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73 Cards in this Set
- Front
- Back
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SEE slide 5
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catalase test
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Staphylococcus aureus Virulence Factors
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Capsule: inhibits phagocytosis by PMNs
Slime layer: extracellular stuff involved in biofilm formation Coagulase = clumping factor: binds to fibrinogen, converts to fibrin Fibrin-coated cells resist phagocytosis Protein A: binds to Fc region of Ig Carotenoid pigment: (golden color) antioxidant resists superoxides O· Catalase: converts H2O2 into O2 and water Staphylokinase (also called fibrinolysin: activation of plasmin from plasminogen can target Fc cleavage, cleavage of antimicrobial peptides cleavage of C3b to C3i. |
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Staph aureus has CHIPS which is
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Chemotaxis Inhibitory Protein of Staphylococci: binds C5a and formyl peptide receptors on neutrophils
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Staph aureus cytotoxins
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Alpha
Beta Gamma Delta |
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Alpha toxin
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targets membranes of many cells (erythrocytes, leukocytes, hepatocytes, platelets, smooth muscle in blood vessels)-cell lyses
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Beta toxin
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sphingomyelinase C – targets sphingomyelin and lysophosphatidylcholine, forming pores in erythrocytes, fibroblasts, leukocytes, macrophages.-cell lyses
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Delta toxin
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very small (3,000 da), surfactant/detergent action.
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Gamma toxin and PVL
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specifically targets leukocytes.PVL associated with MRSA community based.
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Staph Exfoliative toxin A and B
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causes SSSS = Staphylococcal Scalded Skin Syndrome
Found in 5-10% of S. aureus strains. Serine protease—splits intercellular bridges in stratum granulosum of epidermis Not associated with inflammation or cytolysis Bacteria not found at site of shedding skin Seen in primarily in young children |
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Staph Aureus Enterotoxins
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Eight serologically distinct toxins:
A-E, G, H, I (food poisoning) |
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Staph Aureus Heat and protease resistant
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Food poisoning, upset stomach, vomiting
Incubation period ~ 4 hours |
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S. Aureus Toxic Syndrome Toxin 1
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Heat and protease resistant
Menstruation-associated toxic shock Able to cross mucosal barriers Superantigen release of cytokines, leakage of endothelia Requires high oxygen and neutral pH (therefore not often found to act during other types of staph infections where abscess forms because abscess are acidic) |
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Staphylococcus epidemiology
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Found in oropharynx, GI tract, urogenital tract. ~30% of normal health adults are persistent nasopharyngeal carriers of S. aureus – higher percentage in hospital patients and staff.
Shedding of bacteria is common and responsible for many hospital acquired infections. The bacteria can survive on dry surfaces for long periods of time, and can be spread by direct contact or by fomites. |
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Staphylococcus disease
Toxin-mediated |
SSSS, food poisoning, Toxic Systemic Shock
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Staphylococcus disease Suppurative infections
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cutaneous, bacteremia, endocarditis, pneumonia, empyema, osteomyelitis, septic arthritis
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Staphylococcal Scalded Skin Syndrome SSSS= Ritter’s Disease
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1st sign: peri-oral erythema, expanding to entire body. Large bullea form—no bacteria within bullae. Result of toxin. Low mortality
Bullous Impetigo: localized SSSS; fluid-filled blisters; Staph cells within blisters; erythema does not extend beyond blister Only the top layer of the skin, bullae with no bacteria and results as part of the toxin. Mortality low. Immunocompromised adults |
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Staphylococcal Food Poisoning
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Very common. Symptoms result from intoxication, not infection.
Toxin is present in food, contamination often occurs during food preparation 4 hour incubation, doesn’t last longer than 24 hours Vomit, diarrhea, stomach cramping, No Fever Staph may cause enterocolitis…often following broad-spectrum antibiotic treatment |
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Toxic Shock Syndrome( menstruating women, tampon)
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Localized growth of S. aureus and release of toxin into blood. Requires high oxygen, neutral pH. Fever, hypotension, macular erythematous rash - entire skin can desquamate
Fatality has been reduced to 5% with treatment Recurrence can be high…protective Ab not generated in patients |
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S. aureus cutaneous infections
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Impetigo: Superficial infection of epidermis
Pus-filled vesicles; following rupture of vessicle, crusts over 2° infection and spread likely occurs after rupture. Most common in children |
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S. aureus Folliculitis:
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infection around hair follicle; pus-filled lesions form around follicle
If occurs at base of eye – stye |
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S. Aureus Furuncles (aka Boils)
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extension of folliculitis. Large, painful, underlying collection of necrotic tissue. Erythemitous, raised, swollen.
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S. Aureus Carbuncles
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coalesced furuncles; extend to deeper tissues; can lead to spread to other sites of body and bacteremia
Often include chills and fever indicates systemic spread |
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S. Aureus Bacteremia
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Staph is a common cause of bacteremia. Large number of cases have unknown primary site of infection (likely skin infection)
Half of cases follow surgical procedure or prolonged catheter use. |
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S. Aureus Accute endocarditis
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staph in blood can adhere to heart tissues; can be sudden onset of high fever (103°-105°F). High mortality (50%). Valvular destruction and embolisms to brain or lung can occur.
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S. aureus Aspiration pneumoniae
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: inhaled from oral secretions; characteristic chest x-ray
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S. aureus Hematogenous pneumonia
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acquired during bacteremia or rarely from the community – strains typically express the PV leukocidin ((MRSA Community based)
Can lead to rapid destruction of parenchyma, or development of empyema (pus in the pleural space) |
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Necrotizing pneumonia
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Community-acquired MRSA strains. High mortality.
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S. aureus Osteomyelitis
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occurs following hematogenous dissemination to the bone
in children, occurs at metaphyseal area of long bones in adults, typically occurs in vertebrae both present severe pain and fever |
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S. aureus Septic arthritis
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invasion of the joint.
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Staphylococcus epidermidis
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(coagulase-negative staph…normal flora of skin)
Endocarditis in artificial valves Catheters and shunts (50%) originate from skin Artificial joint infections |
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Staphylococcus saprophyticus
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UTI in young, sexually active women
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Staphylococcus aureus Identification primarily by culture and nucleic acid-based methods
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Organism grows rapidly in culture on nutritionally enriched sheep blood agar. Can be isolated selectively on mannitol-salt agar.
A variety of tests can then be used to differentiate Staphylococci (coagulase, presence of protein A). Can also use commercially developed fluorescent antibodies and microscopy. PCR is used to survey for methicillin-resistant S. aureus. Microscopic detection in patient samples depends on type of infection and quality of material submitted for analysis. May see in a scrape at the base of an abscess, but not in pus or blood. |
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Staphylococcus aureus treatment
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staph sensitive to penicillin
New, semisynthetic penicillins (nafcillin, oxacillin, dicloxacillin) |
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Staphylococcus aureus MRSA txt
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Vancomycin is 1st line of defense against MRSA
targets cell wall one step earlier than b-lactams |
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Streptococcus
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Commonly arranged in pairs or chains, catalase negative.
Facultative anaerobes, some require CO2. |
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Streptococcus pneumoniae
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no Lancefield antigen); a-hemolytic
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Lancefield antigen
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= C-polysacharide; Groups A thru S, (there >30 spp. of Strep, not all have Lancefield antigen
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Streptococcus Viridans
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(large group of many species; verde = green, a-hemolytic); various Lancefield antigens; most important = Streptococcus mutans (dental caries).
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Group A streptococcus – Virulence Factors
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M-Protein
Hyaluronic acid capsule Hemolysins Streptolysin S: Streptolysin O: Proteases Nucleases Toxins |
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M-Protein
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M-like proteins:
antiphagocytic factor. Binds factor H; binds fibronectin; some bind Fc region of Abs |
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Hyaluronic acid capsule.
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Interferes with phagocytosis
Non-immunogenic (looks like host connective tissue) |
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. Hemolysins
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make pores in host membranes
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Streptolysin S:
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Oxygen-Stable; non-immunogenic.
Major factor leading to b-hemolysis on blood agar plates. |
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Streptolysin O:
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Oxygen-sensitive hemolysin (will not contribute to b-hemolysis on blood agar plates when grown aerobically
immunogenic—can be used to diagnose rheumatic fever and glomerulonephritis (anti-streptolysin O antibody test = ASO test) |
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Proteases
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SpeB, Mac1/Mac2, SIC, ScpA, ScpC : cleaves immunoglobulins, antimicrobial peptides (cathelicidin) , complement factors (C3b, C5a), cytokines (IL-8)
Streptokinase: conversion of Plasminogen to Plasmin (breaks down clots; spread?) |
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Nucleases
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Streptodornase (Dnase). Breaks down NETS (neutrophil extracellular traps)
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. Toxins
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Pyrogenic exotoxins:
These are phage-encoded superantigens. Superantigens are mitogenic factors that cross-link MHC class II to T-Cell Receptors (TCR). Induces T-cell activation and massive cytokine production. Results in non-productive and non-specific immune response. Causes massive inflammation and Toxic Shock. |
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Diseases caused by Group A streptococcus
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Pharyngitis
Scarlet Fever may accompany pharyngitis Impetigo (aka Pyoderma) Erysipelas. Cellulitis. |
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Pharyngitis;
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; fever >102°F, chills, headache, painful to swallow; possible nausea; (viral pharyngitis more common…runny nose, post-nasal drip, etc.)
most common cause of bacterial pharyngitis (“strep throat”) repeated infections common Common among 5-15 year-olds, but possible in all ages Highest incidence in winter and spring Self-limiting, but treatment advisable to avoid sequelae |
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Scarlet Fever may accompany pharyngitis
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Streptococcal Pyrogenic Exotoxins are superantigens;
Encoded on prophage |
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Impetigo (aka Pyoderma)
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Superficial infection. Common in children. Common in warm and humid summer months.
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Erysipelas.
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Infection of the dermis; sharply demarcated edge; localized pain, erythema, systemic signs of fever, chills, leukocytosis
Most common in young and elderly. Accompanied by fever; progresses rapidly; usually at extremities. |
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Cellulitis.
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Deeper dermal infection. Not sharply demarkated.
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Group A strep Necrotizing fasciitis.
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flesh-eating disease”
Necrosis of connective tissues, fat tissues, and lymphatics Preceded by cellulitis, bullae formation, gangrene extremely painful, rapid progression along fascial plane débridement typically required often accompanied by Streptococcal Toxic Shock Syndrome (STTS) due to pyrogenic exotoxins (superantigens) more likely than Staphylococcal toxic shock to have bacteremia |
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Non-Suppurative Sequelae: Autoimmune reactions post-GAS infection
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Acute Rheumatic Fever/Reumatic Fever (ARF/RF)Acute Glomerulonephritis (AGN)
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Acute Rheumatic Fever/Reumatic Fever (ARF/RF)
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Antibodies raised against M-protein and other bacterial antigens cross-react with heart tissues (muscle and valves).
Follows pharyngeal infectioins Immune reactions to joints, CNS, and skin also possible. Recurrence can happen following each GAS infection (due to many different M-types) Strains (M-types) causing ARF/RF called rheumatogenic strains |
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Acute Glomerulonephritis (AGN)
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Follows pharyngeal and skin infections
Antibody-antigen complexes deposit on glomerular basement membrane—leads to complement fixation and inflamation (Type III Hypersensitivity) Less likely to recur because nephritic strains are less common. |
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Strep A txt
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Highly susceptible to Penicillin G
Mixed infections with S. aureus should include vancomycin days of onset will prevent rheumatic fever |
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Group B Streptococcus (GBS) = S. agalactiae
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Largest cause of neonatal meningitis, sepsis and pneumonia
Women testing positive during pregnancy (tested at 35-37 weeks) should be given antibiotics during labor. |
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Streptococcus pneumoniae = Pneumococcus
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a-hemolytic, aerotolerant anaerobe
Commensal species, residing in upper respiratory tract Most common cause of bacterial meningitis in adults and children |
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Impetigo (aka Pyoderma)
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Superficial infection. Common in children. Common in warm and humid summer months.
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Erysipelas.
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Infection of the dermis; sharply demarcated edge; localized pain, erythema, systemic signs of fever, chills, leukocytosis
Most common in young and elderly. Accompanied by fever; progresses rapidly; usually at extremities. |
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Cellulitis.
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Deeper dermal infection. Not sharply demarkated.
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Group A strep Necrotizing fasciitis.
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flesh-eating disease”
Necrosis of connective tissues, fat tissues, and lymphatics Preceded by cellulitis, bullae formation, gangrene extremely painful, rapid progression along fascial plane débridement typically required often accompanied by Streptococcal Toxic Shock Syndrome (STTS) due to pyrogenic exotoxins (superantigens) more likely than Staphylococcal toxic shock to have bacteremia |
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Non-Suppurative Sequelae: Autoimmune reactions post-GAS infection
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Acute Rheumatic Fever/Reumatic Fever (ARF/RF)Acute Glomerulonephritis (AGN)
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Acute Rheumatic Fever/Reumatic Fever (ARF/RF)
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Antibodies raised against M-protein and other bacterial antigens cross-react with heart tissues (muscle and valves).
Follows pharyngeal infectioins Immune reactions to joints, CNS, and skin also possible. Recurrence can happen following each GAS infection (due to many different M-types) Strains (M-types) causing ARF/RF called rheumatogenic strains |
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Acute Glomerulonephritis (AGN)
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Follows pharyngeal and skin infections
Antibody-antigen complexes deposit on glomerular basement membrane—leads to complement fixation and inflamation (Type III Hypersensitivity) Less likely to recur because nephritic strains are less common. |
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Strep A txt
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Highly susceptible to Penicillin G
Mixed infections with S. aureus should include vancomycin days of onset will prevent rheumatic fever |
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Group B Streptococcus (GBS) = S. agalactiae
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Largest cause of neonatal meningitis, sepsis and pneumonia
Women testing positive during pregnancy (tested at 35-37 weeks) should be given antibiotics during labor. |
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Streptococcus pneumoniae = Pneumococcus
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a-hemolytic, aerotolerant anaerobe
Commensal species, residing in upper respiratory tract Most common cause of bacterial meningitis in adults and children |
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Pneumococcus Prominent Virulence Factor
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polysaccharide capsule
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Group D Streptococcus
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No longer streptococcus; reclassified as Enterococcus
Enterococcus faecalis and E. faecium Normal flora of intestinal tract (large and small intestine) Major carriers of antibiotic resistant cassettes Source of b-lactamase and Vancomycin resistance (van genes) Has been transmitted to Staphylococcus aureus Treatment of VRE: linezolid, daptomycin, tigecycline |
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Strep Viridans = Oral Streptococci
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Very large group of species within the genus Streptococcus
Commensal species commonly found in the oral cavity and GI tract Viridis: Latin for Green – many are a-hemolytic (greenish color surrounding Many species responsible for dental caries – tooth decay (S. mutans) Dental manipulations can send Viridae into the blood stream these bacteria can target heart tissues, esp. valves. repeated buildup of Viridae can lead to Subacute Endocarditis higher risk in patients with history of rheumatic fever or heart defects antibiotic prophylaxis previously recommended before dental work |
