain rich in M protein will resist phagocytosis and multiply quickly
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13
Q

How is virulence of GAS or immunity to GAS related to M protein?

A
  • GAS with lots of M protein is more virulent [resists phagocytosis, multiplies quickly]
  • host with strong response to M protein will be more immune to infection
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14
Q

What is protein F in GAS?

A
  • cell membrane virulence factor

- helps organism adhere to mucosal sites

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15
Q

What is streptolysin O?

A
  • most important extracellular product of GAS

- causes hemolysis and damage to WBCs, platelets, heart cells

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16
Q

What is streptolysin S?

A
  • dmages WBCs, platelets, herat cells
  • responsible for GAS causing beta hemolysis on blood agar
  • extracellular compound of GAS
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17
Q

What do hyaluronidase and streptokinase do?

A
  • extracellular compounds of GAS

- speeds up liquefaction of pus, enhance spread of infection in tissues

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18
Q

What are suppurative vs non-suppurative complications of pathogenesis

A 
suppurative = direct invasion, pus/abscess
non-suppurative = manifestation of disease remote from primary site of colonization or infection
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19
Q

What are suppurative vs non-suppurative complications of host immune response?

A

suppurative: neutrophil response

non-suppurative: host response causes clinical manifestations of disease

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20
Q

What are 4 suppurative complications of GAS?

A
  • pharyngitis
  • cellulitis
  • impetigo [skin infection
  • necrotizing fasciitis
21
Q

What causes streptococcal pharyngitis? treat? What kind of complication is it

A
  • usually GAS
  • can sometimes be caused by other strains
  • goes away in 3-5 days but can be shortened by penicillin
  • suppurative complication
  • can lead to abscess or rheumatic fever
22
Q

What causes erypsipelas? treat?

A
  • form of cellulitis
  • suppurative complication of GAS
  • occurs near mucosal, epidermal junctions [around nose and mouth]
  • spreads rapidly
  • responds to antibiotics quickly
  • rarely causes more serious infection
23
Q

What is streptococcal impetigo?

A
  • found in young children in crowded conditions [developing countries]
  • starts as papule, then vesicle, then pustule
  • treat with antibiotics
  • never causes acute rheumatic fever
  • can lead to post-strep glomerulonephritis
24
Q

What is necrotizing fasciitis?

A
  • suppurative complication of GAS
  • common in diabetics, elderly
  • rapid destruction subcutaneous fascia
  • leads to shock and acidosis
  • only effective treatment is to surgically remove necrotic tissue
25
Q

What are 4 non-suppurative complications of GAS?

A
  • acute rheumatic fever
  • poststreptococcal glomerulonephritis
  • scarlet fever
  • streptococcal toxic shock syndrome
26
Q

What are epi features of acute rheumatic fever? What age group and type of people get it?

A
  • usually in children 5-15
  • primary ARF never seen over age 20
  • relapse can occur later in life after GAS pharyngitis
  • more common in impoverished countries
27
Q

What is acute rheumatic fever?

A
  • complication from pharyngeal infection with GAS
  • never from skin infection ALWAYS pharyngeal
  • antibodies to GAS cross react with endocardium because of molecular mimicry
  • immune system causing the disease
28
Q

What two things associated with increased susceptibility for ARF [one on host side one on bacteria side]?

A
  • GAS strain rich in M protein [particularly M 12]

- DR2 and DR4 HLA types increase risk of ARK after strep pharyngitis

29
Q

What are 4 clinical manifestations of acute rheumatic fever? How long does after strep pharyngitis does it occur?

A
  • 1 to 5 wks between strep pharyngitis and onset symptoms
  • migratory arthritis
  • carditis [long term can cause valve damage]
  • sydenham’s chorea [jerking movements]
  • erythema marginatum [pink rings on trunk and inner surface limbs]
30
Q

What is the pathogenesis of post streptococcal glomerulonephritis?

A
  • cause by nephritogenic strains of GAS via skin or pharyngeal infection
  • antibodies/complement components bind and form immune complexes with strep antigens
  • immune complexes deposit in renal glomerulus
31
Q

What are the clinical manifestations of post-streptococcal glomerulonephritis?

A
  • affects children
  • hypertension
  • edema
  • blood urine [hematuria]
  • self-limited [resolved on its own]
  • associated with higher rates of hypertension in adulthood
32
Q

True or false there is cross-creating in post strep glomerulonephritis?

A

false – there is cross-reacting in ARF not post strep glomerulonephritis

33
Q

What is scarlet fever?

A
  • nonsuppurative complication of GAS
  • from infection with strain that releases erythrogenic exotoxin
  • can follow pharyngeal or skin infection
34
Q

What are clinical manifestations of scarlet fever

A
  • get red rash and characteristic distribution on upper chest spreading to trunk
  • red “strawberry tongue” studded with white marks
35
Q

What is pathogenesis of streptococcal toxic shock syndrome?

A
  • from skin/soft tissue infections with strains that have lots of M protein
  • pyrogenic exotoxins [SPEA, SPEB, SPEC] released from organism
  • ## act as superantigens and bind to t lymphocytes and MHC II and cause cytokine storm
36
Q

What are clinical manifestatiosn of streptococcal toxic shock?

A
  • shock
  • multi-organ system failure
  • fever
  • more often in diabetics, chronic alcoholics,
37
Q

What is difference antigens and superantigens?

A
  • antigens processed by APC and presented to T lymphocytes by MHC II
  • superantigens directly bind MHC II and TCR so don’t need to be processed
38
Q

What group and hemolysis pattern is streptococcus agalctiae?

A

group b

beta-hemolytic

39
Q

What diseases is streptococcus agalactiae associated with?

A
  • neonatal sepsis and maternal sepsis
  • soft-tissue infection in diabetics
  • urinary tract infection
  • [rarely] bacterial endocarditis
40
Q

What are the two major pathogenic species of enterococcus?

A

enterococcus fecalis

enterococcus faecium

41
Q

Do enterococcus cause soft tissue or pharyngela infections? where do they inhabit? What drugs are they susceptible or resistant to? What lancefield group?

A
  • do not cause soft tissue or pharyngeal infection
  • relatively resistant to antibiotics
  • found in GI tract
  • very resistant to penicillins and cephalosphorins and other beta-lactams
  • considered lancefield group D
42
Q

What diseases is enterococcus associated with?

A
  • UTI
  • billiary tract infection
  • peritonitis
  • bacterial endocarditis
  • nosocomial [hospital acquired] superinfection [bacteremia]
43
Q

What pathogen is major cause of neonatal sepsis?

A

streptococcus agalactiae

44
Q

What type of hemolysis pattern for strep viridans?

A

alpha hemolytic

45
Q

What family is S. mutans? what does it cause?

A
  • type of strep viridans

- causes dental caries [tooth rot]

46
Q

What family is S. sanguis? what does it cause?

A
  • type of strep viridans

- associated with subacute bacterial endocarditis on previously damaged valves

47
Q

How do you distinguish pneumococci from strep viridans?

A
  • both are alpha hemolytic

- distinguish by the optochin test –> pneumococci are sensitive to optochin and strep viridans are not

48
Q

Where do strep viridans normal live?

A

mouth and upper respiratory tract

49
Q

What are the causes of bacterial endocarditis on native heart valves?

A
  • 60-80% streptococci [30-40% viridans]
  • 10-27% staphylococcus aureus
  • 1-13% gram negative aerobes

Microbiology Part 1 (24 decks)

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