Gram-positive cocci:
Staphylococcus
Streptococcus
Prof. Beata Sobieszczańska
University of Medicine
Dept. Of Microbiology
Staphylococcus
Virulence factors:
Coagulase (CF)
Glycocalix
A protein
Enzymes: hyaluronidase
Cytolytic exotoxins
=hemolysins
Leukocidin Panton-
Valentine
Superantigens (SAgs):
exfoliatins
enterotoxins
toxic shock toxin
(TSST-1)
Staphylococcus
Source of infection (the origin from which a
host acquires the infection):
Human carriers
Transmission:
directly (contact with carriers or infected
individual)
indirectly (contaminated surfaces or medical
equipment)
Staphylococci – resistant to drying (prolonged
survival), disinfectants, antimicrobials
Staphylococcus aureus
Skin infections: localized: superficial or
subcutaneous abscesses (furuncles, boils),
larger, deeper infections (carbuncles) – can lead
to bacteremia
Diffuse skin infection – impetigo (pyoderma)
Deep localized infections: osteomyelitis, arthritis
Other infections: acute endocarditis, septicemia,
severe necrotizing pneumonia
Toxicoses: shock syndrome, gastroenteritis,
intoxication staphylococcal scaled skin
syndrome (marked epithelial desquamation)
SSSS
Staphylococcus – types of
infections
INFECTION
INVASIVE TOXICOSES MIXED
Staphylococcal
Furuncles
scaled skin
Carbuncles
syndrome
Wound infections
Food poisoning (SSSS)
Postoperative
TSST-1 shock
Postatraumatic
syndrome
Endocarditis
Bacteremia
(heart surgery)
sepsis
INVASIVE INFECTONS
pathogen in situ =
local infections:
furuncles
carbuncles
wound infections
postoperative or
posttraumatic
ostitis/osteomyelitis
What virulence factors
are important?
The effects of peptidoglycan fragments and
teichoic acids released during GP infections
The effects of peptidoglycan fragments and
teichoic acids relerased during GP infections
diapedesis
vasodilation
capillary damage during SIRS
SIRS
Systemic inflammatory response
syndrome:
hypotension + hypovolemia + DIC (diffuse
intravascular coagulation) + loss of
perfusion + ARDS (acute respiratory
distress syndrome) = acidosis &
decreased cardiac output =
irreversible septic shock and MOSF
(multiple organ system failure) & death
Superantigens (Type I toxins)
Unusual bacterial toxins that
interact with exceedingly large
numbers of T4 lymphocytes
This results in the secretion of
excessive amounts of cytokine IL-2
and the activation of self-reactive
T-lymphocytes
Superantigen
superantigen activation T-lymphocytes
circulation IL-2 self-reactive
• fever T-lymphocytes
• nausea TNFα, IL-1
• vomiting IL-8, PAF autoimmune attack
• diarrhea endothelial neutrophils
• malaise damage
ARDS
DIC proteases
MOSF toxic oxygen
shock radicals
excessive inflammatory response
damage to capillary walls
adherence of IL-8
neutrophils
capillary permeability
blood and plasma
leave bloodstream prolonged vasodilation
vascular resistance
hypovolemia
coagulation pathway hypotension
DIC
reduced
Shock
perfusion
and death
of blood
Superantigens (Type I toxins) - examples
• Toxic shock syndrome toxin-1
(TSST-1) some strains of Staphylococcus
• Staphylococcal enterotoxins (SE)
• Staphylococcal exfoliative toxin
• Pyrogenic exotoxin (Spe) – toxic shock-like
syndrome (TSLS) – rare invasive strains and
scarlet fever strains of Streptococcus pyogenes
(group A)
Other staphylococci
Staphylococcus epidermidis
Part of normal flora of the skin and anterior
nares
Important cause of infections from prosthetic
implants (catheters, heart valves)
Virulence factors: glycocalyx – biofilm
Staphylococcus saprophyticus
Part of the normal vaginal flora
A frequent cause of cystitis in women
Virulence factors: urease, glycocalyx, lipase
Streptococcus
Virulence factors:
Hyaluronic acid
capsule
M protein
Streptolysin O
Pyrogenic
streptococcal
exotoxins (PSE):
A, B, C
Streptokinase
Hyaluronidase
Streptococcus
Source of infection:
Carriers, infected indyviduals – direct/close
contact
Streptococci are very susceptible to drying
and antimicrobial agents
Streptococcus – types of
infections
INFECTION
INVASIVE SEQUELAE
acute
Skin and mucous
membranes Glomerulonephritis
infections Acute rheumatic
Scarlet fever fever
Necrotizing fasciitis
Septic infections
Erysipelas
Streptococcus pyogenes
The most common cause of bacterial
pharyngitis or pharyngotonsilitis
Scarlet fever (pyrogenic exotoxin in non-immunized
individuals)
Acute rhumatic fever
Glomerulonephritis
Impetigo
Cellulitis (diffuse spreading inflammation)
Puerperal sepsis (disease of uterine endometrium)
Invasive infections: necrotizing fasciitis/myositis
Streptococcus pyogenes
• Erysipelas
• Streptococcal toxic shock syndrome (PSE)
• Bacteremia
• Pneumonia
Other streptococci
Streptococcus agalactiae
Meningitis and septicemia in neonates
Infections in adults: endometritis in postpartum
women, septicemia, pneumoniae in
immunosupressed individuals
Streptococcus pneumoniae –
Capsule – antiphagocytic (90 serotypes)
Hyaluronidase
IgA protease
STREPTOCOCCUS PNEUMONIAE
Infections
Serotypes:
2, 3, 5, 8, 14
INVASIVE:
Purulent:
meningitis
Otitis media
bakteremia, sepsis
sinusitis
endocarditis
pneumonia
peritonitis
Mortality:
15-25%
ENTEROCOCCI
► Enterococcus faecalis &
E. faecium cause >90% infections
in human
► normal intestinal flora of humans
and animals
► resistant to environmental
factors and many antimicrobial
agents
Source of infections: endogenous
Indirect: contaminated surfaces &
medical equipment
ENTEROCOCCI:
virulence factors
► proteins binding ECM = colonization
► lipoteichoic acid = fibronectin binding,
induction of cytokines
► hyaluronidase = invasion into tissue
Most common infections: UTI,
endocarditis, catheter-related infections
Other: intraabdominal and pelvic infections,
bacteremia, sepsis, postoperative wounds
infections, meningitis – uncommon
(neurosurgical procedures)
Streptococci in oral cavity
Streptococcus: mitis, mutans, salivarius,
sanguis, milleri
► normal flora: oral cavity, intestines, urethra
► endogenous infections: dental carries,
endocarditis, mixed infections within oral
cavity (e.g. abscesses)
