streptococci, enterococcus, pneumococcus and staphylococcus (2/8/18) Flashcards
what kind of pathogen are streptococci, enterococcus, pneumococcus, and staphylococcus (+/-)
all gram possitive
who first described streptococci
leuis pastuer in 1879
what is the first microbes identified in cause contagious disease (germ theory)
puerperal fever in maternity ward
discovery of streptococci and subsequently germ theory was essential to what in hospitals
hygiene and aseptic practices
number of species of streptococcus
100+
how were streptococci originally classified
lancefield groups
serological classification based on major cell-wall carbohydrate antigens (A-H) (works well for pyogenic strep)
lancefield groups
can all strep be classified using lancefield groups
no, many strep are un-typeable
no antisera reacts to their cell wall antigens
what lancefield groups of streptococci are pyogenic strep
Group a: streptococcus pyogenes
Group b: streptococcus agalactiae
morphology of streptococci
gram positive cocci arranged in chains
small and more ovoid than staphylococci
do streptococci react with catalase
negative
do streptococci form spores
no
are streptococci motile
no flagella
do streptococci have a capsule
variable (carb or hyaluronic acid
can streptococcus be classified on hemolysis on blood agar
yes
alpha hemolysis pattern
partial hemolysis and green discoloration of hemoglobin
beta hemolysis pattern
clear zone of complete hemolysis (can kill blood cells)
gama hemolysis
no zone of clearing
what streptococcus does alpha hemolysis patterns
viridans strep mostly in oral cavity
whatstreptococcus does beta hemolysis
GBS and GAS
what do biochemical reactions what classifying strep look at
particular enzymes
what do DNA sequences look at for classifying strep
16s rRNA (doesn’t work well for mitus strep)
types of Group A strep (GAS)
primarily infect respiratory tract , blood stream, and skin
- suppurative pus diseases: direct damage by organism
- toxin mediated disease- systemic response cuased by strep exotoxins secreted in bloodstream
- non-suppurative sequelea- late manifestations-autoimmune-aberrant immunological reaction to GAS antigens
who does GAS infect
exclusively humans
how does GAS spread
respiratory droplets and direct person to person contact
What are the virulence factors of GAS (S pyogenes)
M protein Protein F Hyaluronic Acid (HA capsule) Hyaluronidase C5a peptidase streptolysis S and O Strptokinase Pyrogenic exotoxins
roll of M protein in GAS( S pyogenes)
adhesin binds to keratinocytes (outer layer of skin)
roll of protein F in GAS( S pyogenes)
Fibronectin binding protein
roll of hyaluronic acid (HA) capsule in GAS( S pyogenes)
anti-phagocytic
roll of hyaluronidase in GAS( S pyogenes)
spreading factor that allows S pyogenes to spread through tissues
roll o C5a peptidase in GAS( S pyogenes)
degrades complement protein c5a-blocking phagocyte chemotaxis
roll of streptolysin S and O in GAS( S pyogenes)
hemolysins the lyse various host cells
roll of streptokinase in GAS( S pyogenes)
binds human plasminogen converting it to plasmin-breaks fibrin clots allowing tissue spread
roll of pyrogenic exotoxins in GAS( S pyogenes)
superantigens causing fever neutropenia, rash of scarlet fever
how does GAS adhere to mucosal surface via fibronectin
pili, M protein, LTA and protein F
how does GAS adhere to sub corneal keratinocytes in the epidermis
M protein and protein F
can GAS infecet non-phagocyctic cells
yes, but not completely understood
what does GAS do once past host barriers
GAS secretes virulence factors that allow host immune evasion and deeper infections to occur
what does M protein look like
myosin
function of M protein
bind to keratinocytes
prevents opsonization by complemnt
antibody against M protein opsonize where
against the hypervariable region
opsonization against M protein hypervariable region is difficult becuase
200 distinct M protein serotypes responsbile for subtypes of GAS and inmunity to one serotype does not confer protection to others
regions of M protein of GAS
Type specific Ab (hypervariable region)
fibrogen binding region (semi-conserved)
serum factor H (conserved) and inserts into cell wall
what does M protein type determine
what disease GAS can cause (different serotypes cause different diseases) with some overlap though
binding of fibrinogen to M protein prevents binding of:
C3b
M proteins bind was complement control protein to inhibit alternative compliment pathways
Factor H
C5a peptidase degrades what
C5a- the peptide mediator of inflammation (degredation leads to prevention of chemotaxis)
purpose of the Hyaluronic acid capsule (HA)
antiphagocytic structure by camouflaging against the immune system, pretending to by Non-antigenic (HA is found in connective tissue
problem with Hyaluronic Acid (HA) capsule for pathogens
interferes with adherence to epithelial cells
how does S. pyogenes spread through tissue despite having a hyaluronic acid capsule
secretes hyaluronidase to digest the capsule
a pore forming toxin the can lyse Red bood cells and kill phagocytes and lse various host cell
streptolysin s and o
a toxin the lyses red bllod
hemolysin ( Beta-hemolysis on blood agar)
toxin that kills phagocytes
leukocidin
why release a toxin to kill host cells
release nutrients for growth
stability of streptolysin S and streptolysin O in oxygen
S-stable in O2
O- labile in O2
what binds to plasminogen to perform enzymatic conversion to plasmin
streptokinase (invasin)
what can plasmin coated GAS do:
degrade and spread through fibrin (blood clots) resulting in invasive disease
what do some strains secrete into the blod stream
pyrogenic exotoxins (speA, SpeB, and SpeC)
pyrogenic exotoxins cause
rash associated with scarlet fever (toxin spread through blood)
the most abundant extracellular protein by GAS
SpeB
what is SpeB
cysteine protease-degrade immunoglobulins and cytokines preventing complement activation (degrades C3b)
other name for speA and speC
superantigens
speA and SpeC non-specificall activate large subsets of what that leads to
T-cells cuasing streptococcal toxic-shock syndrome (STSS) (strepSAgs)
most common manifestations of GAS
Acute pharyngitis (strept throat) pyoderma - GAS infection of skin (impetigo)
who has acute pharyngitis
school age children with 20% are asymptomatic carries
who are the most contageous with GAS
nasal carriers
who has Pyoderma
preschool children
mortaility from S pyogenes (GAS)
500,000 death/year worldwind (influenced by strain, host and portal of entry)
symtoms of scarlet fever
high fever (101 degrees F)
deep red cheecks (white around mouth and nose-circumoral pallor)
red tongue with yellow-white exudate that peals after a few days (straberry tongue)
sand paper rash develops after several days
how to treat S pyogenes (GAS upper repiratory tract infections
10 days of penicillin
strep throat is characterized by
swollen white pus on the tonsils
skin infections cuased by GAS
impetigo-infection of the epidermise
erysipelas
Cellulitis- acute inflamatory process involving subcutaneous tissue
symptomes of impetigo
transient skin colonization+ trama (insect bite)
intraepidermal vesicles filled with exudate- eventually crust over
not systemic, but nephrogenic GAS can lead to post streptococccal glomerulonephritis
sysmpotms of erysipelas
superficial erythematous and edematous lesions
spreads in superficial ymp of the dermis
rash is confluent, salmon red, with sharp demarcations
symptos of cellulitis
red, heat, tender
indistinct boarders
rapid progression to septicemia
autoimmune diseases (non-suppurative infections) due to S. pyogenes (GAS)
acute Rheumatic Fever (ARF)
Acute Post streptococcal Glomerulonephritis (APSGN)
what does ACute Rheumatic fever follow
pharyngeal infections by rheumatogenic strains
what does Acute post streptococcal Glomerulonephritis follw
pharyngeal or skin infections by nephritogenic strains
Hypersensitivity reaction cuased by cross-reacting antibodoies ( M proteins) to effect the heart, joint, skin and brain.
Acute Rheumatic Fever (ARF)
when does ARF appear
1-4 weeks after strep throat (even asymptomatic infection) but only 10% of people are susceptible
who sees ARF
not-developed counties
Since ARF has a high susceptibility for recurrence, what is done
prophylactic antibiotics into adulthood or life is required (3-4 week IM dose)
how to prevent ARF
treating strep throat with a full course of Penicillin
symptoms of ARF
Fever Painful joints (arthritis) Chorea- (fidgety or abrnormal movement) heart murmur non-itchy erytheme marginatum rash
who gets acute post streptococcal glomerulonephritis
2-12 years old after strep throat or impetigo 5-21 says before
incidence of Acute Post streptococcal Glomerulonephritis
rare(6-20: 100,000 in the west)
what strain of GAS causes acute post streptococcal glomerulonephritis
only nephritogenic GAS strains (type M12 and 49)
what cuases acute post streptococcal glomerulonephritis
immune complexes (antibody-antigen) containing steptococcal antigens are deposited in affected glomeruli causing type III hypersensitivty
symptoms of Acute Post Streptococcal Glomerulonephritis
Edema
Gross Hematuria )tea colored urine)
Hypertension)
how to treat acute post streptococcal glomerulonephritis
sodium restirction
diuretics
(95% recovery)
what severe invasive infections can S pyogenes (GAS) cause
subdermis (cellulitis)
Connective FAscia (necrotizing fasciitis, i.e. flesh-eating disease)
muscle(myositis)
Blood (septicemia, streptococcal toxic shock syndrome)
streptococcal toxic shock syndrome can occur with what
necrotizing fasciitis- nausea, vomiting, diarrhea, hypotension, shock, organ failure…
what is effective against GAS
penicillin G
Beta-lactams and macrolides also work
becuase antibodies are protective against future infections with the same M type, they are considered
type specific immunity
Vaccine agianst GAS
none yet but specific M-protein vaccines that do not cross react with host protein are being tested with good results
what group of strep is streptococus pneumoniae
mitis
morphology of streptococcus pneumoniae
gram-possitive oval cocci found in pairs (diplococcus)
hemolysis of streptococcus pneumoniae
alpha-hemolytics (partial hemolyisis, green colonies on blood agar)
capsule on streptococcus pneumoniae>
yes, required for virulence with antigenic carbs
lysis of streptococcus pneumoniae
autolytics
where does pneumococcal colonize
nasopharynx in 5-40% of healthy perons, highest in children in winter months
how does pneumoccal spread
person to person via direct contact, microaerosoles
what pneumococcal serotypes produce disease
20 of the 90 serotypes produce more disease due to enhanced virulence factors
Virulence factors for Pneumococci
Capsule (necessary)
Choline-binding Proteins_asherence to host tissues
Pneumolysin- transmembrane pore-forming toxin
Neuraminidase- cleaves sialic acid present in host mucin, glycolipids, and glycoproteins- exposing binding sites
how is pneumolysin released
pneumococci must lyse itself to release the pneumolysin
pathogensis for pneumococcal pneumonia
aspiration of respiratory secretion containing pneumococci
adherence to host epithelial cells in aveoli of lungs
neuraminidase aids in addition recetpors being exposed
capsule acts to block phagocytosis disrupting complement-C3b
Bacterial cells lyse causing release of pneumolysin injurying host cells
what normally clears pneumococcal pneumonia when breathed into the lungs
the mucocilliary blanket
what helps with binding of pneumococcal pneumonia to epithelial cells of aveoli
cell-wall choline binding proteins and carbs on host cells
what causes the lungs to fill with fluid in pneumococcal pneumonia
the neutrophils come in in response to injury of host cells due to pneumolysin
what makes up the capsle ofpneumococci
high molecular weight polysaccharide polymers with 90 different serotypes with unique antigens
how does the capsule work in pneumococci
interferes with deposition of complement protein C3b on bacterial cell surface
if antibodies recognize the capsule of pneumococci, what happens
opsonophagocytosis
what is pneumolysin related to
staph alpha-toxin and streptolysin O produced by GAS
action of pneumolysin
cytokines relase
pore formation
discupts cilia of human respiratory epithelial cells
pneumococcal disease is the leading cuase of
pneumonia (500k cases) otitis media (ear infections- millions of cases) acute purulent meningitis (3000 cases) bacteremia other infections
who dies from pneumococcal disease
5 million deaths in children per year
symtoms of pneumococcal pneumonia
shaking chill and high fever initally
Productive cough with pink and rusty color(blood)
Sharp chest pain when inhaling and exhaling
Pulmonary consolidation (fluid filled lungs)
when do symptoms of pneumococcal pneumonia clear
5-10 days due to adaptive immunity-opsonizing antibody arrival
after the sysmptoms of pneumococcal pneumonia clear what may happen
bacteremia is common and may be followed by pneumococcal meningitis
who is at risk for pneumonia
people over the age of 50
how to treat pneumococcal pneumonia
penicillin works on susceptible strains
cephalosporins also used
fluoroquinolones
vaccines for pneumococcal pneumonia respond because
capsular polysaccharides
types of vaccines for pneumococcal pneumonia
PPV23-pneumococcal polysaccharide vaccine-
purified polysaccharide from 23 serotypes of invasive S pneumoniae
PPV13- pneumococcal conjugate vaccine- from 13 strains conjugated with protein for type 2 response
who is recommended for the PCV13 vaccine
children 2 months to 2 years of age
the leading cause of neonatal sepsis and miningitis in newborns
Group B streptococci (GBS) - S. agalactiae (aeobic)
where is GBS/S. Agalactiae found
inhabit lower GI and female genital tracts
how babies get GBS/S. agalactiae
during burth because 15-40% of women are carriers
how to prevent babies from getting GBS/S. agalactiae
screen female at 35-37 week of gestation and if possitive, mother takes intrapartum antibiotics
GBS/ S. agalactiae causes what in adults with chronic diseases
Cellulitits, arthritis, and meningitis
roll of polysaccharide sialic acid capsule of GBS
prevent opsonization and phagocytosis
how may one become immune to GBS
because the polysaccharide sialic acid capsule has type-specific antibodies, infection leads to immunity along the complement pathway
serotypes of GBS polysaccharide sialic acid capsule
9 serotypes, with type III most common in neonatal sepsis in USA
what are Group C and G streptococci
commensal bacteria that live in the airway, skin, and Digestive tract and female genitals
what does s. dysgalactiae cause
bovine mastitis
what does s. equi cause
strangles in horses
what do C and G streptococi have that make them similar to other streptococci
M proteins that bind fibrinogen and secreate similar extracellular enzyme
does C or G streptococci have a hyalueonic acid capsule
Group C
what infections can group c and G streptococci cause
Similar to GAS- tonsillitis, respiratory and deep tissue
gRoup C and G streptocci are implicated in what
AGN no ARF
hemolytic type of group D
alpha or gamm
are group D streptococi enterococci or non-enterococci
both!
where are group D streptococci found
in the normal flora of GI and genitourinary tracts
why are enterococci coined as the worlds toughest pathogenic bacteria
grow in high salt and detergents (bile)
Inhibited but not killed by penicillin (Altered PBP’s)
resist most antibiotics
what does Enterococci cause
nosocomial opportunistic infections
how to kill enterococci
antibiotic synergism(penicillin-weakens cell wall and aminoglycoside-reaches inside
why are Vacomycin resistant enterococci emerging
subtle changes in peptidoglycan precurses, so beta-lactams bind much less
the last resort antibiotic for enterococci
linezolid
who does Enterococci give its Vancomycin resitance to in a lab
staphylococci
main virulence factor of enterococci are from
resisting environmental and antimicrobial agent stress
hemolytic description of viridans (greening streptococci)
alpha
where is Viridans(greening streptococci found
30-60% of oropharyngeal flora
what does Viridans greening strptococci causea s a pathogen
if introduced into the blood stream by dental procedues, can cause subacute bacterial endocarditis, affecting abnormal heart valves
what is used to treat Viridans (greening) streptococci in high risk patients
prophylaxis antibiotics
what is subacute bacterial endocarditis
bacterial infection on endocardium when abnormal values or heart disease is present
symptoms of subacute bacterial endocarditis
fever chills muscle aches abdominal pain heart murmur
morphology of staphylococcus
large and more round than strptococci and bunch together
hemolytic properties of staphylococcus
beta-hemolytic
motility of staphylococcus
non-motile
spore of staphylococcus
non-spore forming
catalase reaction with staphylococcus
positive
coagulase of staphylococcus
positive(variable)
where staphylococcus can be found
in the normal flora
cell wall of staphylococcus aureus
contains peptiodglycan with lots of Teichoic acid (TA)
also polysaccharide capsule
and surface proteins
surface proteins of staphylococcus aureus
Clumping factors (bind fibrinogen)
FnBP (bind fibronectin)
Surface protein A (bind the Fc portion of IgG molecules- stimulates cytokines (TNF-alpha), platelets and activates B cells
virulence factros of S. aureus
cytolyitc toxins (alpha, beta gamma, delta) that cause cell lysis PVL exfoliatin toxin Staphylococcal superantigens toxic shock syndrom toxin
what toxin is secreted by all S. aureus except coagulase negative strains to create pore
alpha toxins
what is active against platelelts and neutrophils to cuase tissue necrosis
Panton-Valentine leukocidin (PVL)
protease that cleaves specific cell membrane fatty acids forn in keratinized epidermis of skin to disrupt intraepidermal junction
exoliatin toxin
what does exfoliatin toxin cause
staphlococcal scald skin syndrome (SSSS)- fluid filled blisters
secreted proteins that stimulate systemeic effects when absorbed in the gut or when produced in vivo by multiplying bacteria
SAgs(staphylococcal superantigen)
Enterotoxins cause
vomiting and diarrhea
resistance of enterotoxins
V. stable to boiling and digestive enxymes
cause toxic shock syndrome (TSS)
toxic shock syndrom toxin leads to
massive cytokine release, binding to class II MHC to activate T cell non-specifically
primary infection by staphlococcal diseases lead to
Furuncle (boil)
impetigo
deep tissue lesions
pneumonia
where do furuncles begin
in hiar follicle, sebaceous gland, or sweat glands
multiple boils under the surface
carbuncle
what is impetigo secondary to
GAS infection
but can also act as a primary infection
deep tissue lesions of staphylococcal diseases
in bones, joints, and soft tissues
toxin mediate disease can result from
primary infections via staphlococcus with strains that produce toxins
what are toxin mediated disease
Scaldd skin syndrome
toxic shock syndrome
staphylococcal food poinsing
how does one get infected by staphylococcus aureus
normal transmission via nasal carriers (10-30% of population has it in their nose)
hospital spread- hands of medical personnel
what can staphylococcus aureus
survives drying-spread from contaminated clothing
pathogensis of staphylococcus
inital atachement via nBP
alpha-toxin injures keratinocytes to allow in
immune evasion
inflammator cells create the boil
and spontaneously resolves via drainage of puss
how does stphylococcus evade the immune system
antiphagocytic properites of protein a
pVL limited innate defence
Coagulase and CIF-limit host phagocytes
what causes toxic shock syndrom
toxin from a local infection enters blood stream
what is the most common superantigen adsorbed across the mucosal membranes
TSST-1
what does TSST-1 bind to
T-cell receptors andclass II MHC receptors- stimulating massive cytokine release (IL-1 and TNF)
what other way can Toxic shock syndrom occure
non-mentrual TSS without TSST-1
