BACTERIAL CAUSES OF SORE THROAT I: Streptococcus
characteristics of Streptococcus agalactiae (GBS)
G+ chain cocci, Catalase -, beta-hemolytic bacitracin resistant positive CAMP test (amplified hemolytic activity with S. aureus)
characteristics of Streptococcus pyogenes (GAS)
G+ chain cocci, Catalase -, beta-hemolytic bacitracin sensitive negative CAMP test
characteristics of Enterococcus
G+ cocci in pairs and chains facultative anaerobe previously group D catalase neg or weak pos a,b, or non hemolytic not very virulent but multiantibiotic resistant HAI (nosocomial) (E. faecalis or faecium)
characteristics of Streptococcus
G+ cocci, pairs or chains, facultative anaerobe, catalase negative
differentiating Viridan Streptococci
S. pneumoniae are optichin-sensitive and lysed by bile S. mitis are optichin-resistant and not lysed by bile
Strep throat
caused by S. pyogenes 2-4 d incubation, sore throat/fever/headache erythematous (red) pharynx with an exudate and cervical lymphadenopathy
pathogenesis and virulence factors of S. pyogenes
cell wall Ag -A is carb Ag -M is protein Ag (type I or II), strain-specific has an anti-phagocytic hyaluronic acid capsule that mimics the host (HA in connective tissue) adhesin: (fibronectin-binding), lipoteichoic acid, M and F proteins spreading factors: hyaluronidase, streptokinase, DNase
Scarlet fever
complication of strep throat occurs 1-2 d after sore throat chest --> neck/trunk/arms/legs strawberry tongue disappears in a week phage integrate into bacteria and produce a toxin
diagnostic testing of S. pyogenes
direct/rapid tests for A Ag (throat swab, must confirm negative results by culture), culture for biochem properties and A Ag, ASO test, anti-DNase B test
epidemiology of S. pneumoniae
endogenous spread from NP or OP to distal site common in kids and in cold months clinical significance in fetus, can get into blood or CNS and cause bacteremia or meningitis, pneumonia in URT
catalase test
enzyme catalase catalyzes degradation of H2O2 into water and oxygen, produces bubbles
S. agalactiae epidemiology
express antiphagocytic sialic acid capsule asymptomatic colonization of upper resp./GI/UG tracts normal flora on many people can have vertical transmission bad if in blood immunocompromised (diabetes mellitus, cancer, alcoholism) are at increased risk for disease
characteristics of S. pneumoniae
fastidious facultative anaerobe diplococci or chains catalase-negative alpha-hemolytic virulent are often capsulated many serotypes
Viridans Streptococci
green, collection of alpha and gamma hemolytic streptococci colonize OP, GI, UG S. mitis has penicillin-resistance - S. pneumoniae is most virulent (endocarditis, sepsis, pneumonia, meningitis) S. mutans involved in cavities and bacteremia
clinical significance of S. agalactiae
leading cause of neonatal meningitis, pneumonia, sepsis UTI/endometritis/wound infections in pregnant women
viral vs. bacterial causes of pharyngitis
major causes are viral but strep pyogenes (GAS) is most common bacterial and most likely to have complications
pathogenesis of S. pneumoniae
manifestations caused by host response teichoic acid, peptido, pneumolysin activate inflammatory response and classic complement IgA protease (mucosal) and pneumolysin capsule
epidemiological significance of Enterococcus
normal flora of GI, skin, OP can grow at high [NaCl] and bile salt survive in env for a long time
clinical significance of S. pyogenes
suppurative (pharyngitis) and non-suppurative (acute rheumatic fever, glomerulonephritis) sequelae can elicit autoimmune response
S. pyogenes exotoxins
Streptolysin S and O: form pores, anti-O titer to check recent infection in diagnosing rheumatic fever Exotoxin B: flesh-eating protease