Strep Micro Lecture 2 Flashcards
The three strep that are most important human pathogens are:
Streptococcus pyogenes (group A strep)
S. agalactiae (group B strep)
S. pneumoniae
Strep grows in what conformation?
chains
if very short = diplococci
What types of strep are alpha hemolytic?
S. pneumococci
viridans strep such as S. mitis, S. mutans
What types of strep are beta hemolytic?
S. pyogenes
S. agalactiae
What types of strep are gamma hemolytic?
S. salivarius
What are the growth requirements for strep?
Facultative anerobes (can make ATP by aerobic respiration when oxygen is present, but can switch to fermentation if oxygen is not present)
Fastidious (need amino acids, vitamins, etc.)
S. pyogenes is group ____ strep and ____-hemolytic
A
beta
S. agalactiae is group ____ strep and ____-hemolytic
B
beta
What isn’t typable by the Lancefield system?
S. pneumoniae (pneumococcus)
viridans strep (S. mutans, S. sanguis, S. mitis, S. salivarius, etc.)
Strep are catalase (+/-) and oxidase (+/-)
What is the significance?
- and -
staph are catalase +
neisseria are oxidase +
Viridans and enterococci are ___-hemolytic
alpha
What are some pretty freaking serious Group A Streptococcal Diseases?
toxic shock
necrotizing fasciitis
What causes rheumatic heart disease?
pharyngitis from S. pyogenes
What causes acute glomerulonephritis?
S. pyogenes (often) following skin infection
What are SLO and SLS?
potent virulence factors
SLS is oxygen stable; responsible for hemolysis surrounding colonies on the surface of blood agar plate
SLO is oxygen sensitive; responsible for the clearings below the surface of the agar
What is hyaluronic acid capsule?
group A strep virulence factor which prevents phagocytosis
Structurally similar to human hyaluronic acid, thus there are no antibodies produced against it
What is M protein?
group A strep virulence factor which is:
- a major antiphagocytic factor in most strains; binds fibrinogen and other host proteins that mask the bacteria from the immune system
- an adhesin
What is lipoteichoic acid?
group A strep virulence factor which is thought to be an adhesin
aids in group A strep binding to mucosal surfaces in the host, but it is also a PAMP (activates innate immune system)
What is the difference between the N and C terminus in protein M?
C-terminal half is conserved
N-terminus varies under immune pressure, forms the basis for serotyping
What are the strep superantigens?
Streptococcal pyrogenic exotoxin A
Streptococcal pyrogenic exotoxin B
(there are others)
How does pharyngitis spread?
droplets, especially in a crowd (asymptomatic carriage rates are 15-30%)
Should you treat strep pharyngitis?
it’s self-limiting, but you should treat with penicillin to decrease the risk of developing ARF
Acute rheumatic fever follows:
strep pharyngeal infections, not skin infections
How does M protein relate to recurrence of strep pharyngitis?
When pharyngitis occurs again, it will be from a different M type strain of S. pyogenes
The patient has antibodes against the previous strand’s M (which bind to the amino terminus of the M protein)
Why is endometritis, or puerperal fever, uncommon now?
we wash our hands…
Who common becomes infected with group A strep impetigo?
kids, especially after insect bites (kids have strep on their fingers, then scratch the bites)
What is a pyoderma?
an infection of the skin that produces pus
How does group A strep impetigo present?
weeping vesicles with honey-colored crusts
What is ecthyma?
a form of impetigo that has invaded more deeply, forming round lesions with pus and ulceration in the center
What is erysipelas? What does it look like?
form of strep cellulitis that involved both the dermis and epidermis
“fiery red” erythema and edema with rapidly advancing, well-demarcated edges
What are the symptoms of erysipelas? (4)
rapid-onset of cheek redness
pain
fever
lymphadenopathy
Erysipelas normally affects:
kids and elderly
How are staph and strep cellulitis different?
staph: usually associated with localized infection (folliculitis, foreign body, etc)
strep: spreads more rapidly and usually has fever and lymphangitis
What are the symptoms of strep cellulitis?
localized pain
erythema
swelling
heat
Why would a strep cellulitis have a negative blood culture?
a small number of bacteria secreting toxins can cause this
What is necrotizing fasciitis? How serious is it?
deep tissue infection that spreads along the fascial planes
can be life threatening–40-70% mortality
What causes strep toxic shock and necrotizing fasciitis, and how does it progress from there?
innocuous infection (bruise, skin trauma) Necrosis then progresses quickly (~1 inch per hour)
What symptoms is very indicative of strep toxic shock and necrotizing fasciitis?
extreme pain out of proportion to the appearance of the lesion
(crescendo pain: rapid ramping up of the degree of pain)
What are the early and later signs of strep toxic shock and necrotizing fasciitis?
early:
flu-like symptoms
brawny edema
extreme pain out of proportion to lesion
later:
spreading erythema
eccymosis (hematoma) with vesicles enlarging to purple bullae
What is the proper treatment for strep toxic shock and necrotizing fasciitis?
Debridement
Aggressive use of broad spectrum abx immediately–penicillin and clindamycin if S. pyogenes is detected
Massive amounts of IV fluids may be needed
Monitor CO closely
What causes the shock related to strep TSS and necrotizing fasciitis?
- streptococcal pyrogenic exotoxins
2. peptidoglycan fragments, lipoteichoic acid, etc
Why is clinda very useful in strep TSS?
protein synthesis inhibitor – does not break down cell walls.
Therefore: less peptidoglycan, LTA and other cell wall substances released (innate immune system is not activated so broadly)
What is usually different about the appearance of strep TSS versus staph TSS?
Streptococcal toxic shock causes a widespread rash that blanches when pressure is applied
How do you confirm a diagnosis of strep TSS?
- Isolate GAS from a clinically significant specimen in a hypotensive pt (SBP <90)
- Two/more of the following:
- -renal impairment- -coagulopathy
- -liver dysfunction
- -acute respiratory distress syndrome
- -generalized eryth macular rash
- -soft-tissue necrosis (NF, myositis or gangrene)
What is a fulminant infection?
one occurring suddenly and quickly, and one that is intense and severe to the point of lethality
What are the non-suppurative sequelae of S. pyogenes?
ARF and AGN
Usually develops in young children after pharyngitis:
ARF
What are the major manifestations listed in the guidelines for diagnosis of ARF (Jones Criteria)?
*Carditis
*Polyarthritis
Chorea
Erythema marginatum
Subcutaneous nodules (uncommon)
What are the minor manifestations listed in the guidelines for diagnosis of ARF (Jones Criteria)?
Arthralgia Fever elevated ESR elevated CRP Prolonged PR interval
Non-suppurative sequelae of S. pyogenes are most frequent in:
children 5-15
Usually develops after throat or skin infection:
acute glomerulonephritis
What titer is high in non-suppurative sequelae of S. pyogenes?
anti-SLO
What are the major clinical findings listed in the guidelines for diagnosis of AGN?
Edema
Hypertension
Malaise, headache
Back pain
What are the major lab findings listed in the guidelines for diagnosis of AGN?
Ig complement C3 strep antigens Hematuria (rust-colored urine) Proteinuria
How are kidneys affected by AGN?
Increased glomerular intracapillary cellularity
Almost all glomeruli involved, some tubules
Treatment of AGN:
Benzathine penicillin (slow-release) **no treatment alters long-term prognosis, treat to manage acute kidney problems
Treatment of most S. pyogenes infections:
penicillin
For patients with allergies: clindamycin, azithromycin
Treatment of serious/invasive S. pyogenes infections:
Initiate broad spectrum abx if Group A strep is identified: high levels of penicillin and clindamycin (which is more effective in deep infections)
Surgical debridement required
IVIG (may protect against superantigens)
SUpportive therapy (fluids to treat hypotension, dialysis for renal failure, etc)
What does GBS cause (but this is declining)?
septicemia and meningitis in neonates and infants <3mo
pregnancy-related morbidity
GBS are resistant to:
Bacitracin
What is CAMP factor?
GBS factor which synergizes with S. aureus hemolysin to cause increased lysis of red cells
What substance is hydrolyzed by GBS (thus a useful test)?
Bile esculin
What is an example of a GBS?
S. agalactiae
5 VFs in GBS?
- Capsule (serves as an antiphagocytic factor and reduces adhesion); *major
- Adhesins:
a-protein
fibrinogen-binding proteins (FbsA, FbsB) - Surface beta-protein (binds factor H and downregulated complement deposition)
- beta-hemolysin (damage cells if bacteria evade phagocytosis)
- peptidoglycan and lipotechoic acid (stimulate cytokine secretion)
What does neonatal GBS cause? Who is infected?
Septicemia, respiratory distress, meningitis
7 days or younger (often pre-term) whose mothers had intraamniotic infection
What does early GBS cause? Who is infected?
Bacteremia
Meningitis
Permanent neurologic sequelae
2wks to 2mos, 50% pre-term
What has reduced incident of GBS in neonates and infants?
- Prenatal screening (35-37 weeks)
2. intrapartum IV penicillin to infected mothers and mothers with risk factors
Viridans Streptococci are ___-hemolytic and are commonly found in:
alpha
plaque biofilm on teeth (normal oral flora)
Viridans Streptococci are distinguished from enterococci by:
inability to grow in 6.5% NaCl
Viridans Streptococci are distinguished from pneumococci by:
resistance to optochin (ethylhydrocupreine)
Viridans Streptococci contribute to what conditions?
caries, periodontal disease and endocarditis (if you have damaged heart valves)
Why do patients with damaged heart valves require prophylactic antibiotics before dental procedures?
- Transient bacteremia occurs after dental procedures (S. sanguis and other viridans strep)
- Damage of heart valves leads to exposure of fibronectin and deposition of fibrin and platelets
- Viridans strep have adhesins for fibronectin, fibrin and other host proteins that accumulate on injured valves.
- Once they adhere, form biofilms (vegetations)
_____ shows reaction for Lancefield antigens, but _____ do not.
Enterococcus
Viridans
What do enterococcus cause?
nosocomial infections, many of which are vanc-resistant
Why are enterococcus infections problematic after a course of antibiotics?
killing competing organisms with antibiotics leads to overgrowth
Once they increase in number, they can gain access to lymphatics or blood
Why are enterococci a big problem, in terms of drug resistance?
extremely proficient at taking up DNA (plasmids, transposons) and passing it along to other species
When is intrapartum prophylactic penicillin not necessary?
planned c-section in absence of membrane rupture or negative GBS screen
When is intrapartum prophylactic penicillin necessary?
Unknown GBS with:
Intrapartum temp >100.4
Amniotic membrane rupture >18h
Delivery at <37 weeks
Previous infant with GBS
Current GBS bacteremia
