strept-entro-pnemo Flashcards
Streptococcus, gram/catalase
gram +, catalse -
strepto(=chain) cocci (shape)
Some streptococci are typically seen as diplo-cocci: _________
Streptococcus pneumoniae
Classification based on Hemolysis (on blood plates)
species
pneumolysin
b-hemolysis on blood-agar plates causes clearing at and around colonies in = Streptococcus pyogenes, staph aureus
a-hemolysis shows greening due to partial lysis of erythrocytes in S.mitis and S.pneumoniae.
pneumolysin degrades hemoglobin= green
Streptococcal classifications
based on hemolysis: a, b or gamma
Lancefield groups:
serological (=antiserum) differences (mostly based on cell wall carbohydrates)
Group A: N-Ac-glucosamine + rhamnose
Group B: rhamnose + N-Ac-glucosamine + galactose
Rapid strep throat test is based on? useful for?
Group A serological response.
Useful for rapid distinction from viral strep throat
Virulence factors of streptococci
m protein capsule f protein lipoteichoic acid g protein C5a peptidase membrane damaging toxins super Ag
m protein where found in cell? how many serotypes? Ab to this? binds to? effects?
M protein - cell wall component, >100 serotypes, membrane anchored: is an important virulence factor
• anti-M antibodies prevent infection of S.pyogenes but many serotypes. So protective immunity is type specific
• M protein binds keratinocytes, the main cell type in outer skin layer
• M protein binds fibrinogen, blocking surface from complement system components
• M protein binds complement control proteins
• Inhibits formation of opsonins by complement cascade
M protein anti-complement action through Factor H
capsule of strep
how does group A avoid pahgo?
antibodies are ineffective against glycocalyx-covered surface antigens
Ø Group A strains have capsules of hyaluronic acid, mimicking
mammalian connective tissues, preventing phagocytosis.
F protein
F protein (cell wall adhesin) provides adherence to the fibronectin of throat epithelial cells
lipoteichoic acid
lipoteichoic acid (species-specific form) also adheres to the fibronectin epithelial cell coat
. Capsular C3 peptidase
destroys opsonizing C3b complement opsonization
Thus: CR1 does not work! Phagocytosis only by IgG opsonization (FcR)
G protein
G protein (cell surface) binds Fc of IgG, preventing phagocytosis based on FcReceptors
C3b peptidase
C5a peptidase in which group? how it works
C5a peptidase in Group A Streptococci
membrane damaging toxins of strep. pyogenes
streptolysins s and o
tissue degrading enzymes
streptolysins S, O
lysis of erythrocytes (direct lysis; basis of β-hemolysis) and of phagocyte lysosomal membranes (indirect lysis of leukocytes)
secretion of tissue degrading enzymes by strep pneumo.
clinical use?
DNase, protease, hyaluronidase (spreading factor), streptokinase (degrades blood clots)
streptokinase is clinically useful in early vascular attack treatment because its activates plasminogen and the resulting plasmin will degrade fibrin clots formed in stroke and heart infarct.
super Ag of strep pneumo
overrides t cell response= excess
SPE
scarlet fever
strain?
virulence factor causing this?
Streptococcus pyogenes
Virulence factor: a superantigen SPE
Streptococcal Pyrogenic Exotoxins
Other results of pyrogenic SPEs
Pyoderma (impetigo) = skin infections of face, arms, legs (pus)
Erysipelas: erythros = red, pella = skin, bullae = blisters
streptococcal gangrene
Strept.pyogenes
Progression to deep, systemic infection leads to multi-organ failure and death.
necrotizing fasciitis
Acute Pharyngitis/ Strep throat sequence and late complications
encounter>symptoms>recover late complications possible: glomerulonephritis- type III hyper rheumatic fever- type II hyper, can lead to myocarditis/ arthritis chorea- brain function impairment
Rheumatic Heart Disease by Streptococci
Acute Rheumatic Fever:
• non-suppurative sequela with some strains of strep
• <10% of population is susceptible
• fever is non-responsive to penicillin because disease is autoimmune
• high frequency of reoccurrence
weaking of mitral valve and backflow
Comparing Strep and Staph: characteristics
strep: gram + cocci in chains , b-hemolytic, cell wall with A polysac and M pro
staph: gram + cocci in clusters, cream colored, M protein
Comparing Strep and Staph: extracellualr products
strep: L
staph: R
Comparing Strep and Staph: diseases caused
strep: L
staph: R
Streptococcus agalactiae group? hemolytic? aerobic? capsule? effects of children, elderly and preganant? Ab for this?
Group B, β-hemolytic (<2% non-hemolytic), chain-like growth, aerobic, polysaccharide capsule
• pneumonia in neonates (neonates: <7 days of birth)
• bacteremia and meningitis (neonates: >7 days of birth)
• various symptoms in elderly suffering from chronic diseases (often complicated by penicillin allergy)
urinary infections, bacteremia (pregnant women)
Neutralizing antibodies against group B polysaccharide Ag develop quickly and protect.
(maternal Abs prevent infection of neonate)
Strains different from S.pyogenes or S.agalactiae may cause:
opportunistic streptococcal toxic shock syndrome (AIDS)
Enterococcus faecalis gram? shape? hemolysis? virulence? aggration substance? adhesin for? cytolysin? attracts what cells? gelatinase? Ax resistance?
Gram+ cocci (Lancefield Group D streptococci) α- and non-hemolytic
Facultative anaerobes, normal part of gastrointestinal flora
Virulence (low):
Ø aggregation substance – epithelial adhesion
Ø enterococcal adhesin for collagen
Ø cytolysin facilitates colonization
Ø neutrophil chemo-attractant
Ø gelatinase – protease for gelatin, collagen, hemoglobin
Ø high, multiple antibiotic resistances (plasmid and chromosomal)*
elderly; long hospitalization= (high nosocomial risk antibiotic resistance)
Streptococcus pneumoniae
hemolytic, gram, shape
causes?
only what strains are virulent?
α-hemolytic, Gram+ diplococci
cause of pneumococcal pnemonia
Only encapsulated strains (smooth colonies) are virulent
pneumonia causing species
pnemococcal pneumonia, klebsellia pneumonia, mycoplasmal pneumonia
pneumococcal pnemonia carrie rates and vax
high carrier rates and vax available
klebsiella pneumonia where found? resistant? cause of? vax
enterobacteria
often resistant to Ax
fatal nosocomial pneumonia
no vax
mycoplamasmal pneumonia
cause of?
vax?
mild pneumo
no vax
streptococcal pneumonia sequence
infection of alveoli>neutrohils invade> fluid filled> macrophages and Ax assit to beat infection
S.pneumoniae virulence factors
a hemolysin capsule IgA protease c polaysac phosphoryl choline f antigen
a hemolysins of strep pneumo
erythocyte lysis by pneumolysin: cholesterol-dependent action, hemoglobin destruction
pneumolysin also suppresses oxidative burst in phagocytes
capsule, s. pneumonia
is anti what?
what action does it facilitate?
capsule (>90 serotypes) is antiphagocytic and its anti-complement facilitates bacteremia (presence in blood circulation) and thus spreading to other tissues like brain (meningitis)*, peritonitis, arthritis, endocarditis
c poly sac of s pneumonia
C polysaccharide rich in choline; precipitates CRP (C-reactive Protein, an early inflammatory signal)
phosphoryl-choline of s. pneumo
phosphoryl-choline in cell wall activates PAF º allowing entry of bacteria into cells
lipoteichoic acid/ F antigen of s. pneumo causes? results in?
alternative complement activation produces C5a
Result: typical pneumococcal leukocyte aggregation in lower respiratory tract (lungs)
S.pneumoniae and meningitis
Thousands of cases of pneumococcal meningitis per year in USA
is main agent with increased age, although young children more susceptible to group B strepococcus meningitis
