LG 3.6 Micro Joint Infections Flashcards

1
Q

3 most common organisms that cause NJI:

A
  1. Staph aureus (nongonococcal) 2. Neisseria gonnrrhoeae (gonococcal) 3. Borrelia burgdorferi
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2
Q

2 most common organisms causing PJI:

A

S. aureus, S. epidermidis

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3
Q

IDing info for S aureus

A

o Gr+ cocci, clusters o Catalase +, Coagulase +, Mannitol fermenter, beta-hemolytic o Facultative anaerobe o Ubiquitous, normal microbiota (nares, skin, mucous membranes)

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4
Q

virulence factors S aureus

A

• SCCmec chromosome → Panton-Valentine leukocidin (PVL) • Protein A • SCCmec chromosome → mecA gene • Enzymes • Fibronectin-binding protein

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5
Q

ID info for Staph epidermidis

A

o Gamma-hemolysis, catalase +, coagulase -, mannitol fermentation -

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6
Q

virulence factors for Staph epidermidis

A

o Slime layer o Adhesins o biofilms

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7
Q

ID info for Eikenella corrodens

A

o Gr- rod - facultative anaerobe o Normal microbiota (mouth, GU, GI) (Human bite/clenched fist injury infix.) o Pit agar o Bleach-like odor

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8
Q

ID info for Kingella kingae

A

o Gr- coccobacillus o Human reservoir (normal microbiota: oropharynx) mostly kids o Facultative anaerobe o Beta-hemolytic o Oxidase +

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9
Q

Virulence factors K kingae

A

(Low virulence) damage to respiratory mucosa (e.g. viral) facilitates invasion bloodstream

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10
Q

ID info for Neisseria gonorrhoeae (morphology and habitat only)

A

o Gr- diplococci o Human reservoir

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11
Q

other ID info for Neisseria gonorrhoeae

A

• Aerobe to facultative anaerobe • Oxidase + • Catalase + • Oxidizes glucose • chocolate or Thayer-Martin (=chocolate agar + antibiotics)

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12
Q

Gonococcal virulence factors (5 of them)

A
  1. Adhesions (Opa, pili) 2. IgA1 protease 3. facultative intracellular 4. antigenic and phase variation (Opa, pili, LOS) 5. outer membrane blebbing
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13
Q

symptoms of DGI and gonococcal arthritis

A
  1. main (red) one: septic arthritis 2. also low-grade fever, petechial skin lesions migratory polyarthralgia
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14
Q

nongonococcal arthritis symptoms

A

o fever, joint pain (hot, swollen), impaired range of motion • usually monoarticular o knee most common

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15
Q

gonococcal arthritis symptoms

A

o DGI symptoms plus… o polyarticular (less often mono) arthritis (knee, wrist, ankle, elbow) o less joint damage than non-gonococcal arthritis

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16
Q

describe the three-part diagnostic strategy for NJI

A

• I.D. bacteria in synovial fluid is definitive o WBC count + gram-stained smear + culture

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17
Q

Diagnosing PJI (*not a posted objective)

A

o More difficult than NJI • less inflammation • infecting agent may be lacking in synovial fluid • biofilms not readily cultured

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18
Q

explain the role of biofilms in the pathogenesis and diagnosis of PJI

A

• biofilms complicate! o resting state • smaller inflammatory response • antibiotic protection • tougher to isolate microbes

19
Q

what’s Lyme Disease vector?

A
  1. blacklegged tick (‘deer tick’) Ixodes scapularis in hyperendemic regions eastern U.S 2. nymph is primary vector
20
Q

What’s Lyme Disease reservoir

A

rodent reservoir, esp. white-footed mouse

21
Q

In US, where are most reported Lyme Disease cases?

A

northeast and upper midwest US

22
Q

Describe seasonality of Lyme Disease

A
  1. between 2001 - 2010, most cases by far in June/July (70 - 80K) 2. second most in August and May (30K and 20K, respectively). 3. Lyme’s is most commonly reported vectorborne illness in US
23
Q

describe interplay between deer tick, rodent, human in Lyme Disease

A
24
Q

ID factors for Borrelia burgdorferi

A

Gr- spirochete
Microaerophile

25
Q

virulence factors for burgorferi

A

very motile

(bundles of axial filaments between plasma membrane and outer membrane)

26
Q

descibe Early localized Lyme Disease

A

Tick bite –> several days to 1 month later erythema migrans = bull’s eye rash appears (80% get this)

27
Q

describe early disseminated Lyme disease

A
  1. weeks to months after bite
  2. at this point Lyme disseminated systemically (skin, heart, CNS, joints) 3. could have corresponding systemic symtoms
28
Q

Late Lyme symptoms

A
  1. after months to years
  2. usually manifests as chronic arthritis = Lyme arthritis
  3. 60% untreated get this
  4. occasionally with constitutional symptoms
    large joints most common (knee monoarthritis most common
    even w/out antibiotics usually resolves, but can last for years
29
Q

Not really helpful to culture Lyme. why?

A

there are few spirochetes in blood, tissues

and culture not available most clinical labs

30
Q

name and describe 2 types of immunologic (serologic) methods of diagnosis

A
  1. direct

looking for presence of microbe antigens
uses known antibody

  1. indirect

looking for host antibodies directed against microbe antigens
uses known antigens
current exposure, previous exposure

31
Q

titer

A
  1. results of many immunologic tests expressed as titer
  2. highest dilution (lowest concentration) of specimen (e.g. serum) that gives a positive reaction in test
32
Q

how is titer expressed?

A

expressed as reciprocal of highest dilution (lowest concentration)

33
Q

how does titer confirm new infection?

A

to confirm a new infection→ usually have to demonstrate either seroconversion or a rising titer→ a fourfold ↑ in a convalescent titer obtained 2-3 wks after the acute titer is considered diagnostic in most situations

34
Q

ELISA

A
  1. enzyme-linked immunosorbent assay
  2. uses an enzyme as label
  3. reaction of the enzyme with its substrate produces a colored product → positive test
  4. can detect either antibody or antigen
  5. indirect more common in I.D.
  6. quantitative
35
Q

Western blot procedure

A

microbial proteins separated

         ↓transferred to membrane

incubated w/ patient serum

secondary antibody (w/ enzyme or radioactive isotope as label)

add substrate for enzyme

bands ‘light up’ where antibody recognizes each antigen

36
Q

How to diagnose early localized Lyme

A

made on clinical grounds alone when characteristic erythema migrans lesion present in patient who lives or has recently traveled to endemic area

37
Q

How to diagnose early dissiminated/late Lyme

A

based on clinical + serology when patient lives or has recently traveled to endemic area

38
Q

What are the 3 ways that native joint infections can occur?

A

*Hematogenous spread.

Direct inoculation (trauma, bite).

Extension of osteomyelitis.

39
Q

What is the most common infectous agent to cause early PJI, late PJI?

A

Early = Staph. Aureus, more virulent.

Late = Staph. Epidermidis, less virulent.

40
Q

When would you use a chocolate agar plate vs. a Thayer-Martin plate for ID of N. Gonorrhoeae?

A

Chocolate for fluid from joint. (nothing else should be in the joint so easy to ID alone).

Thayer-Martin for rectal, blood, throat (many other organisms here so you want to screen them out).

41
Q

Regarding PMN counts how can you tell between gonococcal and nongonococcal infiltration?

A

S. aureus large infiltration PMNs

N. gonorrhoeae smaller infiltration PMNs

42
Q

What is seroconversion?

A

Test patient serum, they don’t have it.

Check again at a later time, now they do have it.

43
Q

K kingae leading cause of _____ infx in _______ age-group.

A

septic arthritis, osteomyelitis <4 years age