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Infectious Disease 1 > TBL 1 > Flashcards

TBL 1 Flashcards

1
Q

What color does staph grow on agar?

A

S. Aureus colonies are gold

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2
Q

How is S. Aureus spread?

A

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

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3
Q

What can S. Aureus cause? (Symptoms and diseases)

A

Skin and soft tissue infections; Bacteremia - sepsis, metastatic seeding; Endocarditis; Musculoskeletal Infections; Respiratory tract infections; TSS; Food poisoning

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4
Q

How does S. Aureus invade?

A

Elaboration of enzymes (lipase, coagulase, hyaluronic are, etc) causing tissue damage; Presence of different adhesions may facilitate seeding of different tissue sites

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5
Q

What can staph toxins cause?

A

TSS; Food poisoning; Scalded skin syndrome

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6
Q

What is TSS caused by?

A

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

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7
Q

How does staph cause food poisoning?

A

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

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8
Q

What is staphylococcus epidermis associated with?

A

Prosthesis; It is coagulase negative and can elaborate a biofilm that allows it to adhere to prosthetics

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9
Q

What are some distinct characteristics of coagulase negative staph?

A

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)

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10
Q

What is the primary host response to staph?

A

PMNs (which is why patients w/ qualitative or quantitative leukocyte defects are at increased risk of staph infection)

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11
Q

What is the biochemical mechanism of TSS?

A

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

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12
Q

Define: Infective Endocarditis

A

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

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13
Q

How is endocarditis described?

A

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)

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14
Q

What are the top 3 causes of infective endocarditis?

A

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

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15
Q

What are the risk factors for infective endocarditis?

A

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)

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16
Q

What is the pathogenesis of endocarditis?

A

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

17
Q

What host factors affect pathogenesis of infective endocarditis?

A

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

18
Q

What are some immunologic manifestations of infective endocarditis?

A

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

19
Q

What are some common symptoms of endocarditis?

A 
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
20
Q

How can endocarditis be diagnosed?

A

History and physical
Blood cultures
EKG (trans esophageal echocardiography)

21
Q

How should endocarditis be treated?

A

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

22
Q

When should prophylaxis be used for prevention of infective endocarditis?

A 
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
23
Q

How has epidemiology of endocarditis changed?

A

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)

24
Q

What hemodynamics features affect the anatomic site of vegetation formation in infective endocarditis?

A

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)

25
Q

What are characteristics of staphylococci? (Coagulase, growth, staining, spores, etc)

A

Extracellular
Pus-forming micro organisms (pyogenic)
Form abscesses
S. Aureus is coagulase positive, others are coagulase negative
Nonsporulating, nonmotile
Grow in clusters (grape-like)
Surrounded by a micro capsule and a cell wall
Gram positive
Cocci
Extremely hardy - survive a variety of environmental stress
Catalase positive

26
Q

How is sepsis defined?

A

Inflammatory response to micro organisms or invasion of normally sterile tissue
+ >=2 SIRS criteria

27
Q

What are the SIRS criteria?

A

Systemic Inflammatory Response Syndrome

T>38C or 90; RR>20 or pCO2 12K or 10% bands

28
Q

What defines septic shock?

A 
Severe sepsis (sepsis + organ dysfunction, lactic acidosis, altered mental status)
AND hypotension despite fluid resuscitation (BP 40)
29
Q

What can cause sepsis?

A

Bacteria, fungi, viruses
LPS (even without bacteria; “endotoxin reaction”)
Exotoxins (TSS toxins, superantigens)

30
Q

What is the pathophysiology of sepsis?

A

LPS initiates the stereotypic inflammatory response
Targets are initially the macrophage and vascular endothelial cell
TLRs are also affected (TLR4 for gram neg, TLR2 for gram position)
TNF and NFkB are activated

31
Q

What are the shock syndromes of sepsis?

A

Hypovolemic or oligemic
Cardio genie
Vascular obstructive
Distributive or Vasodilatory

32
Q

What is the mechanism of Vasodilatory shock?

A

ATP-sensitive K channels are activated causing hyper polarization of smooth muscle cells
Activation of the inducible form of NO synthase
Deficiency of vasopressin
(Remember: pituitary holding vasopressin like a small Gucci bag)

33
Q

What is SIRS?

A

A clinical response arising from a nonspecific insult with 2+ of the SIRS criteria

34
Q

What is severe sepsis?

A

Sepsis with =>1 of the following system dysfunction:

  • cardiovascular
  • renal
  • respiratory
  • hepatic
  • hemostasis
  • CNS
  • metabolic acidosis (unexplained)
35
Q

How does sepsis change from early to late phase?

A

Skin goes from warm and dry to cold and clammy
Urine output usually plummets
Lactic acid greatly increases
Pulse increases and is “thready”

36
Q

How is sepsis managed?

A

Ventilators support; Antibiotics (early); Resuscitation of fluids, blood, vasoactive agents; Close monitoring; Assess for cause; Modulate the host response (restore balance); Minimize complications

37
Q

What checklists seem to be helpful in treating sepsis?

A

Central line bundle (hand hygiene, barrier protections, skin antisepsis, daily review of line)
Ventilator Associated Pneumonia (VAP) Bundle (elevation of the head of the bed, sedation vacations and assessment of readiness to extubate, DVT prophylaxis, peptic ulcer prophylaxis)
Sepsis/Resucitation Bundle Bundle (lactate if >4 memos/L - give at least 20-30 ml/kg in first 6 hours until lactate

38
Q

What are Dr. Chong’s take-home messages about sepsis?

A

Send a lactate if patient doesn’t look right; You don’t need a central line to treat; Severe sepsis and septic shock are emergencies; Lots of fluids; Use the sepsis order set; Crackles don’t always mean pulmonary edema

Infectious Disease 1 (10 decks)

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