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

24
Q

ID factors for Borrelia burgdorferi

A

Gr- spirochete
Microaerophile

25
virulence factors for burgorferi
very motile (bundles of axial filaments between plasma membrane and outer membrane)
26
descibe Early localized Lyme Disease
Tick bite --\> several days to 1 month later erythema migrans = bull’s eye rash appears (80% get this)
27
describe early disseminated Lyme disease
1. weeks to months after bite 2. at this point Lyme disseminated systemically (skin, heart, CNS, joints) 3. could have corresponding systemic symtoms
28
Late Lyme symptoms
1. after months to years 2. usually manifests as chronic arthritis = Lyme arthritis 4. 60% untreated get this 5. occasionally with constitutional symptoms large joints most common (knee monoarthritis most common even w/out antibiotics usually resolves, but can last for years
29
Not really helpful to culture Lyme. why?
there are few spirochetes in blood, tissues and culture not available most clinical labs
30
name and describe 2 types of immunologic (serologic) methods of diagnosis
1. direct looking for presence of microbe antigens uses known antibody 2. indirect looking for host antibodies directed against microbe antigens uses known antigens current exposure, previous exposure
31
titer
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
how is titer expressed?
expressed as reciprocal of highest dilution (lowest concentration)
33
how does titer confirm new infection?
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
ELISA
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
Western blot procedure
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
How to diagnose early localized Lyme
made on clinical grounds alone when characteristic erythema migrans lesion present in patient who lives or has recently traveled to endemic area
37
How to diagnose early dissiminated/late Lyme
based on clinical + serology when patient lives or has recently traveled to endemic area
38
What are the 3 ways that native joint infections can occur?
\*Hematogenous spread. Direct inoculation (trauma, bite). Extension of osteomyelitis.
39
What is the most common infectous agent to cause early PJI, late PJI?
Early = Staph. Aureus, more virulent. Late = Staph. Epidermidis, less virulent.
40
When would you use a chocolate agar plate vs. a Thayer-Martin plate for ID of N. Gonorrhoeae?
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
Regarding PMN counts how can you tell between gonococcal and nongonococcal infiltration?
S. aureus large infiltration PMNs N. gonorrhoeae smaller infiltration PMNs
42
What is seroconversion?
Test patient serum, they don't have it. Check again at a later time, now they do have it.
43
K kingae leading cause of _____ infx in _______ age-group.
septic arthritis, osteomyelitis \<4 years age