House-style Bacterial Clin Stuff Flashcards

1
Q

Staph bacteria are catalase positive, what does that mean? (picture staff with cats)

A

* catalase is an enzyme that converts H2O2-> H20 + O2

that is, Staph aureus, etc can convert hydrogen peroxide into water and oxygen (bubbles appear when staph present)

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2
Q

What are alpha, beta and gamma hemolytic bacteria?

A

Bacterial description:

beta - can fully lyse RBCs (they are cultured on sheep blood agar, so leave white spots as RBCs get killed, with red aroung)

alpha - can partially lyse RBCs, greenish colour on agar

gamma - cannot lyse RBCs

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3
Q

What can group A Strep do?

A

Can cause strep throat (pharyngitis), skin infections, glomerulonephritis, Toxic Shock Syndrome

Can also cause delayed antibody response diseases: scarlet fever (pyogenes class), rheumatic fever.

think PHaryingitis can also lead to glomerulonePHritis and rheumatic PHever

Group A - beta hemolytic (can kill sheep RBCs on agar completely)

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4
Q

So why does Group A Strep cause delayed antibody responses?

A

scarlet fever (pyogenes class), rheumatic fever

Also has pyrogenic exotoxin - can cause scarlet fever, superantigen - directly stimulates a sea of T cells -> massive cytokine rlease -> toxic shock syndrome

  • scarlet fever: extensive rash on trunk and neck, spares face; skin may peel off in fine scale (happens due to exotoxin that Strep produces)
  • toxic shock syndrome - (Strep or Staph), mediated by release of pyogenic toxin, need high dose of penicillin and clindamycin to stop toxin synthesis (blocks protein synthesis by blocking bacterial ribosomes)
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5
Q

Testing for Strep pharyngitis?

A

exudative pharyngitis common, swab tonsils and send for a rapid antigen detection test (RADT), in minutes, highly specific for Strep pyogenes, but can be misleading in kids (get throat culture in them as backup, b/c get strep often but results can be negative).

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6
Q

Skin infections in Strep?

A
  • folliculitis: infection of hair follicles
  • cellulitis: deep infection of skin cells, producing red, swollen skin hot to touch
  • impetigo: vesicular (volcanic-lava like), blistered, skin with crusty yellow tops, frequent around mouth (can also be S. aureus); frequently pyoderma (=pus on skin) = impetigo contagiosa
  • erysipelas - step infection of the superficial skin (dermis), raised, bright red rash with a sharp border that advances from the initial site of infection (S.aureus rare)
  • necrotizing fasciitis : flesh eating streptococcus - swelling, heat, redness day one, then colour changes to purple to blue in a day and large blisteres (bullae form). then skin dies and msucle may also be infected (myositis). in this case fascia has to be surgically removed and rapid antibiotic therapy is crucial. add clindamycin to penicilin G treatent to shut down toxin production. also can be caused by Staphylococcus, Clostridium, etc
  • scarlet fever: extensive rash on trunk an dneck, spares face; skin may peel off in fine scale (happens due to exotoxin that Strep produces)

image up front is erysipelas

on this page, impetigo

  • necrotizing fasciitis

usually fo

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7
Q

Risk of untreated pharyngitis?

A

Rheumatic fever

usually in 5-15 years old, often follows untreated pharyngitis by Group A Strep

Think JONES

J for Joints: joitn swelling, arthritis

O for heart <3 (can’t type it) : myocarditis

N for nodules: subcutaneous nodules = rubbery nodules just under skin

E is for erythema marginatum: red margin rash that spreads from centre

(erythema is like red and marginatum like margins)

S is for St. Vitus dance = uncontrolled dance-like movements of the extremities

antibody-mediated, risk of developing arrythmias and heart failure, after recurrent infections heart can become permanently damaged, but takes many years for valves to show problems after initial myocarditis (rheumatic valvular disease develops). most often mitral valve.

remember CLIN: causes for valvular disease are #1 rheumatic, #2 rheumatic, #3 rheumatic

give prophylactic penicillin, b/c patients susceptible to repeats.

no permanent injury to the joints though

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8
Q

Antibody mediated diseases from Strep?

A

- rheumatic fever

-post-streptococcal glomerulonephritis

about 1 week after infection of either the pharynx or skin by nephritogenic (strains that can cause glomerulonephritis) strains of group A strep. antigen-antibody complexes travel to kidneys, get stuck in glomerular basement memgrane, activate complement cascade leading to glomerular destricution

1) puffy face (b/c retaining fluid)
2) dark pea (b/c blood in urine = hematuria)
3) high BP secondary to hypervolemia due to impaired kindey function

ASK ABOUT SORE THROAT A WEEK OR SO AGO

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9
Q

What do Group B Strep do?

A

B for baby

25% of women have these bugs vaginally, so baby can acquire during delivery, can cause neonatal meningitis, pneumonia and sepsis (<3 months old)

nonspecific signs: fever, vomiting, irritability, poor feeding.

act rapidly: diagnose by lumbar puncture, start antibiotics as soon as suspected, not when diagnosis confirmed.

Most common causes of meningitis in neonates: Strep Group B, E.Coli and Listeria = cover for all.

BABY brain saved by the BEL (saved from meningitis knowing it could be group B strep, E.Coli or Listeria)

Group B can cause pneumonia and sepsis in immunocompromised (diabetes, malignancy, renal failure, etc or elderly)

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10
Q

Criteria for SIRS?

A

SIRS = systemic inflammatory response syndrome

diagnosis is made if two+ of the following present:

  • HR > 90 BPM
  • RR > 20 breaths/min
  • WBC <4,000 cu/mm or >12,000cu/mm or > 10% bands
  • temperature <36 C or > 38C
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11
Q

Possible complications from otitis media?

A

  • *1. Vertigo
    2. Tinnitus
    3. Facial paralysis
    4. Mastoiditis
    5. Meningitis**
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12
Q

What predisposes someone to accute sinusitis?

A
  1. Dental infections
  2. Allergies
  3. Swimming
  4. Mechanical obstruction of nose
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13
Q

What bacterias commonly cause UTIs?

A
  • Enterobacteria: E.coli, Klebsiella, Proteus
  • Enterococcus spp (+ve but anaerobic, looks like strep)
  • Staphylococcus sapprophyticus (#2 in young females)
  • Strep. agalactiae (GBStrep)

Community:

E.coli (80%), Staph sapprophyticus, other Staph, enterococci, etc

Nosocomial:

E.coli (40%), Gram -ves (25%) = klebsiella, enterobacter, pseudomonas; then gram +ves, etc

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14
Q

Whats this Staph saprophyticus?

A

From Wikipedia:

In humans, S. saprophyticus is found in the normal flora of the female genital tract[3] and perineum.[4] It has been isolated from other sources too including meat and cheese products, vegetables, the environment, and human and animal gastrointestinal tracts.[4] S. saprophyticus causes 10-20% of urinary tract infections (UTIs). In females 17–27 years old, it is the second most common cause of community-acquired UTI, after Escherichia coli.[5] Sexual activity increases the risk of S. saprophyticus UTI because bacteria are displaced from the normal flora of the vagina and perineum into the urethra.[3] Most cases occur within 24 hours of sex,[3]earning this infection the nickname “honeymoon cystitis”.[6] S. saprophyticus has the capacity to selectively adhere to human urothelium. The adhesin for S. saprophyticus is a lactosamine structure. S. saprophyticus produces no exotoxins.[3]

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15
Q

Risk factors for UTI?

A

Anything to hold urine longer:

  • Kidney infection
  • Prostate problems (hypertrophy)
  • short urethra in women
  • catheters
  • neurologic (bladder can have problems emptying)
  • vesicoureteral reflux (urine travels up from bladder to ureter and kidneys (in kids, think reflux as going up)
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16
Q

Most likely cause of UTI in hospital?

A

Catheter - risk of UTI increases by 3% for every day with catheter

DO NOT FORGET about it , take it off patient as soon as you can

Make sure collection bag is below patient (use gravity to clean catheter!), intermittent catheter is better than continuous catheter

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17
Q

What is vesicoureteral reflux?

A

Vesicoureteral reflux (VUR) is an abnormal movement of urine from the bladder into ureters or kidneys. Urine normally travels from the kidneys via the ureters to the bladder. In vesicoureteral reflux the direction of urine flow is reversed (retrograde).

In healthy individuals the ureters enter the urinary bladder obliquely and run submucosally for some distance. This, in addition to the ureter’s muscular attachments, helps secure and support them posteriorly. Together these features produce a valvelike effect that occludes the ureteric opening during storage and voiding of urine. In people with VUR, failure of this mechanism occurs, with resultant retrograde flow of urine.

WIkipedia

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18
Q

Approach to UTI diagnosis:

A
  1. History and physical
  2. Urinalysis (urine test with electrolytes, proteins in urine, etc)
  3. Urine culture and susceptability (collect before starting antibiotics, dah)
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19
Q

Signs and symptoms of UTI?

A
  • Dysuria (burning or discomfort when peeing)
  • Fever
  • Costovertebral angle tenderness (pyelonephritis)
  • Frequency of urination changes
  • Higher urgency of urination
  • Hesitancy ?
  • New onset incontinence in elderly

malodorous and cloudy urine is not a symptom of UTi

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20
Q

What sample of urine to collect?

A

* midstream urine (after you started peeing but before you finished to decrease chance of bacterial contamination, as first urine washes residual bacteria out)

* Foley catheter - ideally from newly inserted catheter, b/c those over 24 hrs will be colonzied, DO NOT collect from collection bag (usually there is bacteria there and overgrown)

* Suprapubic aspiration (needle over pubic bone)

* ileal conduit (piece of ileum used as bladder, always will be some bacteria in urine after that procedure)

* nephrostomy tube - conduit directly in kidneys

* cystoctomy tube - tube directly in bladder (cyst = bladder)

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21
Q

What is in urinalysis?

A
  • test for leukocytes (leukocyte estarase + if WBC)
  • test for nitrites (positive if there are bacteria that can transform nitrate to nitrite (NO3->NO2. think nitRITE is right, so NO2)
  • Proteus, Klebsiella, E.Coli (enterobacters)
  • WBC count = infection, cancer or catheters (can produce inflammation)
  • RBC = infection, kidney disease, renal stones, urinary tract cancers, bleeding disorders, contamination
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22
Q

Urine culture

A

try mistream urine

> 10^5 bacteria in 1 ml = significant bacteriuria (for midstream urine only!)

if over 3 organisms found, likely contaminated sample instead

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23
Q

T or F?

Signs and symptoms, positive urinalysis and positive culture are required to assess for UTI

A positive quntitative urine culture alone just indicates bacteriuria (not UTI, could be asymptomatic)

A positive leukocyte esterase just indicates inflammation (not necessarily infection)

A positive nitrite just indicates the presence of bacteria that can reduce nitrate (Klebsiella, E.coli, proteus)

A

All true

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24
Q

When to get BLOOD culture when suspecting UTI?

A
  • when presented with sepsis
  • immunocompromised with fever, pyelonephritis and UTI symptoms (fear worse = bacterimia)
  • all pediatric patients with fever (need to know what is goign on and can’t get all history, so resort to tests)
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25
Q

Commonly used UTI antibiotics?

A

TMP/SMX and ciprofloxacin have really good gram -ve coverage, were used empirically, but not anymore as develops resistance

nitrofurantoin and fosfomycin are good, for cystitis (bladder infection) but do not use in pyelonephritis

amoxicillin-clavulanate for gram +ves

Pregnancy: avoid TMP/SMX in first and third trimester, avoid nitrofurantoin and quinolones (ciprofloxacin)

IV: piperacillin+ tazobactram + gentamycin for broad spectrum

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26
Q

Treatment of acute cystitis (bladder infection)?

A

may resolve spontaneously

recurrent cystitis common in sexually active women

in men, if recurrent cystitis, screen for prostatic hypertrophy and prostatitis

response to antibiotics should be seen in 48 hrs, if not, consider other genitourinary infections, including STIs

treat with nitrofurantoin (remember that Klebsiella, proteus and E.coli make nitrate out of nitrite, so nitrofurantoin (5 days) or fosfomycin (1 day). NOT FOR PYELONEPHRITIS

alternative TMP/SMP, ciprofloxacin or trimethoprim (but resistance from E.coli

27
Q

What if cystitis symptoms reoccur?

A

Reinfection (most likely after 1 month), more common >90%

Relapse (most within 2 weeks of completing treatment), treat with longer course of antibiotics

28
Q

What is pyelonephritis? How does it present? How do you treat?

A

Pyelonephritis = kidney infection: fever, costovertebral angle tenderness, lower urinary tract symptoms

can damage kidney -? loss of renal fucniton in recurrent pyelonephritis

can result in secondary bacterimia (since kidneys filter blood)

treat 7-14 days

community: cefixime 10-14 days or TMP/SMX (14)

hospital: gentamicin IV or ceftriaxone IV

29
Q

What do you do with asymptomatic bacteriuria?

A

Do not treat unless:

  • pregnant (risk of pyelonephritis, preterm labour or becoming symptomatic); screen regularly throughout
  • about to undergo urinary tract surgery (can then get baad infection)
  • do not treat all because of C.diff, bacterial resistance nd other risks
30
Q

Symptoms of catheter - associated UTI?

A

typical symptoms like dysuria, frequency and urgency absent (dah, catheter takes care of that)

would have vefer, rigors, costovertebral angle tenderness)

remember cloudy urine or badsmelling urine is not a symptom of UTI and not indication for obtaining urine culture

catheter needs to be changed or removed

31
Q

UTI in kids

A

if delayed response to antibiotics > 48 hrs , ultrasound

if recurrent fevers, ultrasound

if abnormal urine stream, ultrasound

if abdominal or bladder mass felt, ultrasound

can have voiding cystourethrogram - put contrast in bladder to see if urine flows back up into kidneys (vesicoureteal reflux)

32
Q

What is septic shock?

A

Sepsis-induced hypotension inspite of adequate fluid resuscitation along with presence of perfusion abnormalities which can include lactic acidosis, oliguria (passing little urine) or an acute alteration in mental status.

33
Q

What is sepsis?

A

SIRS+confirmed infection

34
Q

What is septic shock?

A

Sepsis + hypotension

35
Q

SIRS->sepsis->severe sepsis-> septick shock

what is severe sepsis?

A

sepsis + organ failure

36
Q

Organisms most common in septic shock?

A

E.coli

Staph aureus

Strep pneumoniae

Klebsiella

37
Q

List some clinical features of sepsis?

A

Fever (remember SIRS <36 or >38C)

Tachycardia (remember SIRS >90 bpm)

Tachypnea (remember SIRS RR >20 bpm)

Organ failure (definition of severe sepsis)

Leukocytosis (remember SIRS WBC <4,000 or >12,000)

Reduced vascular tone (something has got to cause hypotension in septic shock)

Hypotension (septic shock!)

Altered mental capacity (again, definition of sepsis)

38
Q

What is warm shock?

Cold shock?

A

Warm shock, think warm as blood, blood still circulating

so… Hyperdynamic state

heart beating fast (tachycardia)

elevated or normal cardiac output

but in shock… so decreased systemic vascular resistance

Cold shock, opposite, heart not too keen on beating…

low cardiac output

39
Q

What are key principles of septic management?

A
  • Fluid level!
  • getting cultures to gage antibiotic management
  • early targeted antibiotics and establishing/treating source
  • using vasopressors and inotrops to get bp up
  • drain, debride and remove devices if applicable

Also:

  • prophylax for deep vein thrombosis & ulcers
  • prevent nosocomial pneumonia by lifting head by 45degrees
  • interrupt daily sedation, so extubation will be easier
  • narrow antibiotic spectrum when possible
40
Q

What is endocarditis?

A

Infection of endocardial (inner) layer of the heart

with fever and persistent bacterimia

vegetation on endothelial surface, variable in size, has fibrin and platelets

  • Native valve IE
  • Prostetic valve IE
  • Nosocomial IE
  • IVDA IE
41
Q

Difference between acute and subacute infectious endocarditis?

A

Acute

  • usually staph aureus (gold medal in eating hearts)
  • usually in normal heart valves,etc
  • metastatic
  • progresses very quickly (can be 6 weeks to fatality if not treated

Subacute

  • usually Strep
  • affects damaged heart valves
  • if not treated, fatal within a year or so
42
Q

Risks for Infective Endocarditis?

A
  • prostetic valves
  • congenital defects
  • IVDU
  • intravascular catheters
  • acquired heart defects (aortic stenosis and regurg, mitral problems)
43
Q

Causative agents of Infective Endocarditis (native and prostetic)?

A
  • Staph aureus (25% in native)
  • Strep (50% in native, 1% prostetic)
  • non-coagulase staph (30% prostetic)
  • enterococcus sp.
44
Q

Pathology of infective endocarditis?

A

IE often occurs when there is an underlying cardiac abnormality (3/4 of all cases) that creates a high-low pressure gradient. The resultant turbulent blood flow disrupts the endocardial surface by peeling away the endothelium.

The body’s natural response to endothelial damage is to repair it by laying down a sticky platelet-fibrin meshwork, which harbors infection.

Temporary bacteremia delivers the offending organism to the endocardial surface where is sticks to the platelet-fibrin meshwork. This festers into an infection that eventually invades the cardiac valves.

The pathophysiology is slightly different with IVDA. It has been postulated that repeated injections of drugs and particulate material causes microtrauma to the cardiac valves, thereby starting the infection cascade.

45
Q

Clinical features of infective endocarditis?

A

Fever (80-90%)

splenomegaly (30%)

heart murmurs 85%

new or changing murmur 10-40%

peripheral signs

emboli in up to 40%

Osler nodes (called mycotic anuerysms in lecture 2-10%)

46
Q

What are Osler’s nodes?

A

Osler’s nodes are painful, red, raised lesions found on the hands and feet. They are associated with a number of conditions, including infective endocarditis, and are caused by immune complex deposition.

Also look for splinter haemorrhage (nail haemorrhage)

Memory aid: O-oooh Osler’s are raised and immune

47
Q

What are Janeway lesions?

A

Janeway lesions are non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles only a few millimeters in diameter that are indicative of infective endocarditis. Pathologically, the lesion is described to be a microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis. They are caused by septic emboli which deposit bacteria, forming microabscesses. Janeway lesions are distal, flat, blanching, and painless.

Similar to Osler’s nodes, but Olser’s nodes are raised and painful, and associated with immune response.

48
Q

What are Roth’s spots?

A

Roth’s spots are retinal hemorrhages with white or pale centers composed of coagulated fibrin. They are typically observed via fundoscopy (using anophthalmoscope to view inside the eye) or slit lamp exam.

They are usually caused by immune complex mediated vasculitis often resulting from bacterial endocarditis. Roth’s spots may be observed in leukemia, diabetes, subacute bacterial endocarditis, pernicious anemia, ischemic events, and rarely in HIV retinopathy.

49
Q

What are some investigations for Infective Endocarditis?

A
  • CBCs
  • Blood cultures (without antibiotics) - get 2 or more blood cultures separated by 12 hrs, or 3 with at least 1 hr in between
  • Urinalysis (meh)
  • Renal and hepatic profile (meh)
  • ECG (rarely helpful)
  • Transthoracic Echo (TTE)
  • Transesophageal Echo (TEE) - way better than TTE; indicated in definite of suspected endocarditis, in persistent bacteremia over 5 days, or persistent emboli
50
Q

What is the modified duke criteria?

A
  • 2 major criteria
  • 3 minor and 1 major (4)
  • 5 major
  • think 2-1+3-5 (1,2,3,4(1+3),5)

Major

I. Positive blood culture for EI

a) typical microorganisms for EI in 2 separate blood cultures
b) persistently positive blood culture
c) single positive blood with coxiella or IgG antibodies 1:800>

II. Evidence of endocardial involvement

a) echo positive for IE (abscess, intracardial mass, etc)
b) new valvular regurgitation
c) new partial opening of a prosthetic valve

Minor:

a) predisposing heart condition or IVDU
b) fever >38C
c) vascular phenomena (ex. septic pulmonary emboli, etc)
d) immunologic phenomena (glomerulonephritis (remember urine tests = pyuria, proteinuria, hematuria + low serum complement), Osler nodes, Roth’s spots, rheumatoid factor (occasionally elevated rheumatoid factor in IE, especially if infected for over 6 weeks)

51
Q

What is phlebitis?

A

= vein inflammation. A needle or a catheter inserted into a vein and left in place will in time cause inflammation at the entry site. When this process involves the vein, it is called phlebitis. Phlebitis is one of the most common causes of fever after the third postoperative day. The symptomatic triad of induration (hardening), edema, and tenderness is characteristic. Visible signs may be minimal. Prevention of phlebitis is best accomplished by observance of aseptic techniques during insertion of venous catheters, frequent change of tubing (ie, every 48–72 hours), and rotation of insertion sites (ie, every 4 days)

52
Q

When to suspect catheter colonization?

A

if >15 cfu of organism is isolated from the catherer surface or >1,000 cfu/ml of organism is isolated from the lumen of catheter, without prior infection

53
Q

what is cfu?

A

cfu = colony forming unit ; estimate of viable bacteria or fungi

54
Q

What is tunnel infection? exit site infection?

A

**tunnel infection - **tenderness, erythema, and/or induration (hardening) > 2 cm from the catheter exit site, along subQ tract of a tunneled catheter

exit-site infection - erythema, tenderness and induration (think endure = endurance hardends you) <2 cm of the catheter exit site, may be associated with other signs and symptoms of infection, such as fever or pus emerging from the exit site, with or wihtout concominant bloodstream infection

55
Q

Sources of catheter related infections?

Risk factors?

A
  • operator
  • skin flora
  • contamination of the catheter hub/lumen
  • contamination of infusate

Risk factors:

  • loss of skin integrity
  • severity of underlying illness
  • thrombogenicity
  • number of catheter lumens
  • location of catheter
  • duration of placement (>72 hrs)
  • nursing staff ratio
56
Q

When do you suspect CAI (catheter - associated infection)?

A
  • local cellulitis
  • bacterimia without source
  • sepsis without source
  • non-functioning catheter
  • positive tip culture
  • pus at insertion site
  • rigors during the use of catheter

Diagnose if blood sample has 1:5 cfu of catheter sample (peripheral vs CVC)

OR

positive result of culture from a CVC is obtained at least 2 hr earlier than is a positive result of culture from peripheral blood

57
Q

Treatment of catheter associated infection? specifically, should catheter be removed?

A

For coagulase-negative Staph

  • CVC can be retained, if necessary, in patients with uncomplicated, catheter-related bloodstream infections
  • if CVC is retained, patients shoudl be treated with systemic antibiotic therapy for 7 days
  • threatment failure is a clear indication for removal of the catheter

Most likely organism in catheter associated infections is coagulase-negative Staph

58
Q

Prevention of catheter infections?

A
  • Try not to use femoral vein (probably b/c sweaty and more likely to be infected)
  • wash hands
  • use full-barrier precautions during placement of catheters
  • cleaning skin with chlorhexidine
  • removal of catheters that are no longer needed
59
Q

Risk factors for prosthetic joint infections?

A

memory aid: think about what old people often have:

primary:

  • rheumatoid arthritis
  • diabetes mellitus
  • poor nutritional status
  • obesity

revision:

  • prior joing surgery
  • prolonged OR time
  • preoperative infection (teeth, skin, UTI)

Main offenders:

  • Staph aureus
  • coagulase-negative staph
  • Strep
  • gram -ve bacilli
60
Q

What is antimicrobial therapy of Prostetic Joint Infections?

A
  • empirical therapy not recommended
  • treatment is based on culture and sensitivity
  • duration of at least 6 weeks after removal of infected prosthesis
  • MSSA: IV cloxacillin + PO rifampicin
  • MRSA/MRSE: vancomycin + rifampicin
  • Strep: IV penicillin G or ceftriaxone
61
Q

Key clinical features of septic shock as per notes?

A
  • myocardial depression (think cold shock)
  • altered vasculature (vasodilation!)
  • altered organ perfusion (vasodilation -> low bp -> less blood gets to tissues -> low perfusion (also reason for organ failure! in severe shock)
  • imbalance of O2 delivery and consumption (low bp -> less blood delivered to tissues)
  • metabolic (lactic) acidosis (low bp -> less blood delivered to tissues -> glycolysis stops at pyruvate and pyruvate cycles to lactic acid to regain NADH -> since O2 lacking lots of lactic acid produced -> lactic acidosis)
62
Q

What imaging clinical investigations can you order to confirm IE?

A

Chest X ray - more to rule out other causes, ex to see emboli or calcifications of heart valves

ECG - can show evidence of EI complications, like ST changes, arrhythmias

TransEsophageal Echo * is the shit, sensitivity of 75-95%, compared to TransThoracic Echo (TTE), with sensitivity of <60%

63
Q

Complications of EI?

A
  • Neuro complications (20-40%)
  • systemic emboli
  • splenic abscess
  • acute renal vailure in native valve 21% in prostetic 27%
  • prolonged fever
  • congestive heart failure
64
Q

Is surgery recommended in infective endocarditis?

A

Yes, mortality with medical intervention alone is 56-86% and with medical+surgical therapy it falls down to 11-35%