Lec3 Streptococci Flashcards
Where does strep normally live [3 places]
- skin
- mucous membranes
- GI tract
What is name for group A beta hemolytic strep?
streptococcus pyogenes
What is name for group B beta hemolytic strep?
streptococcus agalactiae
What are the 4 main types of strep?
- streptococcus pyogenes
- streptococcus agalactiae
- strep viridans group
- streptococcus pneumoniae
Are streptococci gram neg or pos? what shape?
- gram positive
- cocci in chains
What distinguishes streptococci from staphylococci biochemically?
streptococci are catalase negative
Does strep grow aerobically or anerobically?
both!
What are the 4 nomenclature systems?
- lancefield grouping
- hemolysis pattern on blood agar
- genus and species
- traditional term
What are lancefield groups?
system of dividing streps by the surface antigens they have
- group A, group B, group C, etc
What are the three types of hemolysis patterns?
- beta [clear zone around colony]
- alpha [ green zone]
- gamma [no zone of hemolysis]
How do you distinguish GAS from other beta-hemolytic streptococci?
GAS is sensitive to bacitracin
What is the M protein of GAS?
- main virulence factor
- anchored in cell membrane
- strain rich in M protein will resist phagocytosis and multiply quickly
How is virulence of GAS or immunity to GAS related to M protein?
- 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
What is protein F in GAS?
- cell membrane virulence factor
- helps organism adhere to mucosal sites
What is streptolysin O?
- most important extracellular product of GAS
- causes hemolysis and damage to WBCs, platelets, heart cells
What is streptolysin S?
- dmages WBCs, platelets, herat cells
- responsible for GAS causing beta hemolysis on blood agar
- extracellular compound of GAS
What do hyaluronidase and streptokinase do?
- extracellular compounds of GAS
- speeds up liquefaction of pus, enhance spread of infection in tissues
What are suppurative vs non-suppurative complications of pathogenesis
suppurative = direct invasion, pus/abscess non-suppurative = manifestation of disease remote from primary site of colonization or infection
What are suppurative vs non-suppurative complications of host immune response?
suppurative: neutrophil response
non-suppurative: host response causes clinical manifestations of disease
What are 4 suppurative complications of GAS?
- pharyngitis
- cellulitis
- impetigo [skin infection
- necrotizing fasciitis
What causes streptococcal pharyngitis? treat? What kind of complication is it
- 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
What causes erypsipelas? treat?
- 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
What is streptococcal impetigo?
- 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
What is necrotizing fasciitis?
- 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
What are 4 non-suppurative complications of GAS?
- acute rheumatic fever
- poststreptococcal glomerulonephritis
- scarlet fever
- streptococcal toxic shock syndrome
What are epi features of acute rheumatic fever? What age group and type of people get it?
- 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
What is acute rheumatic fever?
- 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
What two things associated with increased susceptibility for ARF [one on host side one on bacteria side]?
- GAS strain rich in M protein [particularly M 12]
- DR2 and DR4 HLA types increase risk of ARK after strep pharyngitis
What are 4 clinical manifestations of acute rheumatic fever? How long does after strep pharyngitis does it occur?
- 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]
What is the pathogenesis of post streptococcal glomerulonephritis?
- 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
What are the clinical manifestations of post-streptococcal glomerulonephritis?
- affects children
- hypertension
- edema
- blood urine [hematuria]
- self-limited [resolved on its own]
- associated with higher rates of hypertension in adulthood
True or false there is cross-creating in post strep glomerulonephritis?
false – there is cross-reacting in ARF not post strep glomerulonephritis
What is scarlet fever?
- nonsuppurative complication of GAS
- from infection with strain that releases erythrogenic exotoxin
- can follow pharyngeal or skin infection
What are clinical manifestations of scarlet fever
- get red rash and characteristic distribution on upper chest spreading to trunk
- red “strawberry tongue” studded with white marks
What is pathogenesis of streptococcal toxic shock syndrome?
- 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
What are clinical manifestatiosn of streptococcal toxic shock?
- shock
- multi-organ system failure
- fever
- more often in diabetics, chronic alcoholics,
What is difference antigens and superantigens?
- 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
What group and hemolysis pattern is streptococcus agalctiae?
group b
beta-hemolytic
What diseases is streptococcus agalactiae associated with?
- neonatal sepsis and maternal sepsis
- soft-tissue infection in diabetics
- urinary tract infection
- [rarely] bacterial endocarditis
What are the two major pathogenic species of enterococcus?
enterococcus fecalis
enterococcus faecium
Do enterococcus cause soft tissue or pharyngela infections? where do they inhabit? What drugs are they susceptible or resistant to? What lancefield group?
- 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
What diseases is enterococcus associated with?
- UTI
- billiary tract infection
- peritonitis
- bacterial endocarditis
- nosocomial [hospital acquired] superinfection [bacteremia]
What pathogen is major cause of neonatal sepsis?
streptococcus agalactiae
What type of hemolysis pattern for strep viridans?
alpha hemolytic
What family is S. mutans? what does it cause?
- type of strep viridans
- causes dental caries [tooth rot]
What family is S. sanguis? what does it cause?
- type of strep viridans
- associated with subacute bacterial endocarditis on previously damaged valves
How do you distinguish pneumococci from strep viridans?
- both are alpha hemolytic
- distinguish by the optochin test –> pneumococci are sensitive to optochin and strep viridans are not
Where do strep viridans normal live?
mouth and upper respiratory tract
What are the causes of bacterial endocarditis on native heart valves?
- 60-80% streptococci [30-40% viridans]
- 10-27% staphylococcus aureus
- 1-13% gram negative aerobes
