TBL 1 Flashcards
What color does staph grow on agar?
S. Aureus colonies are gold
How is S. Aureus spread?
Humans are the primary reservoir of this organism - opportunistic infection; Most infections (community and HAI) are the result of auto-inoculation; 20-40% of healthy people are colonized w/ staph aureus; Unlikely to cause local or systemic disease in the absence of some (minor) trauma
What can S. Aureus cause? (Symptoms and diseases)
Skin and soft tissue infections; Bacteremia - sepsis, metastatic seeding; Endocarditis; Musculoskeletal Infections; Respiratory tract infections; TSS; Food poisoning
How does S. Aureus invade?
Elaboration of enzymes (lipase, coagulase, hyaluronic are, etc) causing tissue damage; Presence of different adhesions may facilitate seeding of different tissue sites
What can staph toxins cause?
TSS; Food poisoning; Scalded skin syndrome
What is TSS caused by?
S. aureus that typically expresses TSST-1 (toxic shock syndrome toxin 1) - >95% of menstruation-associated TSS and ~50% of non-menstrual; TSST-1 is an exotoxin subject to regulatory control; TSST-1 gene (txt) is chromosomal and may be part of a mobile element
How does staph cause food poisoning?
Enterotoxin-mediated disease (does not require viable staphylococci) that results from ingestion of heat stable enterotoxin; These toxins stimulate the vagus nerve and the CNS vomiting center, increasing peristalsis; NOT the same site as the induction of TSS
What is staphylococcus epidermis associated with?
Prosthesis; It is coagulase negative and can elaborate a biofilm that allows it to adhere to prosthetics
What are some distinct characteristics of coagulase negative staph?
Relatively avirulent bacteria; Part of the normal skin flora; S. Epidermidis is the most common pathogen; Typically found in IV catheters, prosthetic heart valves; Frequent contaminant in cultures; Tend to be more antibiotic resistant than other bacterial species; Often require surgery to remove (have to take out prosthesis)
What is the primary host response to staph?
PMNs (which is why patients w/ qualitative or quantitative leukocyte defects are at increased risk of staph infection)
What is the biochemical mechanism of TSS?
Toxins bind to antigen-presenting cells MHC II molecule outside the peptide groove; Super antigens then bind T cells, resulting in massive T cell activation and cytokines storm (IL-1, IL-2, TNF, and IFN-g); Results in a syndrome similar to septic shock
Define: Infective Endocarditis
A microbial infection of a cardiac valve or the endocardium cause by bacteria or fungi; Path findings include the presence of friable valvular vegetation so containing bacteria, fibrin, and inflammatory cells; There is typically valvular destruction w/ extension to adjacent structures; Embolism lesions may demonstrate similar findings
How is endocarditis described?
Acute (48h) or subacute (go on for weeks or months) based on the rapidity of the clinical course; Can also be typed of risk factor (nosocomial, prosthetic valve, IV drug use-associated)
What are the top 3 causes of infective endocarditis?
S. Aureus (32%); Viridians strep (18%); Enterococcus spp. (11%); Culture negative is the worst b/c you don’t know how to treat; Can be caused by gram negatives (HACEK); NOTE: Primary pathogen for subacute is Viridans strep
What are the risk factors for infective endocarditis?
Dental procedures(Viridans strep, nutritionally variant strep, HACEK); Poor dental hygiene; Prosthetic valves (coag neg staph, S. Aureus, v. Strep in late); Gastrointestinal or genitourinary procedures (enterococcus or s. Bovis); Nosocomial (s. Aureus, gram negatives, candida)
What is the pathogenesis of endocarditis?
Inoculation of bacteria colonizing a mucosal or peripheral tissue site in the bloodstream
Transient bacteremia of serum-resistant pathogen capable of adhering to a cardiac valvular surface
Turbulent blood flow across the valve
Bacterial adherence to cardiac valvular surfacePathogen-host tissue interaction resulting in vegetation formation and local tissue damage
Dissemination of infection to other tissue sites and elimination of systemic findings
What host factors affect pathogenesis of infective endocarditis?
Valvular surface (no bacterial thrombus forms on damaged valves; suture line, valve surface of prosthetic valves)
Platelets dual role (platelet microbicidal proteins BUT bacteria induce platelet aggregation, part of no bacterial thrombus surface)
Leukocytes, complement, and cytokines play a more limited role
What are some immunologic manifestations of infective endocarditis?
Hypergammaglobulinemia
Polyclonal B cell activation (rheumatoid factor)
May block IgG opsonic response, accelerate micro vascular damage or stimulate phagocytosis
Vascular is
“Lumpy bumpy” glomerulonephritis with deposition of complexes with complement
What are some common symptoms of endocarditis?
Tachycardia Petichiae Abscess Heart murmur Lesions on arms and nails Swelling on foot or leg Roth spots Splinter Hemorrhages Osler's Node Fatigue Fever Anorexia General malaise Janeway Lesion
How can endocarditis be diagnosed?
History and physical
Blood cultures
EKG (trans esophageal echocardiography)
How should endocarditis be treated?
Antibiotics for weeks (prolonged therapy)
Treatment is best started after multiple sets of blood cultures have been taken
Synergistic combinations of antibiotics are used when available
Some patients have to go right into surgery even if they still have bacteremia
When should prophylaxis be used for prevention of infective endocarditis?
When having dental procedure/surgery involving the respiratory tract, infected skin, or skin sutures: Prosthetic valve Complex congenital heart disease Previous endocarditis Cardiac transplantation w/ valvulopathy
How has epidemiology of endocarditis changed?
Incidence has stayed constant for the last 25 years (1.7-6.2/100,000)
Age has increased (30-40 to 47-69)
Major shift in underlying issue and change in microbiology (more staph)
Increase in nosocomial endocarditis
Increased risk in IV drug users, hemodialysis, IV catheters, diabetics, HIV infected (150-2,000/100,000 person years)
What hemodynamics features affect the anatomic site of vegetation formation in infective endocarditis?
Presence of high-pressure source (eg left ventricle)
High velocity flow throw a narrow orifice (such as an insufficient mitral or aortic valve)
Low-pressure chamber or “sink” beyond the orifice (such as left atrium or left ventricle during diastole)
