Module 11 Flashcards
(40 cards)
Clinically relevant members of the Streptococcaceae family
Streptococcus, Enterococcus, Aerococcus
Aerococcus viridans
Opportunistic organism from the environment that rarely causes infections in humans
Relatively uncommon isolate
Beta hemolytic Streptococci groups
Group A (S. pyogenes) Group B (S. agalactiae) Group C (S. equisimilis) Group F and G (rarely of clinical significance in humans)
Non-hemolytic Streptococci group
Group D Enterococcus (Enterococcus faecalis, Enterococcus faecium, Enterococcus durans)
Group D Non-enterococcus (Streptococcus equinus, Streptococcus bovis)
Alpha hemolytic Streptococci
S. pneumoniae, S. viridans
Not identified by group antigens
Streptococcus anginosus-milleri
Small colonies, require increased CO2 for growth, may be alpha, beta, or gamma hemolytic and may or may not have a group antigen
May have a butterscotch smell
Erysipelas
Streptococcal cutaneous infection affects the underlying dermis
Skin shows reddish patches that enlarge, thicken and swell at the margins
Streptococcal cutaneous infection affects the underlying dermis
Erysipelas
Strep throat
Caused by S. pyogenes
Characterized by sudden onset of a sore throat, swollen lymph glands, fever and headache
Complications include ear and sinus infections, meningitis
Scarlet fever
Caused by a pyrogenic exotoxin from S. pyogenes
Pharyngitis accompanied by a rash starting on the upper chest and spreading to other parts of the body
“Strawberry tongue”
Symptoms of invasive infections caused by S. pyogenes (Invasive Group A Streptococcal disease)
Cellulitis with pain Fever Septic shock with decreased blood pressure Respiratory distress Necrotizing fasciitis Renal and liver dysfunction
Antibiotic given for invasive Group A Streptococcal disease
Penicillin G and inclusion of erythromycin
Two post-Streptococcal diseases
Rheumatic fever and acute glomerulonephritis
Rheumatic fever
May follow Streptococcal pharyngitis by 1-5 weeks
Streptococcal antibodies attach to heart muscle causing an inflammatory reaction and the scarring of heart valves
Acute glomerulonephritis
May follow Streptococcal pharyngitis or cutaneous infection
Antigen-antibody complexes are deposited on the glomerular membranes of the kidney. This activates complement resulting in damage to the membrane, allowing blood and protein to pass into the urine
Most serious infection of Streptococcus agalactiae
Neonatal sepsis
Rapid onset neonatal sepsis
Neonate is infected in utero or during birth from Streptococcus agalactiae colonizing the mother’s vagina
Neonate is critically ill at birth with respiratory distress along with septicemia and meningitis
Mortality rate is high
Late onset neonatal sepsis
Streptococcus agalactiae infection seen after the first week; mean age of onset is 4 weeks
Meningitis is the usual manifestation seen
Mortality rate is lower
The most common cause of sepsis and death in the neonate
Streptococcus agalactiae (GBS) infection (neonatal sepsis)
When are mothers-to-be screened for GBS?
34-36 weeks gestation
Treatment for GBS
Penicillin and ampicillin
Streptococcus pyogenes antimicrobial susceptibility
Universally susceptible to Penicillin
Erythromycin and tetracycline can also be used
When is antimicrobial susceptibility testing for S pyogenes required?
When indicated by treatment failure
Streptolysin S
Oxygen stable, acid labile
When a blood agar base with fermentable carbohydrates is used, acid produced from fermentation can kill Streptolysin S and interfere with hemolysis
