ICL 2.8: Streptococci Flashcards
what is the microbiology of streptococci?
gram (+) coccus shape
how is steptococci classified?
- hemolysis
subdivided based on their ability to lyse red blood cells
- group specific carbohydrates
further subdivided based upon serological reactivity to different cell wall sugars = Lancefield groups
- biochemical characteristics
do NOT have catalase, while other gram (+) pathogens are catalase positive
what are the 3 hemolysis categories that streptococci can be divided into?
- α-hemolytic = green color, incomplete hemolysis
- β-hemolytic = gold color, complete hemolysis
- γ-hemolytic = no hemolysis!
what are the 5 groups of streptococci?
A,B,C/G,D, viridans
what is the organism and associated diseases of group A streptococci?
S. pyogenes = β-hemolytic
Pharyngitis, pyoderma, scarlet fever, toxic shock,
Impetigo, erysipelas, cellulitis, necrotizing fasciitis, puerperal sepsis, acute rheumatic fever, glomerulonephritis
causes 800 diseases so this is the group we’re most concerned with
what is the organism and associated diseases of group B streptococci?
S. agalactiae = β-hemolytic
neonatal sepsis, meningitis, puerperal sepsis
what is the organism and associated diseases of group C/G streptococci?
S. dysgalactiae = β-hemolytic
upper respiratory infections; septicemia, deep-tissue infections
what is the organism and associated diseases of group D streptococci?
- enterococcus = γ to α hemolytic
genitourinary tract infections, wound infections, endocarditis
- s. pneumoniae = α hemolytic
upper respiratory infections, septicemia, deep-tissue infections
what is the organism and associated diseases of viridans streptococci?
viridans streptococcus = α hemolytic
native valve subacute bacterial endocarditis (SBE)
which streptococci are α-hemolytic?
- s. pneumoniae
2. viridans
what is GABHS?
GABHS = group A β-hemolytic strep
GABHS differentiated from other β-hemolytic Strep based upon sensitivity to bacitracin so it WILL have a zone of inhibition!!
ex. streptococcus pyogenes
what is the composition of the capsule of group A streptococcus pyogenes?
hyaluronic acid capsule = antiphagocytic
poorly immunogenic
what is the rapid strep test?
it uses an antibody that is specific to group A capsule
group A capsule = hyaluronic acid!
what is the reason that sreptococci pyogenes is virulent?
there is an M protein that’s attached to the bacterial cell wall and it adheres to host cells!
it binds to fibrinogen to block C3 convertase (blocks classical complement pathway) and binds complement factor H (blocks alternative complement pathway)
group A streptococcus pyogenes is further divided into serotypes based on which M protein they have (130 serotypes)
the issue is that Abs against one M-type do not protect against other M-types; serotype-specific antibodies protect from re-infection –> so you need tons of antibodies because each serotype generates its own antibodies and you’ll get sick from each one
what does the M protein do?
protein of group A streptococcus pyogenes
it binds fibrinogen to block C3 convertase (blocks classic complement pathway) and binds complement Factor H (blocks alternative complement pathway)
what are the steps in the pathogenesis of grou pA streptococcus pyogenes?
- adherence
- immune evasion
- invasion and spread
- strep toxic shock syndrome
how do you diagnose s. pyogenes?
- culture
- rapid antigen detection test (RADT)
- DNA PCR
- Streptex (older, being phased out)
what would a s. pyogenes culture show?
gram-positive cocci in chains
β-Hemolytic; bacitracin sensitive
what is a dipstick test? what’s it used for?
it’s a type of rapid antigen detection test (RADT) used to diagnose s. pyogenes
throat swab is collected; carbohydrate extracted; add dipstick
it’s based on the group A carbohydrates!
if the red line comes up it’s positive
only takes 5 minutes
how is streptococcus pyogenes transmitted?
- contact with carriers
20% of school-age children carry GABHS during winter and early spring and it’s also in the normal flora of pharynx and skin
- air
distances of beds directly correlated with GABHS throat colonization (think military)
- hygiene
spread of all types of GAS infection can be reduced by good hand washing
what parts of the body does streptococcus pyogenes effect?
tonsilitis and pharyngitis
adenitis
what are the disease manifestations of s. pyogenes?
SUPPURATIVE INFECTIONS (pus forming)
- pharyngitis
- scarlet fever
- pyoderma
- erysipelas
- cellulitis
- necrotizing fasciitis
- streptococcal toxic shock syndrome
NONSUPPURATIVE SEQUELAE
- acute rheumatic fever
- acute glomerulonephritis
what are the symptomsm of s. pyogenes pharyngitis?
aka strep throat!!
- sore throat and fever = rapid onset of sore throat with malaise and fever (>101°F)
- tonsils enlarged = erythematous w/ patchy exudate
- tender anterior cervical lymph nodes = enlarged, palpable, tender at or below angle of the mandible
- ABSENCE of cough, choryza, hoarseness, or conjuntivitis (these are indicative of viral infections)
- non-pharyngeal signs = headache, nausea, vomiting, abdominal pain
- other signs = tongue is red & swollen “strawberry tongue”; soft palate shows petechiae
what are the complications associated with s. pyogenes pharyngitis?
- tonsillar abscess = serious infection of the tonsilar area
- cervical adenitis = infection of the cervical lymph node forms an abscess; ust operate to drain abscess in both cases
literally a giant bulge in the neck…
how do you treat s. pyogenes pharyngitis?
- Penicillin V: oral, 10 days, common Rx if ARF not endemic –> this is always what you treat with first!
- Benzathine penicillin G: i.m., once, lasts 10 days
- cephalosporins or macrolides: in cases of penicillin allergy
- acetaminophen or ibuprofen for symptom relief
what do you need to consider when treating s. pyogenes pharyngitis?
antibiotics reduce the risk of acute rheumatic fever (ARF)!! (:
with antibiotics, throat cultures negative after 24 hrs BUT children should NOT return to school until 24 hrs after treatment
without antibiotics, GABHS can persist for > 6 weeks and can lead to acute rheumatic fever, scarlet fever, etc.
what is opsonophagocytosis?
you need time for antibodies against s. pyogenes M protein to develop
what is serotype-specific immunity?
antibodies to s. pyogenes M protein are specific to the infecting GABHS only
if a new strain infects, there is NO immunity
different serotypes fluctuate through a population within the same year
what is streptococcus pyogenes scarlet fever?
- **toxin-mediated disease: Group A Strep secrete Streptococcal pyrogenic rxotoxins (Spe A, B, C) into bloodstream
- throat or skin colonization: Scarlet Fever is most commonly associated with untreated pharyngitis
- fever as high as 107-108∘F with severe headaches
- Pastia’s lines = characteristic reddish lines in folds of skin around elbows, underarms, stomach, and neck
- strawberry and raspberry tongue: Initially yellowish-white coat that progresses to a beefy red appearance
- “sandpaper rash”
what are Pastia’s lines?
characteristic reddish lines in folds of skin around elbows, underarms, stomach, and neck seen in scarlet fever
describe the sandpaper rash associated with scarlet fever?
scarlet fever is caused by streptococcus pyogenes
appears day 2 on upper trunk then spreads to rest of trunk, neck, and extremities
occlusion of sweat glands is what leads to sandpaper feel
the rash is maculopapular and blanches to the touch; resembles sunburn
mouth usually exhibits circumoral pallor (white around the mouth, not red)
eventually there’s desquamation = skin literally peels off –> this is localized to the hands and feed during the second week of illness
in what disease do you see a strawberry/raspberry tongue?
scarlet fever
the tongue starts white looking like a young strawberry then turns really red
it’s a disease caused by streptococcus pyogenes
what superficial skin infection is associated with streptococcus pyogenes?
pyoderma/impetigo
what is pyoderma/impetigo from streptococcus pyogenes?
localized purulent streptococcal infection of skin not related to pharyngitis!!
happens in the the epidermis (the top layer of skin which is why it’s a superficial skin infection)
progression = papule –> vasicle –> pustle
the vesicles and pustles are superficial and surrounded by erythema; the pustles resolve over 4-6 days and for thick crust – fluid is “honey colored”
may be associated with trauma (e.g., wound, fly bite)
same as impetigo contagiosa which can also be caused by Staphylococcus aureus)
which populations get pyoderma/impetigo from streptococcus pyogenes?
children 2-5 years old most common
specifically economically disadvantaged children with poor hygiene
what times of the year is pyoderma/impetigo from streptococcus pyogenes most common?
highest incidence in summer in northern climates
year-round in tropical climates
how do you treat pyoderma/impetigo from streptococcus pyogenes?
usually benign and resolves over time
if you need:
- penicillin
- topical mupirocin (bactroban)
**can be expensive
what’s the hallmark clinical feature of pyoderma/impetigo from streptococcus pyogenes?
“honey crusted” legions on kids
what invasive skin and deep tissue infections are caused by streptococcus pyogenes?
- erysipelas
aggressive; high mortality rates
- cellulitis
- necrotizing fasciitis
why do invasive skin and deep tissue infections from streptococcus pyogenes happen?
invasion of GABHS from skin or other sites to normally sterile sites
sterile sites = blood, deep tissue, CSF, organs
what is streptococcus pyogenes erysipelas?
acute inflammation of skin w/ lymphatic involvement
often involves face, trunk and extremities following pharyngitis
facial erysipelas presents with a characteristic “butterfly-winged” lesion and is benign (4-10 days)
localized erythema spreads with advancing red margins that are raised and well demarcated (can mark with pen)
how do you treat streptococcus pyogenes erysipelas?
penicillin
what is streptococcus pyogenes cellulitis?
spreading of acute inflammation in subcutaneous dermis layer as a result of burns, wounds, or surgery
local pain, tenderness, swelling, and erythema
can expand to become large areas, going systemic with bacteremia and lymphangitis
just looks really red and swollen
how does streptococcus pyogenes cellulitis differ from erysipelas?
- lesions are not raised
2. margins are not distinct
what are some predisposing factors for streptococcus pyogenes cellulitis?
- IV drug use
2. coronary bypass surgery
how do you treat streptococcus pyogenes cellulitis?
penicillin
sidenote: make sure it’s not a s. aureus infection
what is streptococcus pyogenes necrotizing fasciitis?
flesh-eating disease
infections of the fascia and deeper subcutaneous tissues
extensive, rapidly spreading necrosis and gangrene of the skin and surrounding tissues
mortality can reach 20% or higher
which bacteria usually causes necrotizing fasciitis?
currently Group A Strep is the most frequent agent
but also can be caused by other organisms like C. perfringens, S. aureus
what’s the progression of necrotizing fasciitis?
begins at site of inapparent trauma on the extremities
after 24-72 h there is extensive spreading inflammation with intense pain
skin becomes dark then blue-purplish, with bullae forming filled with yellowish fluid
bacteremia frequent with gangrenous sloughing skin
looks like blood blisters and red skin
how can you differentiate necrotizing fasciitis from cellulitis?
NF is characterized by:
- high fever and toxicity early in presentation
- extreme prostration
- rapidly spreading inflammation; bullous form
how can you try and save a limb from necrotizing fasciitis?
- I.V. antibiotics to kill remaining bacteria
- debridement = surgical removal of the infected, dead, and gangrenous tissue
may require amputation of infected limbs
what are the purulent, self-limiting diseases you can get from group A streptococcus pyogenes?
- pharyngitis
- impetigo
- erysipelas
- cellulitis
- necrotizing fasciitis
what are the toxin-mediated diseases you can get from group A streptococcus pyogenes?
- scarlet fever
2. streptococcal toxic shock
what are the immunological diseases you can get from group A streptococcus pyogenes?
- rheumatic fever
- glomerulonephritis
- glomerulonephritis
what is streptococcal toxic shock syndrome?
- s. pyogenes grows in wound
- GABHS enters blood stream and produces superantigens and mitogens
- fever, rash, shock +/- myositis and NF
what population is more suceptible to STSS?
STSS = streptococcal toxic shock syndrome
adults»_space;> children
how is STSS transmitted?
person-to-person
how do you treat STSS?
use both penicillin G and clindamycin
penicillin G = bactericidal, but only effective against growing bacteria in low concentrations
clindamycin = bacteriostatic, but prevents production of virulence factors (M protein, toxins, cell wall)
when do you get acute rheumatic fever?
ONLY following GABHS paryngitis
usually 1-4 weeks after GABHS infection
never after skin infactions!!
which population is most suceptible to acute rheumatic fever?
5-15 years old
what is acute rheumatic fever?
you get it ONLY following GABHS paryngitis (s. pyogenes)
immune-mediated; not bacteria, toxins or antigens
what are the symptoms of acute rheumatic fever?
- fever
- carditis (valve damage)
- polyarthritis
- erythema
- chorea = involuntary movements
how do you treat acute rheumatic fever?
so you only get ARF after GABHS pharyngitis
so early intervention of pharyngitis with penicillin Gdecreases chances of immunologic pathogenesis
but once ARF symptoms appear, you need chemoprophylaxis to prevent new GABHS infections or further valve damage:
daily oral penicillin V or monthly penicillin G for at least 5 years and up to age 25
when do you get acute post-streptococcal glomerulonephritis?
following throat OR skin infection from streptococcus pyogenes
which population is susceptible to acute post-streptococcal glomerulonephritis?
primarily in children but can be all ages
what is APSGN?
APSGN = acute post-streptococcal glomerulonephritis
it’s a result of immune complexes in glomeruli with complement fixation following throat OR skin infection
antibiotic treatment of prior infection may not reduce risk
symptoms = dark urine (hematuria), proteinuria, headache, back pain, edema, hypertension
how do you diagnose APSGN?
APSGN = acute post-streptococcal glomerulonephritis
- symptoms = dark urine (hematuria), proteinuria, headache, back pain, edema, hypertension
- GAS infection
- serologic test
how do you treat APSGN?
APSGN = acute post-streptococcal glomerulonephritis
benzathine penicillin G to eradicate Group A Streptococcal infection; supportive care
which bacteria is group B strep?
S. agalactiae = β-hemolytic
diseases = neonatal sepsis, meningitis, puerperal sepsis
how does group B strep grow?
chains
how does group A strep grow?
chains
how does group D enterococcus strep grow?
dipplococci or short chains
how does group D s. pneumoniae grow?
lancet-shaped dipplococci or short chains
how do viridans streptococci grow?
chains
what is group B streptococcus resistant to?
bacitracin
GBS differentiated from other B-hemolytic Strep based upon resistance to bacitracin
NO zone of inhibition!!
what is the capsule of group B streptococcus agalactiae?
sialic acid capsule carbohydrate (mimicry)
it blocks complement and inhibits phagocytosis
where does group B streptococcus agalactiae colonize in the body?
usually an asymptomatic colonizer of the genital and the gastrointestinal tracts
~25% of pregnant women have GBS in vagina or rectum; transient infection
so you have to do vaginal-rectal cultures weeks 36-37 gestation
~50% of infants born to GBS colonized mothers become colonized with GBS but only 1-2% of colonized infants develop disease
Caesarean section greatly reduces risk, even if mother is GBS positive
what is group B streptococcus agalactiae neonatal disease?
newborn infected either through contact in birth canal or by GBS ascending infection of placenta
once in the neonate, two disease courses possible:
- early onset = fulminant pneumonia, septicemia
1st week following birth; high mortality; MOST common
- late onset = meningitis, occult bacteremia, or osteroarthritis
1 wk-3 mo following birth; less common
some cases result in neurologic complications
what are the risk factors in pregnant women for neonatal group B streptococcus agalactiae?
- Colonization with GBS between 36 and 37 weeks gestation
- Fever > 38°C for 18 hours
- Ruptured amniotic membranes
- Premature delivery (<37 weeks)
- Age: women < 20 years old
- Ethnicity: African-American women
how do you diagnose group B streptococcus agalactiae?
vaginal and rectal swabs from pregnant women during weeks 36 – 37
place swab in non-nutritive transport media (Stuart or Amies medium)
culture in selective and antibiotic-containing medium
can further test isolates by rapid latex agglutination or CAMP test
what is the CAMP test?
used to test for group B streptococcus agalactiae
CAMP test examines interaction of presumptive GBS with S. aureus in co-culture
positive reaction is indicated by enhanced β-hemolysis closest to S. aureus
GBS secrete diffusible CAMP factor that enhance S. aureus hemolysis
the result is a characteristic arrowhead pattern!!
this result is distinct for group B streptococcus agalactiae
how do you diagnose maternal step B streptococcus agalactiae infections?
- Urine Detection Tests
possible, but not very sensitive; often requires overnight culture or urine concentration
- Nucleic Acid Amplification Test (NAAT)
PCR detection is sensitive and specific but NAAT availability is limited
how do you diagnose neonatal group B streptococcus agalactiae infections?
direct visualization from normally sterile sites (blood, CSF) is quick diagnostic
use culture to confirm
how do you treat GBS streptococcus agalactiae?
- Pencillin/Ampicillin:
however, MIC is 10x that for GABHS; can combine with an aminoglycoside (Gent, Neo) or cephalosporin (Cefazolin)
- cancomycin or clindamycin in cases of penicillin allergy (check culture sensitivity to clindamycin)
what prophylactic treatment do you do for GBS + pregnant women?
for pregnant women with positive GBS cultures, you want to reduce colonization prior to delivery, thus limiting chances of severe invasive infections of neonate
so do IV penicillin G >4 hours before delivery so that it has time to reach fetal circulation and amniotic fluid
what should you NOT use to treat GBS?
avoid Erythromycin and Tetracycline due to rising resistance
what is the shape of streptococcus pneumoniae? are they catalase +/-?
lancet-shaped diplococci
catalase negative
are streptococcus pneumoniae alpha, beta or gamma hemolytic?
alpha hemolytic = green
what is streptococcus pneumoniae sensitive to?
optochin-sensitive
so there will be a zone of inhibition!
where does streptococcus pneumoniae colonize?
colonizes nasopharynx - respiratory droplets
which population is susceptible to streptococcus pneumoniae infections?
common in children (40-60%)
disease most common in young children and elderly due to reduced immunity
pneumonia is more serious in adults than children
common in cool months
how many streptococcus pneumoniae serotypes are there?
90!!!
you’re usually colonized with one serotype at a time
but you’re gonna get sick after every new serotype…
serotype-specific immunity inhibits colonization by same serotype
what diseases does steptococcus pneumoniae?
- pneumococcal pneumonia
- otitis media
- bacteremia
- meningitis
what is pneumococcal pneumonia?
pneumonia more serious in adults than in children
bacteria replicate in alveolar spaces, leading to inflammation from the neutrophils and macrophages
then erythrocytes leak into alveoli!!
it’s rapid onset, shaking chills, sustained fever, chest pain is common
empyema = collection of pus within pleural space
productive cough with blood-tinged sputum
lobar pneumonia = localized to lower lobes, typically within a single lobe
what is otitis media?
caused by streptococcus pneumoniae; pneumococcus causes 40-50% of otitis media
most common reason for childhood medical visit
not life threatening, but can have other long-term effects
often preceded by viral infection
what is streptococcus pneumoniae bacteremia?
severe disease
children are fairly resistant
adults show 20-35% fatality
what is streptococcus pneumoniae meningitis?
accounts for 1/3 of all meningitis in adults and children
rare in neonates, but more common in children and adults
more severe neurologic issues that with other causes of bacterial meningitis.
what are the virulence factors associated with streptococcus pneumoniae?
SECRETED
1. pneumolysin
- IgA protease
SURFACE
3. capsule
what is pneumolysin?
secreted virulence factor of streptococcus pneumoniae
- forms pores in phagocytes and ciliated epithelial cells of lung
- degrades hemoglobin (a-hemolysis)
- activates complement (alpha Inflammation)
pneumolysin is released and binds to cholesterol in host cell membranes to form large pores. These pores disrupt and damage the cell membrane allowing the contents of the cell to spill out, ultimately killing the host cell
what is IgA protease?
secreted virulence factor of streptococcus pneumoniae
cleaves airway IgA (in mucus) to promote adherence and colonization
how does the capsule of streptococcus pneumoniae act as a virulence factor?
it’s antiphagocytic and secretes soluble capsule fragments that bind antibody
capsule production varies during infection; highly expressed during blood and systemic infections but decreased capsule correlated with competence (DNA uptake)
what is the reason for the damage during streptococcus pneumoniae infections?
host response!!
not toxin-mediated
majority of damage is due to host response to the capsule and PG
how do you diagnose streptococcus pneumoniae?
- Microscopy: direct Gram stain of sputum sample will show neutrophils and diplococci
- culture: sputum inoculated onto blood agar plate to assess optichin sensitivity and a-hemolysis
- antigen detection: commercial immunoassay to detect capsule antigens in sputum, blood and urine
is there antibiotic resistance with streptococcus pneumoniae?
yes, antibiotic resistance in pneumococcus is increasing
how do you treat streptococcus pneumoniae?
- if previously healthy = mcrolide (erythromycin)
- predisposing factors = fluoroquinolone (levofloxacin) or high dose B-lactam plus macrolide
treat until patient able to mount antibody response
also drain the infections of closed spaces (empyema)
is there a vaccine for streptococcus pneumoniae?
- conjugated vaccine
2. polysaccharide vaccine
what is the conjugated streptococcus pneumoniae vaccine?
conjugate vaccine for <2 yrs old (infants); given at 2, 4, 6, and 12-15 months
it’s made of capsular polysaccharides from 13 (13-valent) most common strains conjugated to protein antigen. Prevnar 13 or PCV13
polysaccharides are not processed by APC but, instead, directly stimulate B cells (T-independent).
however, infant B cells aren’t very developed so conjugating a protein to the polysaccharide stimulates the T cells
what is the polysaccharide vaccien for streptococcus pneumoniae?
typically for adults >65 or those with pre-existing conditions (e.g. smokers, HIV+)
uses 23 most common capsular polysaccharides
which bacteria are enterococcus?
group D streptococci
- E. faecalis
- E. faecium
what is the microbiology of enterococcus?
gram (+) diplococci in short chains
alpha-hemolytic or non-hemolytic on BAP
where are enterococcus found?
commensal found in GI tract, urinary tract, and also vagina
grow in harsh conditions = bile acids and salts; BEA agar in lab
**bile resistant in clinical labs
which streptococci is bile resistant?
enterococcus
which diseases does enterococcus cause?
- UTI
- periotonitis
- endocarditis
is there antibiotic resistance associated with enterococcus?
yeah….
there’s a significant reservoir for antibiotic resistance in humans
VRE: Vancomycin-resistant Enterococcus
leads to treatment issues
how do you treat enterococcus infections?
combination of B-lactam (bacteriostatic) and aminoglycoside = antibiotic syngery
ex. Dalfopristin-Quinupristin
which bacteria are viridans streptococcus?
s. mutans
s. sanguis
s. milleri
what is the microbiology of viridans streptococcus?
gram (+) cocci in chains
alpha-hemolytic on BAP
indistinguishable from S. pyogenes in Gram smear
what is viridans streptococcus resistant to?
optochin resistant
no zone of inhibition
where is viridans streptococcus found?
oral cavity
what disease is associated with viridans streptococcus?
native valve subacute bacterial endocarditis
it’s when bacteria entersbloodstream following dental procedures (e.g., tooth extraction or vigorous brushing)
preexisting valve abnormality; fibrin and platelets allow for bacterial adhesion
treat with IV penicillin
FLASHCARD: microbioloty, pathology, epidemiology, clinical, diagnosis, treatment, and immunity of streptococcus pyogenes
MICROBIOLOGY: Gram + cocci; chains; β-hemolytic; catalase negative; bacitracin sensitive; carbohydrate capsule used to group
PATHOLOGY: M protein binds fibronectin, blocks class. comp., binds factor H to block altern path; Spe A,B,C, exotoxins; Spe A,C superAg; Hyaluronidase (tissue spread);
EPIDEMIOLOGY: 20% of school-age kids carry; person-to-person
CLINICAL: Rapid onset sore throat, fever, enlarged tonsils –> scarlet fever (sandpaper rash, Pastia’s lines, strawberry tongue) –> ARF; honey-crusted impetigo; erysipelas (advancing margins); cellulitis; necrotizing fasciitis; toxic shock
Diagnosis: Fever, no cough, swollen lymph nodes, tonsils, <15 yrs, culture, rapid strep test
Treatment: Penicillin V or cephalosporins/macrolides; prevents ARF
Immunity: Ab to M protein protect against same serotype
FLASHCARD: microbioloty, pathology, epidemiology, clinical, diagnosis, treatment, and immunity of streptococcus agalactiae
MICRIOBIOLOGY: Gram + cocci; chains; β-hemolytic; catalase negative; bacitracin resistant; carbohydrate capsule used to group
PATHOLOGY: Capsule blocks phagocytosis by blocking complement; Sialic acid capsule mimics host; CylE pore forming toxin kills nΦ
EPIDEMIOLOGY: 25% of pregnant women have GBS in vagina or rectum
CLINICAL: Neonatal sepsis (early onset) and meningitis (late onset)
DIAGNOSIS: Culture pregnant women wk 35-37; CAMP test
TREATMENT: Pen/Amp pre-delivery or during delivery
FLASHCARD: microbioloty, pathology, epidemiology, clinical, diagnosis, treatment, and immunity of streptococcus pneumoniae
MICROBIOLOGY: Gram +, lancet-shaped diplococci; α-hemolytic; catalase negative; optochin sensitive; 90 serotypes
PATHOLOGY: Capsule (shed; block comp) and peptidoglycan (inflamm); pneumolysin, IgA protease, neuraminidase, hyaluronidase
EPIDEMIOLOGY: 40-60% children (otitis media) vs. 10-30% adults (bacteremia or pneumonia); airborne droplets
CLINICAL: Rapid onset, shaking chills, fever, cough with blood-tinged sputum, chest pain, lower lobe
DIAGNOSIS: sputum Gram stain; culture; Ag detection kit
TREATMENT: Pen but check sensitivity (also erythromycin or levofloxacin)
VACCINE: 13-valent conjugate infants; 23-valent polysaccharide adults
FLASHCARD: micro, clinical, diagnosis, treatment of enterococcus
MICROBIOLOGY Gram +, diplococci, short chain; α or γ-hemolytic
CLINICAL: UTI, wound infections, endocarditis, bacteremia
DIAGNOSIS: Culture on bile acid media
TREATMENT: May be vancomycin resistant; b-lactam+aminoglycoside
FLASHCARD; micro, clinilca, diagnosis, treatment viridans streptococcus
MICROBIOLOGY: Gram +, cocci in chains; α-hemolytic; optochin resistant
CLINICAL: Bacteremia following dental procedures; pre-existing valve defect
DIAGNOSIS: Culture
TREATMENT: i.v. penicillin G
