Mhr Topic 14: Gram (+) Cocci; Staph And Strep

Front 1

S. aureus lab tests

Back 1

1) Produces yellow-gold pigment and is hemolytic on a blood agar plate.
2) Coagulase positive
3) Catalase +

Front 2

S. aureus location

Back 2

Normal flora of:
1) Anterior nares
2) Mucus membrane
3) Skin
4) GI Tract
5) Vagina

Front 3

S. aureus virulence (not counting enzymes or superantigens)

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1) Protein A - Cell wall protein which prevents IgG from activating compliment reducing opsonization.
2) Fibronectin binding protein - Promotes binding to collagen, fibronectin, lactoferrin, and mucosal cells.
3) Hemolysins - lyses erythrocytes and other eukaryotic cells.
4) PVL - Lyses WBCs; important for community acquired MRSA. Causes skin infections, hemohragic pneumonia, and fununculosis.

Front 4

S. aureus secreted enzymes

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1) Lipases
2) Proteases
3) DNAases
4) Hyaluronidases - hydrolizes connective tissue matrix
5) Catalase - converts hydrogen peroxide to water, counteracting neutriphils.
6) Coagulase - Converts fibrinogen to fibrin. Prevents phagocytosis.

Front 5

S. aureus superantigens

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1) SSSS - Causes two exfoliative toxins, ETA and ETB
2) TSST-1 - causes toxin shock syndrome toxin
3) Enterotoxins A-G - Cause food poisoning, can also act as superantigens.

Front 6

S. aureus Diseases

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1) Abscesses anywhere on body
2) Skin/Soft tissue infections
3) Bacteremia
4) Endocarditis
5) Pneumonia
6) Osteomyelitis
7) Septic Arthritis
8) Toxic shock syndrome
9) Gastroenteritis/food poisoning
10) Nosocomial infections

Front 7

3 skin/soft tissue infections which can come from S. aureus and their characteristics

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1) Cellulitis - Spreading infection of skin that involves sub Q tissue. Propensity to spread via lymphatics and blood stream
2) Impetigo - Initially a vesicular, later crusted, superficial infection of the skin. Thick, golden yellow, stuck on crust
3) Erysipelas - Superficial cellulitis of skin with prominent lymphatic involvement. Painful lessions with bright red edematous appearance. Has advancing raised border that is sharply demarcated from adjacent normal tissue.

Front 8

Staph scalded skin syndrome

Back 8

SSSS is a S. aureus toxin mediated disease. Is a superficial skin disorder causing local blistering and scalding.
Caused by 2 exfoliative toxins; ETA and ETB. Act on the strata granulosom of the keratinized epidermis.
Occurs almost exclusively in newborns and infants <1.

Front 9

Toxic Shock Syndrome

Back 9

Caused by TSST-1, a superantigen, and by enterotoxins, both via S. aureus.
Get high fever, sunburn-like rash, desquamation, vommiting, diahhrea, hypotension, and multiple organ involvement. 2 types:
Menstral - associated with use of high absorbancy tampons
Nonmenstral - responsible organisms can colonize any part of body.

Front 10

Gastroenteritis/Food poisoning caused by S. aureus

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Toxin mediated S. aureus disease. Caused by ingestion of food contaminated by preformed toxin produced by S. aureus. Caused by enterotoxins A-G (which are all superantigens?)
Disease starts 2-6 hours post ingestion. Get nausea, vomiting, diarrhea.

Front 11

Lab ID of S. aureus

Back 11

Gram stain: (+) clustered cocci
Colony Characteristics: Hemolytic, yellow
Catalase: +
Coagulase: +
Mannitol: Ferments

Front 12

Antibiotic resistance of S. aureus

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1) Most S. aureus strains are penicillin resistant due to production of beta-lactamase. Therefore methicillin is resistant to beta lactamase and is drug of choice
2) Methicillin resistant S. aureus (MRSA) also exists, can be hospital or community acquired. Treat with vancomycin
3) Rare strains of vancomycin resistant S. aureus have also been I.D.d (VRSA)

Front 13

Coagulase (-) staphylocicci

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Common inhabitatns of the skin. Cause infections in patients with implanted artificial devices like joints, heart valves and catheters.
S. epidermidis produces slime layer that facilitates adherence to devices and acts as a barrier to antibiotics.
S. saprophyticus associated with UTI, particularly in young women with cystitis.

Front 14

Serological grouping of beta-hemolytic streptocicci

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Based on their C-carbohydrate (A through U) A and B are most clinically significant.

Front 15

Streptococcus pyogenes Labs

Back 15

Beta-hemolytic on blood agar
Group A carb antigen
Bacitracin suseptible

Front 16

Streptococcus pyogenes natural location

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Skin and mucous membranes

Front 17

S. pyogenes virulence factors

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1) Major: Fimbriae with M protein. Over 80 antigenic types
2) Capsule - antiphagocytic and non-immunogenic
3) Protein F - Mediates attachment to firbronectin in pharyngeal epithelium
4) Strep pyrogenic exotoxins (Spe)
5) C5a peptidase - prevents attraction of phagocytes to infection site
6) Streptolysin O and S - cytolysins?
7) Hyaluronidase - promotes spread of infection
8) Streptokinase - dissolves clots
9) DNases A-D - stop streptodornases

Front 18

3 types of S. pyogenes Infections

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1) Suppurative - Infections die to direct damage by organism and its secreted enzymes
2) Post-Infections - Late manifestations due to an autoimmune response.
3) Toxin mediated - Disease caused by streptococcal exotoxins secreted into blood stream.

Front 19

Pharyngitis

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A suppurative strep infection. Caused by all group A strep. Very common. Red throat, greyish white tonsillar exudates, enlarged cervical lymph nodes. Treated with antibiotics to prevent acute rheumatic fever.

Front 20

Acute rheumatic fever (ARF)

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Post-Infectious S. pyogenes infection. Autoimmune, occurring 1-4 weeks post pharyngitis. Caused by cross Rx of strep antigens (especially M protein) and heart and joints.
Leads to carditis polyarthritis, spasms, sub Q nodules, rash, eventually cardiac failure (therefore pharyngitis treated with antibiotics).

Front 21

Acute Glomerulonephritis

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Post-Infectious S. pyogenes infection. Autoimmune, occurs 1 week post impetigo or pharyngitis caused by nephritogenic group A strep. Caused by antigen-antibody complexes depositing in golmerular basement leading to compliment and renal injury. Antibiotic therapy does not treat.

Front 22

Scarlet Fever

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Toxin mediated S. pyogenes disease, mediated by delayed type hypersensitivity to the erythrogenic toxins.
Rash appears on second day of pharyngitis beginning on trunk and spreading outward except palms. Pale around the mouth. Tongue goes from white strawberry to red strawberry appearance.

Front 23

Streptococcal toxic shock syndrome

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S. pyogenes toxin mediated disease. Similar clinical presentation as staph TSS. Caused by pyrogenic toxins Spe A and C which act as superantigens.

Front 24

Streptococcus agalactiae (tests, where, virulence factors, disease).

Back 24

Group B beta hemolytic strep. Found in the GI and female genital tracts. Polysaccharide capsule is antiphagocytic. Causes sepsis, meningitis, and pheumonia in newborns, elderly, and immunocompromised. Women screened for group B strep before pregnancy and given antibiotics if +.

Front 25

Streptococcus pneumoniae (where and labs)

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Found in the nasopharynx.
Is gram positive diplocicci.
Is alpha hemolytic, optochin sensitive, and bile sensitive.

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Streptococcus pneumoniae infections and people at risk

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1) Most common cause of bacterial pneumonia which can lead to empyema (abscesses in pleural space).
2) Otitis media
3) Bacteremia
4) Meningitis
At risk people: sickle cell, alcoholism, Hodgkin disease, multiple myeloma, HIV, splenectomized people.

Front 27

S. pneumoiae virulence factors

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1) Polysach. capsule - Antiphagocytic, 84 serotypes. Antibodies against capsule are protective. Vaccine given to children >5.
2) Pneumolysins - Released via autolysins, attack mammalian cell membranes.

Front 28

Viridans streptococci (where, labs, diseases)

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Found in mouth and oropharynx.
Alpha hemolytic strep.
Can cause endocarditis because of bleeding mouth from brushing or bad hygiene. Can cause brain, liver and abdominal abscesses.

Front 29

Enterococci (where, labs, types, diseases)

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Found in GI tract.
Gram + cocci in pairs and short chains. Contain group D antigen. Can be alpha, beta, or non hemolyic. Grow in 6.5% salt. Hydrolyze esculin. Bile salt tolerant.
2 types: E. faecalis and E. faecium.
Cause UTIs endocarditis, intra-abdominal infections, bacteremia. Vancomycin resistant enterococci (E. faecium) are major cause of hospital acquired infection.

Front 30

Antibiotic resistance of strep and enterococci

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1) Groups A-C and G beta hemolytic strep are penicillin susceptible.
2) S. pneumoniae can be resistant to many common antibiotics.
3) Viridians strep can be penicillin resistant.
4) Enterococci can be penicillin and vancomycin resistant.

Front 31

Levels of hemolysis of strep on blood agar

Back 31

beta hemolysis - complete hemolysis
alpha hemolysis - incomplete hemolysis, green
gama hemolysis - no hemolysis