TB

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