Definition
Caseating granulomatous mycobacterium infection
Epidemiology
Great fall in incidence in West
- 1900 80% infected < 20
- 1990 5% infected secondary to immigrants
Found in
- asian immigrants
- aboriginal
- transplant patients 300 x Normal
- drug addicts
- AIDS
Sites
10% extrapulmonary
1% of skeletal
- half in spine
- mono-articular arthritis
Microbiology
2 species affect humans
1. M tuberculosis
- ? Bacilli
- most common
2. M bovis
- thin straight rods
Acid-Fast
- neither Gram positive or negative
- Ziehl-Neilsen Stain
- 2° to waxiness / high lipid in cell wall
Obligate aerobes
- prefer High PO2
Slow growth
- culture in Lowenstein-Jensen Medium
Pathogenesis
Produces no toxins or enzymes
Sensitisation
- occurs 2/ 52 after inoculation
- delayed cell-mediated, hypersensitivity
- positive Tuberculin test
- sensitised for life
Granulomatous Reaction
- initially Bacilli evoke non-specific neutrophilic inflammatory response
- phagocytosed by macrophages
- after sensitisation, reaction becomes granulomatous
- T cells become sensitised & induce macrophages aggregation
- granuloma formation
4 components to Granuloma
1. Epithelioid Cells
- resemble epithelial cells
- rounded & plump macrophages
2. Langhan's Giant Cells
- multinucleated, secondary to macrophages fusion
3. Rim of Fibroblasts
4. Central Caseous Necrosis
- liquefactive & coagulative
Pathology
Primary Infection
TB enters body via
- lung (aerosol) (most important)
- gut (milk)
- conjunctivae or skin (rare)
Primary Complex
Infection of unsensitised patient
- lesion in upper region lower lung
- phagocytosed TB multiply in macrophages
- spread to regional nodes
- 1° or Ghon Complex
- usually no clinical illness
- heals with fibrosis / calcification
If doesn't heal, may progress to
- progressive 1° TB of lung
- haematogenous seeding / Miliary TB
Reservoir of bacilli in nodes
- can be reactivated
Secondary Infection
Infection in previously sensitised
1. Reactivation
- most common
2. Reinfection
Usually in apical lung
- high oxygen content of area
- AKA Simon's focus
Tertiary Lesion
Destructive extrapulmonary lesion from 2° infection
- multiple lesions in 30% (miliary)
- any organ involved
Clinical Features
Initial infection usually asymptomatic
- slight malaise / fever
- lymphadenopathy
- pleurisy
Variable symptoms 2° TB
- fevers with night-sweats
- malaise
- weight loss
- cough / haemoptysis
CXR
Apical lesion
Multinodular infiltration with cavitation
Microbiology
Absolute proof is TB culture
Sputum
- early morning specimen
- bronchial washings
- multiple specimens
Ziehl-Neilsen Stain & Micro
- positive in 30%
Culture for 6/52
- positive in 80%
Tuberculin Skin Test
Mantoux test
- protein fraction of TB injection (0.1 ml injected into volar forearm skin)
- negative excludes diagnosis
- positive - previous sensitisation only or BCG immunization
Delayed hypersensitivity skin oedema in infected patients
Read 2/7
- delayed hypersensitivity
- positive > 10 mm
- negative < 5 mm
BCG Immunisation
- Bacillus Calmette-Guerin
- live attenuated strain of Bovine Tubercle Bacilli
- doesn't eliminate chance of infection
- prevents development of serious disease when infection occurs
- use questionable in areas with low incidence
- invalidates Mantoux
- prevents early detection
Management
Antibiotics
Isoniazid
- interferes with DNA synthesis
- side effects peripheral neuropathy / liver toxicity / anaemia
Rifampicin
- inhibits RNA synthesis
- SE's Jaundice / GIT symptoms / Fever
Protocol
- combination of Isoniazid & Rifampicin for 9/12
- other drugs for Resistant TB
Joint Infection
Cause
- haematogenous seeding of synovium
- direct spread from bony abscess (unusual in that infection can cross physis)
Pathology
- synovium thick & oedematous
- marked effusion
- rice bodies formed ~ fibrin globules
- pannus of granulation tissue spreads across Joint
- gradual destruction of cartilage
- healing usually by fibrous ankylosis
History
- insidious onset
- long history of mild joint pain
- swelling & frequent effusions
- weight loss & night sweats
Examination
- thick synovium / effusion / lightly warm
- late FFD & deformity
- fibrous or bony ankylosis
X-ray
- joint becomes disorganized
- DDx Charcot joint
Management
- antibiotic
TB Spine / Pott's Disease
Epidemiology
L1 most often
- rare in cervical & sacral spine
- usually > one body
Pathology
Disco-Vertebral Lesion
Spread is most likely arterial
- not Batson's venous plexus
TB spreads to adjacent discs
- infection can then extend to involve multiple vertebral bodies
- posterior elements rarely involved
Bony Collapse
- result is sharp kyphotic deformity
- Gibbus
Para-spinal Extension
- usually anterolaterally
- abscess may burrow for long distances
- lumbar Abscess extends under Psoas fascia = Psoas abscess
- may extend into groin & thigh
- abscess may penetrate various organs esp Lung
Cord Compression / Injury
- pressure from abscess / caseous material / sequestrum
- ischaemia 2° spinal artery thrombosis
- progressive kyphosis
Clinical
Long history of ill health
Backache
Kyphotic Deformity
Cold abscess in loin or groin
Paraesthesia / weakness of legs (Pott's Paraplegia)
X-ray
- multiple vertebrae involved
- average 3-4
- collapse of adjacent bodies into each other
- resulting angular deformity
Bloods
- Mantoux +ve
- ± ESR raised
Management
1. Eradicate or arrest disease
- 9/12 Isoniazid and Rifampicin
- 90% favourable outcomes
- no advanatage debridement / bracing
2. Correct deformity
3. Prevent or treat paraplegia