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HMS IDD > Infections of Joints > Flashcards

Infections of Joints Flashcards

1
Q

Three “buckets” for thinking of bacterial joint infection

A
  • Non-gonococcal
  • Gonococcal (N. gonorrheae)
  • Lyme (B. burgdorferi)
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2
Q

Microbial Arthritis etiology table

A
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3
Q

Essential Factors of Septic Arthritis

A
  • Acute onset of painful, warm, swollen, usually monoarticular arthritis
  • Arthrocentesis of synovial fluid >50,000 WBC / μL and >80% PMN
  • Positive synovial fluid culture
  • Staphylococcus aureus the most common cause
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4
Q

Epidemiology of septic arthritis

A
  • Higher incidence in children and elderly
  • Higher incidence in individuals who already have rheumatoid arthritis
  • Higher incidence in prosthetic joints
  • High risk for parenteral drug use
  • Diabetes mellitus is predisposing
  • Immunosuppression (including corticosteroid perscription!)
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5
Q

Sexual activity is a moderate risk factor for septic arthritis. Why?

A

Because it is associated with risk of gonococcal infection, which may lead to disseminated gonococcal infection (DGI), and this condition very commonly results in septic polyarticular arthritis.

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6
Q

Why is it so easy for bacteria in the blood to reach the synovium?

A
  1. The synovial membrane is thin and there is no basement membrane
  2. The tissue is highly vascularized, and so there are many points of entry
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7
Q

Without treatment, ___ may occur within days of joint infection.

A

Without treatment, irreversible subchondral bone loss and cartilage destruction may occur within days of joint infection.

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8
Q

Findings of septic arthritis on physical exam

A
  • Obvious joint effusion
  • Inflammatory signs
  • Pain
  • Marked restriction of both passive and active ROM
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9
Q

A patient with an acute monoarticular arthritis should be ___.

A

A patient with an acute monoarticular arthritis should be considered to have septic arthritis until proven otherwise

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10
Q

__% of cases of septic arthritis involve fever.

A

60-80% of cases of septic arthritis involve fever.

So, if the patient does not present with fever, septic arthritis cannot be ruled out.

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11
Q

Symptoms which indicate possibility of antecedent infection

A
  • Cough
  • GI symptoms
  • dysuria
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12
Q

Antecedent infections may be indentified in ___% of cases of septic arthritis.

A

Antecedent infections may be indentified in 50% of cases of septic arthritis.

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13
Q

Passive motion of the adjacent joint usually does not elicit severe pain unless . . .

A

Passive motion of the adjacent joint usually does not elicit severe pain unless there is stretching of an inflamed tendon

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14
Q

While synovial fluid analysis is critical for the definitive diagnosis of septic arthritis, . . .

A

While synovial fluid analysis is critical for the definitive diagnosis of septic arthritis, arthrocentesis is contraindicated if the needle must pass through an area of cellulitis, a skin lesion, or any lesion which may further introduce bacteria into the joint space.

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15
Q

Synovial fluid analysis for suspected septic arthritis

A
  • Appearance: Color and clarity (purulence and turbidity suggest infection)
  • Cell count and differential
  • Gram stain (positive is diagnostic, negative does not rule out septic arthritis)
  • Culture (positive is diagnostic, negative does not rule out septic arthritis)
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16
Q

Table of common nongonococcal septic arthritis etiologies

A
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17
Q

Plain radiographs for septic arthritis

A

Not very useful, but are done specifically to rule out contiguous osteomyelitis. May show bony changes due to inflammation in late septic arthritis (8 days out or later)

18
Q

Elements of history which may suggest crystal arthropathy over infection

A
  • History of recurrent monoarthritis (gout or pseudogout)
  • Typical podagra (gout)
  • Radiologic evidence of chondrocalcinosis (pseudogout)
19
Q

Major complications of septic arthritis

A
  • Osteomyelitis
  • Persistent or recurrent infection
  • Decrease in joint mobility
  • Aknylosis
  • Persistent pain
20
Q

Essential factors of disseminated gonococcal infection

A
  • Sexually active young person without history of joint disease
  • Triad of polyarthritis, tenosynovitis, dermatitis
  • Negative synovial fluid gram stain and culture
  • Urethral, cervical, pharyngeal, and rectal testing for Neisseria gonorrhoeae in aggregate are positive in up to 90% of cases
21
Q

The time from sexual contact to the onset of DGI varies from ___ to ___.

A

The time from sexual contact to the onset of DGI varies from 1 day to 2 months

22
Q

The disseminated gonococcal infection triad

A

polyarthritis, tenosynovitis, and dermatitis

23
Q

N. gonorrheae infection accounts for __% of monoarticular septic arthritis.

A

N. gonorrheae infection accounts for 20% of monoarticular septic arthritis.

It usually presents as oligo- or poly-articular

24
Q

Course of DGI

A
  • Initially presents as fever, chills, and polyarthralgia
  • Progresses to frank monoarthritis or polyarticular arthritis in knees, ankles, or wrists
  • Migratory tenosynovitis occurs in 2/3 of patients, usually over hand dorsum, wrist, ankle, knee
  • Painless skin lesions observed in 2/3 of patients, but may go unnoticed by patient
25
Q

Laboratory findings for DGI

A
  • Blood culture: Positive in only 20-30% of patients
  • Synovial culture: Positive in 20-50% of patients
  • Synovial cell count and differential: 30,000 - 60,000 WBC/μL
  • Synovial Gram stain: Positive in less than 25% of patients with DGI
  • Nucleic acid amplification tests on urethrum, cervix, pharynx, rectum: 90% sensitive
  • Imaging: Not particularly helpful
26
Q

Treatment of gonococcal septic arthritis

A
  • Closed drainage of purulent effusions required once or twice
  • Antibiotics quite effective in eliminating residual Neisseria
  • Prognosis very favorable in all patients who receive antibiotics, complete recovery in virtually all patients
27
Q

Essentials factors of Lyme arthritis

A
  • Reasonable risk of B. burgdorferi exposure in history or exam
  • Characteristic complex of Lyme symptoms (Stage I, Stage II, Stage III)
  • Supporting B. burgdorferi serology present in most cases, but not in very early infection
28
Q

Reasons B. burgdorferi-mediated disease is difficult to clear

A
  1. Downregulates major antigens (the spirochete lipoproteins) upon host residence
  2. Exhibits antigenic variation in VIsE protein
  3. Possess lipoproteins which bind Factor H and inhibit complement activation
  4. Residual pro-inflammatory products may persist even after B. burgdorferi is gone
29
Q

Borrelia burgdorferi-mediated disease

A

Cause Lyme disease. Begins as local infection and spreads to form erythemia migrans (bull’s eye). This is indicative ot stage I Lyme disease.

Within days to weeks, infection may spread via the blood to distant sites. The first metastasis is indicative of stage II Lyme disease. Cardiac involvement may lead to atrioventricular block or myopericarditis.

After months to years of latent infection, spirochetes may appear in the joints, nervous system, or skin. This is indicative of stage III Lyme disease. Repeated episodes of pauciarticular arthritis are a common presentation.

30
Q

Lyme disease diagram

A
32
Q

Stage I Lyme clinical presentation - Early Localized Infection

A
  • EM in 80% of patients, appears <30 days following infection, usually ~7-10 days
  • Systemic flu-like symptoms: Fever, malaise, neck pain/stiffness, arthralgia, myalgia
33
Q

Stage II Lyme clinical presentation - Acute Dissemianted Disease

A
  • Weeks to months of initial infection
  • May present in many sites, but most commonly: Skin (multiple EM, sometimes necrotizing), heart (conduction system abnormalities), MSK system (pauciarticular arthritis), nervous system (Lyme nervous triad)
  • Persistent, debilitating fatigue and malaise
  • Local symptoms may be intermittent
34
Q

Lyme nervous triad

A
  1. Aseptic meningitis
  2. Cranial neuropathy (usually facial nerve - CNVII)
  3. Painful, peripheral radiculoneuropathy (neuropathy affecting nerve roots)
35
Q

Stage III Lyme clinical presentation - Late Persistent Disease

A
  • Occurs in less than 10% of Lyme patients
  • Manifests in skin (multiple EM), joints (usually chronic monoarticular, especially the knee, may be due to residual antigen), nervous system (cognitive dysfunction, meningoencephalitis, sensorimotor neuropathy)
36
Q

Laboratory findings of Lyme arthritis

A
  • Synovial WBC count and differential: 2,000 - 100,000 WBC / μL, neutrophil predominance
  • Culture: Rare to culture from Lyme patients, not much utility
  • Serologic tests: Positive B. burgdorferi IgM (2-3 weeks post-infection) or IgG (>1 month post-infection) supports diagnosis in patients with >4 weeks of suggestive signs/symptoms
  • Western blot of host serum against purified B. burgdorferi antigen supports diagnosis
  • Radiographic imaging: Used to rule out other diagnoses
37
Q

Essential features of Parvoviral Arthritis

A
  • In children, parvovoris B19 / erythrovirus causes erythema infectosum.
  • Classic finding is a “slapped-cheek” facial rash
  • Minority of childhood cases involve joints
  • In adults, acute erythrovirus infection is associated with self-limited, symmetric polyarthritis that closely resembles rheumatoid arthritis
  • Diagnosis confirmed by detection of anti-B19 antibody in serum
38
Q

Erythrovirus epidemiology

A
  • Aerosol or respiratory secretion transmission
  • Cyclic outbreaks worldwide, winter and spring
  • Children main vector for transmission, and day care workers and school workers are major at-risk population of adult cases
39
Q

Erythrovirus course

A
40
Q

Parvovirus-mediated damage

A
  • Enters via respiratory tract
  • Infection of erythroid precursors
  • ~5 day viremic phase, flu-like symptoms (fever, malaise, cough, etc)
  • Appearance of IgM marks ending of viremic phase, ~1-1.5 weeks after exposure
  • IgG ~2 weeks after exposure
  • This is around when arthralgia/arthritis appear
41
Q

Clinical findings of parvoviral arthritis

A
  • 8% of children, 50-60% of adults experience joint symptoms
  • Typically ~2 weeks post-exposure, ~1 week post flu-like symptom onset
  • Women more commonly experience joint symptoms than men
  • Symmetric joint pattern consistent with typical RA pattern
  • “slapped-cheek” rash in 20% of patients, but general rash in 75%
  • Most symptoms subside on their own in 2-3 weeks, arthralgia may remain longer in absence of permanent joint damage
42
Q

Laboratory findings of parvoviral arthritis

A
  • ESR and CRP usually unaffected, not reliable metrics
  • Diagnosis dependent upon anti-B19 antibody detection (IgG and/or IgM)
  • Almost all infected patients demonstrate antibody response
43
Q

Treatment of parvoviral arthritis

A

Given the self-limited course of the disease, only symptomatic therapy is recommended (eg, simple analgesics or NSAIDs)

HMS IDD (28 decks)

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