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30 Cards in this Set
- Front
- Back
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What is the major cause of hospital- related bacteremias in the US?
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Staphylococcal species
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How do Staph bacteria cause disease?
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Causes disease via INTRAVENOUS CATHETERS and other IMPLANTED PROSTHETIC devices because they are frequently colonized by S. aureus or S. epidermidis
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What is the drug of choice now that 60% of bacteria are resistant to methicillin?
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Vancomycin
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What are the 3 main species of Staph you must learn?
What are some of there characteristics |
1) S. aureus (COAGULASE +)
2) S. epidermidis (COAGULASE -) 3) S. saprophyticus (COAGULASE-) They are all gram + cocci with GRAPE LIKE clusters |
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What is COAGULASE?
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It is a useful distinguishing feature that clots human or rabbit plasma by activating fibrinogen
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Which Staph organisms are of clinical importance?
What does it mean to be CATALASE +? What are faculatative anaerobes? |
Coagulase - Staph (S. hemolyticus, S. hominis)
It means that it converts H202--> O2 + H20, in contrast to Streptococcus Facultative anaerobes can grow with or without O2 |
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1) What are important chracteristics of S. AUREUS?
BACTERIOLOGY |
gram + clusters
coagulse + ferment mannitol produce hemolysins DNase |
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EPIDEMIOLOGY of S. AUREUS?
*How can you trace an epidemic of S. aureus? |
found on the skin, mucous membrane of nares
colonizes nasal passage of 30-40% of people and is higher in diabetics and drug addicts more likely to colonize hospitalized or compromised patients and those with FOREIGN BODIES like catheters or IVs *1) serologically 2) patterns of sensitivity to bacterial phages 3) DNA fingerprinting 4) ribotyping 5) comparing DNA sequence of selected genes among different strains |
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PATHOGENISIS OF S. AUREUS?
What are two types of diseases caused? (1) A) Do you need bacteria to be present at site of infection? B)? C) What are 2 examples of toxins that can produce in the animal model alone? |
1) TOXIN MEDIATED DISEASE
A) contamination with toxin production and don't need bacteria at the site of disease- - can get ENTEROTOXINS that cause food-borne diarrhea) B) colonization with toxin production in host colonization with receptor ligand interaction C) elaboration of toxins that can reproduce in animal model alone ex) TSS and EXFOLIATINS (scalded- skin syndrome) |
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PATHOGENESIS OF S. AUREUS continued... (2)
What factors (3) are involved in invasion of S. aureus? A) What molecles may contribute to adhesion to host's ECM? B)Where are these matrix proteins found? (3) C) What happens upon adhesion? (5) |
2) INVASIVE DISEASES (adhesion, toxins, evasive factors)
A) S. aureus can make multiple adhesive molecules that bind to the host's ECM (fibrinogen, fibronectin, collagen, platelets and others) B) these matrix proteins are found on damaged skin, disrupted airway epithelium, or endothelial cells C) upon adhesion, bacteria will colonize, evade host response, synthesize toxins and enzymes to lyse host tissues and spread to other targets |
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PATHOGENESIS OF S. AUREUS continued... (3)
What are TOXINS RESPONSIBLE FOR HOST CELL LYSIS? (7) |
1) alpha toxin
2) leukocidins 3) proteases 4) coagulase 5) staphylokinase 6) hyaluronidase (dissolves hyaluronic acid, a component of ECM) 7) lipase |
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PATHOGENESIS OF S. AUREUS continued... (4)
How does it EVADE HOST IMMUNE RESPONSES? (4) |
1) PROTEIN A- a cell wall protein that binds to host IgG via Fc receptors, leading to the binding on the "wrong end"
it's less complement- mediated killing it's a B- cell superantigen and it can lead to defective production of specific IgM 2) ENTEROTOXINS A-E, G, H, I- are T-cell superantigens, blunt specific host T- cell response 3) CAPSULAR POLYSACCHARIDES- antiphagocytic 4) EAP (MAP)- a surface protein that impairts neutrophil recruitment |
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What are some major CONSEQUENCES of the S. aureus disease?
What happen if the infection is CONTAINED/ NOT CONTAINED? |
1) If inflammatory and enzymatic actions are CONTAINED by host IR (via Ab, neutrophils, and macrophages), the infection will remain localized (like formation of abscesses..etc)
2) If the infection is NOT CONTAINED, invasion in the bloodstream may occur and bloodborne infections will ensue, and any human organ may be infected in a diseminated infection (spleen, liver, lung, etc.) |
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What are the CLINICAL SYNDROMES for a TOXIN-MEDIATED DISEASE?
(3) A) What enterotoxins is it due to? B) Resist to boiling? C) Do all make all types of enterotoxins? D) What do clinical syndromes include? |
1) FOOD POISONING (common cause of diarrheal outbreaks)
A) due to enterotoxin A-E,G, H, and I (F= TSST-1) B) heat stable, resistant to boiling C) not all strains produce all types of enterotoxins D) many are SUPERANTIGENS that stimulate a sig IL1, IL2 and TNF response clinical syndromes include: NAUSEA, VOMITING, NON- BLOODY DIARRHEA (all explained by T- cell Ag effect) |
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2) TSS characteristics
A) What is it most associated with? B) What factors does it stim? C) Clinical syndromes? |
A) caused by TSST-1, associated with tampon use in menstruating women with wound infections
B) SUPERANTIGEN stim IL1, IL2, TNF C) FEVER, RASH, with DESQUAMATION of palms and soles, HYPOTENSION and SHOCK |
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3) SSSS characteristics
A) What two toxins cause it? B) Secreted by which groups? C) Superantigen?? D) Where do you usually see? |
A) caused by two distinct toxins: exfoliant A and B
B) secreted by specific groups of S. aureus C) ?? D) site of exfoliation may not be same site of toxin production, but usually see in infants, and histology reveals epidermis detaching from underlying dermis |
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What are two types of INVASIVE DISEASES? (2)
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1) Superficial
2) Deep |
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What are characteristics of SUPERFICIAL INFECTIONS?
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impetigo
folliculitis (hair follicle infectoin) carbuncles cellulitis lymphangitis wound infection CATHETER SITE INFECTIONS PARONCHIA (nail bed infections) POSTPARTUM BREAST INF (mastitis) |
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What are characteristics of DEEP SEATED INFECTIONS?
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pneumonia (post- operative patients)
endocarditis (drug addicts, prosthetics in heart valve) osteomyelitis (trauma) arthritis (children) abscess (liver, spleen, kidney) meningitis (trauma) sepsis (from cath site etc..) |
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TREATMENT FOR S. AUREUS?
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1) dicloxacillin (ORALLY)
2) oxacillin (INTRAVENOUSLY) 3) if resistent to PENICILLIN, treat with VANCOMYCIN *note that s. aureus may develop tolerance so may add rifampacin or gentamicin |
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PREVENTION OF S. AUREUS?
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hand washing
discriminate use of ab |
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What are important characteristics of S. EPIDERMIDIS?
BACTERIOLOGY |
Coagulase -
gram - cocci catalase + little hemolysis on blood agar plate does NOT ferment mannitol SENSITIVE TO NOVOBIOCIN |
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S. EPIDERMIDIS EPIDEMIOLOGY?
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1) skin colonizer
2) very opportunistic pathogen 3) adheres to FOREIGN BODIES (pacemakers, prosthetic valves, joints etc) 4) susceptible patients: NEONATES, RENAL FAILRE, IC patients |
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S. EPIDERMIDIS PATHOGENESIS?
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1) may COLONIZE PROSTHETIC SURFACES VERY EFFICIENTLY
2) attachment can lead to proliferation and invasion into the bloodstream 3) surface of carbohydrate of the microorganism amy mediate attachment to synthetic surfaces 4) form biofilms which mediate intracellular adherence or clustering of bacteria embedded in the carb matrix 5) poor und of mechanism of molecules involved in invasion |
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S. EPIDERMIDIS CLINICAL SYNDROMES?
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1) low grade fever, pain, discomfort, course of infection may be indolent
2) bacteremia may result 3) patient not as toxic as S. aureus bacteremia |
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S. EPIDERMIDIS TREATMENT?
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1) remove prosthetic devices if feasible
2) treat with VANCOMYCIN and if toxic consider GENTAMICIN and RIFAMPIN |
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What are important characteristics of S. SAPHROPHYTICUS?
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gram + cocci
coagulase - catalase + does NOT ferment mannitol RESISTENT TO NOVOBIOCIN (compase with S. epidermidis) |
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S. SAPHROPHYTICUS EPIDEMIOLOGY?
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1) skin commensal
2) a common cause of UTI in young women (only second to E. COLI) |
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S. SAPHROPHYTICUS CLINICAL SYNDROMES?
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UTI with POLYURIA and DYSURIA
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S. SAPHROPHYTICUS TREATMENT
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1) trimethoprim sulfamethoxazol (BACTRIM)
2) norfloxacin (QUINOLONE) 3) drug penetration into the urinary bladder us usually very good |
