introduction Flashcards
clinical manifestation of pharyngitis
1) can be viral or bacterial or chemical
2) bacterial
- group a streptococci
pneumonia
1) m. pneumonia
2) s. pneumonia
3) influenza
streptococci
1) A heterogeneous group of bacteria, Gram (+), facultative
anaerobes
2) Cocci arranged in pairs or chains
3) Catalase-negative (unlike Staphylococcus spp.)
4) Bacteria colonize and infect humans
5) Example of diseases caused by Streptocci:
Streptococcal pharyngitis (“strep throat”), pneumonia, cellulitis,
neonatal meningitis, brain abscess, endocarditis, toxic shock
syndrome and necrotizing fasciitis (flesh-eating disease)
classification of streptococci and enterococci
Hemolytic pattern: When streptococci (and enterococci) are
grown on blood agar media in the clinical laboratory, the
colonies may be surrounded by an area of:
1) partial hemolysis that appears greenish (α-hemolysis),
2) a clear zone of complete hemolysis (β-hemolysis), or
3) the absence of a zone (γ-hemolysis or nonhemolysis).
Streptococci & Enterococci
Lancefield classification
serological reactivity to extract cell wall antigens
from various streptococci/enterococci to divide them into groups
lettered A through V.
Note:
Many streptococcal species cannot be assigned to any group
because there are no antisera that react to their cell wall antigens.
group A streptococcus: s. pyogenes clinical manifestation
1) strepthroat and scarlet fever
- Both conditions are self-limited diseases.
However, physicians always treat these conditions pharmacologically
- has to be treated with antibiotics
s. pyogenes characteristics
β-hemolytic
1) Transient colonization in upper respiratory tract and
skin
2) Person-to-person spread by respiratory droplets
(pharyngitis) or through breaks in skin after direct contact
with infected person, or fomite.
3) Most common cause of bacterial pharyngitis
- Children from 5 to 15 years old: high risk group
- Most common in the cold months; no seasonal
incidence for soft-tissue infections
Group A Streptococcus: S. pyogenes
GAS virulence factors
Just remember (from this slide) that:
-Many virulence factors
-Playing a role in establishing infection
- modify host cell and immune resistance for example
anti-phagocytosis
1) M protein
2) Hyaluronic acid capsule hides bacteria from leukocytes
3) Streptolysins (SLO & SLS) lyse phagocytic cells
4) Streptococcal pyrogenic exotoxins B (SpeB) cleaves
IgG bound to GAS (no opsonization)
5) Interfering with ingestion and killing by phagocytes
Group A Streptococcus: S. pyogenes
M protein
1) Anti-phagocytic
- Inhibition of alternative pathway activation by:
- Binding to complement control proteins
- can’t access important bacterial structure
2) Adherence to the surface of human epithelial cells
3) molecular mimicry
- >200 serotypes
- M3 and M18 similar to myosin, keratin, laminin
why must s. pyogenes be limited pharmocologically?
1) prevent more serious infection
facilitating GAS spreading
1) Deoxyribonucleases (DNases)
- Degrade NETs (5/17/24, slide #s41 & 42)
2) C5a peptidase
- Breaks down complement protein C5a (chemokine)
- Decreases movement of white blood cells to the infection
site (**C5a functions as chemotaxis)
3) Hyaluronidase
- Degrade hyaluronic acid in ECM
4) streptokinase
- break down blood clots (fibrin)
streptokinase
1) lyse fibrin clots and restore blood flow
2) for MI
streptolysins
1) Two distinct hemolysin
- Streptolysin O (SLO): immunogenic, oxygen labile.
- reversibly inhibited by oxygen.
- SLO exerts its hemolytic effect in anaerobic cultures.
- SLS: non-immunogenic, oxygen stable
2) Functions:
- Lyse red blood cells (β-hemolysis by SLS), white blood cells
(anti-phagocytic, slide# 17) , and platelets (SLO & SLS)
- Promote apoptosis in keratinocytes (SLS)
streptococcal pyrogenic exotoxin
1) damaging the
plasma membrane of blood capillaries in scarlet fever.
- Superantigens
- They also appear to be involved in the pathogenesis of severe
infection.
2) Streptococcal toxic shock syndrome
GAS diseases
1) pharyngitis
2) scarlet fever which can lead to
- acute rheumatic fever
- post streptococcal glomerulonephritis
3) strep throat
Post streptococcal glomerulonephritis (PSGN): Type III
hypersensitivity
1) glomerular deposition of immune complexes triggered by
nephritogenic strains of GAS (such as M-49) causes PSGN.
- 1-3 weeks after a
streptococcal throat infection
- or 3-6 weeks in cases of skin infection.
2) Clinical manifestations:
- hematuria, proteinuria, hypertension, edema, and elevation in
serum creatinine.
- Adults may suffer irreversible kidney damage
Group A Streptococcus: S. pyogenes
invasive GAS
1) necrotizing fasciitis flesh eating disease
diagnosis
1)Skin infections diagnosed by the presence of Gram-positive bacteria
in short chains or pairs
- Rapid strep test used to diagnose respiratory infections
2) Treatment
- Penicillin is effective (for non-invasive lesions)
- Surgical debridement plus penicillin and clindamycin (for invasive
lesions: necrotizing fasciitis and STSS)
GBS (s. agalactiae)
1) Pathogenicity
- Often infects newborns (often inoculated at birth) without specific antibodies
- Neonatal bacteremia, meningitis, and pneumonia
- Older immunocompromised patients are also at risk
- Produces enzymes whose roles are not yet understood
2) normally doesn’t affect healthy people
CAMP test
1) CAMP factor enhances hemolysis of staphlococcus aureus
viridans streptococci
1) lack group-specific carbohydrates
- Cannot be grouped by Lancefield system
- Inhabit mouth, pharynx, GI tract, genital tract, and urinary tract
2) Opportunistic pathogens
3) Can cause meningitis (rare) and endocarditis if it enters the blood
4) Cariogenic bacteria
- lactic acid
s. penumoniae (pneummococcus)
1) ⍺-hemolytic cocci that most commonly form pairs (diplococcus)
- Lacks Lancefield antigens
2) Closely related to mitis group of Viridans Streptococci
3) Part of the normal bacterial flora of upper respiratory system
polysaccharide capsule
1) playing a critical role in anti-phagocytosis
- Serotype-determining antigen on the organism.
- The basis for antigenic differences among serotypes lies in
the chemical structure of the capsular polysaccharide
2) Target of pneumococcal vaccine
- PPSV23
- PCV (mixing plus conjugating)
quellung test
1) identify serotype of polysaccharide capsule
2) Ab is added and reacts with capsular Ag
- flow of medium changes
- swelling of capsule
s. pneumoniae surface proteins
1) Psp (Pneumococcal surface protein)
- PspA: antiphagocytic (by inhibiting activation of C3 convertases in
classical and alternative complement pathways)
- PspC: antiphagocytic (by inhibiting C3 convertase formation)
2) PsaA (Pneumococcal surface antigen A)
- Mediates binding of cells to epithelial cells of pharynx
3) Secretory IgA protease
- Destroys IgA
pneumolysin
1) A cholesterol-dependent, pore-forming toxin
- Pulmonary, nasal, and tracheobronchial epithelial cells are
damaged as a result of pore-forming activity.
- Breaks down hemoglobin into a green pigment
s .pneumoniae disease
Pneumococcal Diseases
* Pneumococcal pneumonia
* Most common disease caused by S. pneumoniae
* Sinusitis and otitis media
* Sometimes occur following viral infections
* Bacteremia and endocarditis
* S. pneumoniae can enter the blood through lacerations or tissue
damage
* Pneumococcal meningitis
* Mortality rate higher than other causes of meningitis
s. pneumoniae diagnosis
Diagnosis
* Gram stain of sputum smears
* Differentiation methods of S. pneumoniae from
other viridans streptococci
- Susceptibility to optochin
- An optochin (ethylhydrocupreine hydrochloride) disc
is placed on S. pneumoniae culturing agar plate.
There is the zone of inhibition around the disk 24 hours
after incubation at 37°C.
Ø Solubility in bile salts
o S. pneumoniae: bile soluble
s. pneumoniae treatment
1) penicillin
-resistant strains have emerged
2) prevention
- vaccine
staphylococci characteristic
Structure and Physiology
* G(+), catalase positive facultative anaerobes
* Cells occur in grapelike clusters
* Non-motile
* Extraordinary capacity to adapt and survive in a great variety of
environments.
* Tolerant of desiccation/heat
* Salt-tolerant
* Tolerate salt deposited on human skin by sweat gland
Staphylococcus: Characteristic
staph aureus
primarily found only in moist skin folds
* More virulent strain, most often spread to others by direct contact
* Variety of conditions depending on site of infection
staph epidermidis
Normal microbiota of human skin
* Device-related infections, Urinary tract infection (UTI)
staph aureus
Producing toxins-mediated diseases
* Exfoliative toxin: Staphylococcal scalded skin syndrome (SSSS)
* Toxic shock syndrome toxin: Staphylococcal toxic shock syndrome
* Enterotoxins produced by the bacteria that colonize food/beverage: Food
intoxication
staph aureus structural defenses
1) protein A
- binds IgG
- inhibit opsonin
2) bound coagulase (clumping factor)
-Converts fibrinogen into fibrin molecules
-Fibrin clots hide the bacteria from phagocytic cells
- Synthesize polysaccharide slime layers (capsules)
- Inhibit phagocytosis
enzymes staph aureus
1) free coagulase
2) hyaluronidase
3) staphylokinase
4) lipases
5) beta-lactamase
staph aureus toxins
1) cytolytic toxins
2) exfoliative toxins
3) TSS
4) enterotoxins
staph aureus diseases
1) Noninvasive Disease
* Food poisoning
* Due to ingestion of enterotoxin-contaminated food
2) Cutaneous Diseases
* Various skin conditions
* Staphylococcus scalded skin syndrome (SSSS), impetigo, folliculitis
3) TSS
4) meningitis
staph aureus diagnosis
Diagnosis
* Detect Gram-positive bacteria in grapelike arrangements
* Coagulase test
staph aureus treatment
Anti-staphylococcal penicillins (nafcillin, oxacillin, and dicloxacillin)
* They were so designated since their R side chains have bulky residues
that prevent binding by the staphylococcal β-lactamases.
* Vancomycin used to treat methicillin-resistant S. aureus (MRSA)
infections
