Download SDL 17- Infectious Arthritis Infectious arthritis/ septic

SDL 17- Infectious Arthritis
Infectious arthritis/ septic arthritis: synovial inflammatory reaction secondary to joint invasion by microbes
Chronic: caused by slowly progressive/difficult to eradicate organisms (mycobacteria and fungi)
Acute
caused by pyogenic bacteria and termed septic/suppurative
Hematogenous: route of bacteria
Large joints are infected more commonly than small joints
Monoarticular infection (80% or more of cases)
Nongonococcal: Nongonoccal bacteria; Staph aureus is most common cause
Rapidly destructive form of joint disease (days)
Significant morbidity
2 peaks in age:1. children less than 5 years of age (75% in previously healthy children)
2. adults older than 64 years (75% have pre-disposition: prosthetic joint, RA, malignancy, diabetes,
immunosuppressives, skin infection)
Source of Infection
Hematogenous seeding during bacteremia: most common
 Infections of the cutaneous, respiratory, urinary systems or oral cavity.
 Invasive procedures of the cutaneous, respiratory, urinary systems or oral cavity.
 Intravenous catheters.
 Injection of illicit intravenous drugs.
Direct inoculation: second most common
Contiguous source: osteomyelitis (mainly in children)
Infants less than 1 year: metaphyseal blood vessels transverse the epiphyseal growth plate
providing a conduit for infection
Older children: break the outer cortex and cause secondary septic arthritis
Adults: skin infection and diabetic foot ulcer are most common
Microbiology
Staphylococcus aureus (most common) for adults and children
Staph epidermidis (coagulase neg.): major isolate in early onset prosthetic joint infection
Streptococcus spp: second most common; Group B > group A (hemolytic) > S. pneumonia
Gram negative: P. aeruginosa and E. coli
At risk: IV drug users, young children, elderly, immunocompromised, extra-articular infections
Pathogenesis (Multifactoral)
Bacterial colonization: synovium is a highly vascularized structure without a limiting basement
membrane allowing for easy entry of hematogenously spread bacteria. Within the joint space, the
environment is largely avascular (due to hyaline cartilage) that favors colonization. S. aureus can adhere.
Fibronectin-binding proteins are the most important virulence factors (95% of the strains isolated)
Bacterial virulence factors: capsular polysaccharides interfere with opsonozation and phagocytosis
Microcapsule: shown to be important in early colonization of the joint (adhesion)
N-formyl-methionine proteins and techoic acids are potent mediators of joint inflammation due to
binding and activation of toll-like receptors (TLRs)
Pathogenesis (continued)
SDL 17- Infectious Arthritis
Host immune response: acute inflammatory response (IL-1B and IL-6): acute phase proteins from the
liver complement system. TNFa activates neutrophils (phagocytosis); monocytes/macrophages after
Joint damage: If the infection is not rapidly cleared, there is activation of the immune response with
elevated levels of inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8, and granulocyte macrophage colony
stimulating factor), and with reactive oxygen species in the joint space that can lead to rapid joint
destruction. Inflammatory causes release of metalloproteinases and lysosomal and proteolytic enzymes
from invading neutrophils. This can cause degradation of cartilage in 3 days.
Infection with N. gonorrhea causes mild influx of neutrophils
Risk factors: extremes of age, underlying joint disease prosthetic joint, diabetes mellitus and skin infections
Old age: chonic disease, decreased immunocompetence
Underlying joint disease: RA, prosthetic joints
Diabetes mellitus: reduces body’s defense against invading microorganisms
Skin: increases the risk of bacteremia
Clinical Manifestations: typically the patients present with fever, malaise, single joint that is hot, red, severely
painful, swollen, and has a markedly decreased range of motion due to obvious synovial effusion
Monoarticular: 90% and knee (50%) hip (20%) shoulder (8%) ankle (7%) wrist (7%)
Oligoarticular: 2-3 joints (10% of cases)
Laboratory Findings: blood cultures positive 50%; leucocytosis with left shift
ESR and C-reactive protein elevated
Synovial Fluid Findings: via aspiration
90% of cases positive; glucose concentration is 50% below blood glucose level
Imaging Studies
Radiology: Initially normal, earliest plain film radiographic findings are soft tissue swelling around the
joint and a widened joint space from joint effusion. With progression of the disease, plain films reveal
joint-space narrowing. Loss of visualization of the white cortical line over large areas of the joint surface
soon ensues as bone destruction develops
Ultraconography: sensitive modality for the detection of joint effusion
CT and MRI: distinguishes osteomyelitis, periarticular abscesses, and joint effusions. MRI is preferred
because of its greater ability to image soft tissue. Joint effusion, joint-space narrowing, bone and
cartilage erosions, gas within the joint and soft tissue swelling
Treatment: antimicrobial therapy, drainage, immobilization
Antibiotic treatment: Emperical based on organism (culture and gram stain)
S aureus= IV penicillin (nafcillin)
MRSA= vancomycin
Joint drainage: needle aspirate numerous times
Joint mobilization: immobilization to preserve joint function, Isotonic excercise
50% full recovery; 35% irreversible loss of function; 11% mortality rate
SDL 17- Infectious Arthritis
Gonococcal: Neisseria gonorrhea (causes STD; gram neg diplococcus
less morbidity and different clinical presentation
18-35 years of age
4 times more common in women (because gonorrhea is more often asymptomatic in women= not treated)
Affects endocervix and urethra in women and urethra and epididymis in men
Hematogenous spread “disseminated gonococcal infection” DGI
Joint is most common site of colonization of disseminated gonococcus
Risk Factors for DGI
Virulence of N. gonorrhoeae, diagnosis delay, complement system deficiency, systemic lupus erythematosus,
female gender, menstruation, pregnancy, male homosexuality, and low socioeconomic and educational status.
N. gonorrhea virulence: antigenic variation of gonococcal pili; Proteins I, II, III, Lipo-oligosaccharide
Complement system deficiency: 13% patients
Female gender: women 4x more likely; menstruation is major factor for dissemination
Clinical Manifestations
Time from last sexual encounter (initial infection) to initial manifestations of arthritis is 1 day to 2 months
Promodal signs: mirgratory arthralgias in polyarticular patients; arthralgias are asymmetric and involve upper
extremities more than lower (resolve spontaneously in 30-40%)
Two forms of DGI
1. Tenosynovitis: 60% of cases; rare in most other forms of septic arthritis
Inflammation of the synovial sheath that surrounds a tendon (swelling, pain, difficult ROM)
Assymetric in dorsum of hands, wrists, ankles, toes
Dermatitis: extremities or trunk (spares face). Lesions are usually tiny macropapular, pustular,
or vesicular lesions (~5mm) on an erythematous base (painless, nonpuritic)
2. Purulent arthritis: joint symptoms begin within days to weeks (inflammation, synovial WBC count
50,000 (lower compared to non-gonococcal)
Fever, myalgias, malaise
Laboratory studies
Gram stain ID of gram-neg intracellular diplococci(synovial fluid in 50%)
Thayer-Martin agar
Pathogenesis
Clinical presentation resembles serum sickness (tenosynovitis and migratory arthralgias)
Positive genitourinary cultures are found in most patients with DGI (positive synovial fluid ad blood
cultures are found only in a minority of patients)
Tuberculous Arthritis: direct invasion from adjacent focus of tuberculous osteomyelitis or hematogenous dissemination
from lungs, lymph nodes or other viscera
Risk Factors
Certain socio-economic classes: in non-endemic regions generally older people (old-homes, poor,
homeless, prisoners, jail inmates, alcoholics)
Immunocompromised host: HIV, diabetes, malnutrition, alcoholism, chronic renal failure, liver;
corticosteroid therapy, cytotoxic drugs
Local joint and bone tissue factors: joint/bone trauma (RA, systemic lupus erythematosus, gout,
prosthetic joint, osteonecrosis)
Clinical Presentation: 85% with chronic monoarthritis involving large and medium weight-bearing joints
Men older than 50 years
Chronic progressive low-grade joint pain and swelling without warmth or erythema, and stiffness with
slowly progressive loss of function, often with eventual abscess formation. Constitutional symptoms,
including fever, night sweats, weight loss and anorexia, may be present. However, a significant number
of patients may have no systemic symptoms.
Imaging: Phimister triad: periarticular osteoporosis, peripherally loacated osseus erosion, gradual diminution of
the joint space (in RA and pyogenic arthritis the joint space narrows early)
SDL 17- Infectious Arthritis
Diagnosis: synovial fluid findings are variable; acid fast smear positive in 10-20% (80% of synovial fluid cultures
are positive). Typical caseous granulomas (94%)
Disease course: if untreated, complete joint obliteration with fibrous ankylosis
Lyme Arthritis
Spirochete Borrelia burgdorferi transmitted via lxodes or deer tick
Clinical presentation of Lyme disease
Early Localized Infection: erythema migrans arises within 1 month at tick bite site (bulls-eye)
Systemic flulike symptoms (fever, malaise, neck pain, arthralgias, myalgias
Early Disseminated Infection: within weeks of infection it disseminates through skin, blood, lymph
Deabilitating fatigue and appear ill: multiple EM lesions, sign of disseminated infection
Migratory muscle, joint, and periarticular pain (hours to days)
Atrioventricular block occasionally accompanied with mild myopericarditis
Meningitis, headache, photophobia, stiff neck
Late disease: months after the onset of infection, untreated patients can develop arthritis,
encephalomyelitis
Monoarticular or oligoarticular with 80% in knee
Recurrent episodes
Synovial fluid: inflammatory with WBC counts of 24,000 (neutrophils)
Synovial biopsy: chonicicity of arthritis, mononuclear cell infiltration
Antibiotic-refractory: 10% treated with antibiotics for Lyme disease suffers persistent joint
inflammation (maybe due to molecular mimicry via T cell reaction with self-antigen)
Laboratory findings: nonspecific
Diagnosis: detection of antibodies to B. burgdorferi; 5% positive for Lyme disease
ELISA or indirect immunoflourescence assay to detect IgM and IgG reactivity to B. burgdorferi
Western blot to confirm
Imaging: limited role in evaluation of patients with Lyme disease. Plain radiographs of arthritic joints
show changes consistent with an inflammatory arthropathy including joint effusions, synovial
hypertrophy, periarticulas osteoporosis, cartilage loss, bony erosions
Viral Arthritis
Inflammation of the joints caused by a viral infection
Etiology: parvovirus B19; hep A, B, C; rubella virus; alphaviruses (togaviridae family); human immunodeficiency
virus; human T-lymphotropic virus 1; Epstein-Barr virus; mumps virus; varicella-zoster virus; adenovirus;
coxsackievirus, and herpes simplex virus.
Epidemiology: exact incidence unknown and vary with type of virus/age range
Clinical Presentation: symmetrical small-joint involvement (hands, wrists, knees, ankle) with prominent morning
stiffness and fusiform swelling but not erythema
Last from weeks to months, can be severe at onset: progressively resolves and is non-destructive
Diagnosis: usually by symptoms and serology (medical history, recent travel and exclusion of other rheumatic or
febrile illnesses
Most viral arthritides do not result in erosive joint changes and show only ST swelling
Pathogenesis: speculation that autoimmune responses induced by infection lead to autoimmune disease
Mechanism is poorly understood
Treatment: usually involves NSAIDS with steroids or interferon (avtivirals where available)