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