Tuberculosis

By Saad Hmemat

We will talk about…

Epidemiology…

Pathology…

Clinical features…

X-ray…

Investigations…

Diagnosis…

Treatment…

Epidemiology

Decline in its prevalence in developed

countries due to effectiveness of public health

programmes, improvement of nutritional

status & advanced chemotherapy.

Extra-pulmonary TB has risen again in the

last 20 years due to increase in proportion of

elderly people & spread of IV drug abuse.

Skeletal manifestations of the disease chiefly

seen in spine & large joints, but also may

appear in any bone or any synovial or bursal

sheath.

Predisposing conditions include:

Debilitating disorders like AIDs & other

disorders result in reduced defence

mechanism.

Diabetes

Drug abuse

Prolonged corticosteroid use as medication

Pathology Mycobacterium tuberculosis enters human via lung

(droplet infection) or gut (swallowing infected milk

products) or rarely through skin, that will cause

granulomatous reaction which is associated with tissue

necrosis & caseation.

Initial lesion in lung, pharynx or gut is a small one with

lymphatic spread to regional lymph nodes, a

combination called primary complex.

This bacilli usually fixed in nodes with no clinical illness

results but occasionally the response is excessive with

enlargement of glands in neck or abdomen, even

though there is no clinical illness.

Initial infection has two important sequels:

Bacilli within nodes which are apparently

healed may survive for many years so that a

reservoir exists.

Body has been sensitised to the toxin and

reinfection should occur, the response is

quite different & the lesion being a destructive

one which spread by contiguity

Note: a positive heaf test being index of

sensitisation (which is a diagnostic skin test

performed to determine whether or not

someone exposed to TB infection).

If resistance to original infection is low,

widespread dissemination via blood stream

months or years later during period of

lowered immunity & bacilli deposited in extra

pulmonary tissues giving rise to miliary TB or

multiple TB lesion, Secondary spread.

When foci develop into destructive lesions

tertiary term applied.

Bones or joints affected in about 5% of

patient with TB with predilection for the

vertebral bodies & large synovial joints.

Multiple lesions occur in about one third of

patient.

It’s difficult to tell whether infection started in joint

and then spread to adjacent bone or vice versa..

ex: synovial membrane & subchondral bone have

common blood supply and infected

simultaneously.

Once bacilli gain a foothold they elicit chronic

inflammatory reaction, characterised histologically

by tuberculous granuloma or tubercle which is a

collection of epithelia & multi-nucleated giant cells

surrounding area of necrosis with round cells

mainly lymphocytes around periphery.

Within affected area small patches of caseous

necrosis appear, that may coalesce into larger

yellowish mass or centre may break down to form

an abscess containing pus & fragment of necrotic

bone.

Bone lesion spread quite rapidly & epiphyseal

plate is no barrier to invasion & soon infection will

reach joint.

Only in vertebral bodies & more rarely in greater

trochanter of femur or metatarsal and metacarpal

infection persist as a pure chronic osteomyelitis.

If the synovium is involved it become thick &

oedematous giving rise to a marked effusion. A

pannus of granulation tissue may extend from

synovial reflection across the joint, articular

cartilage slowly destroyed.

At the edges of the joint along the synovial

reflection there maybe active bone erosion. In

addition, increased vascularity causes local

osteoporosis.

If unchecked, caseation & infection extend into surrounding

soft tissue to produce abscess that may burst through skin

forming sinus or TB ulcer or it may track along tissue planes

to point at some distant site.

If the disease arrested at an early stage healing maybe by

resolution to apparent normality.

If articular cartilage has been severely damaged, healing is

by fibrosis & incomplete ankylosis with progressive joint

deformity. Within the fibrocaseous mass mycobacterium

remain imprisoned retaining potential to flare up into active

disease many years later.

Clinical features

The patient usually a child or young adult

complains of pain & swelling in joint. In

advanced cases there maybe attacks of

fever, night sweats, lassitude (lack of energy)

and loss of weight.

The joint splinted (secured) by muscle spasm

during waking hours, relaxes with sleep & the

inflamed or damaged tissues are stretched or

compressed causing sudden episodes of

intense pain, term called Night cries.

Muscle wasting, tender, enlarged regional lymph

nodes & movement are limited in all directions.

As articular erosion progresses the joint becomes

stiff & deformed.

TB of spine. Patient may not be present until

there is visible abscess usually in the groin or the

lumbar region to one side of midline, or until

collapse causes a localised kyphosis with slight

pain. Occasionally the presenting feature is

weakness or instability in the lower limb.

In people with lowered resistance we may see

multiple foci of infection with bone & joint lesions

at different stages of development.

X-Ray

Soft tissue swelling & peri-articular osteoporosis are

characteristic.

Bone ends take on a “washed out” appearance & the

articular space is narrowed.

In children the epiphyses maybe enlarged probably

the result of long continued hyperaemia.

Later on there is erosion of subarticular bone seen

on both sides of the joint, indicating an inflammatory

process starting in the synovium.

Cystic lesion may appear in the adjacent bone

ends but there is no or little periosteal

reaction.

In the spine the characteristic appearance is

one of bone erosion & collapse around a

diminished intervertebral disc space, soft

tissue shadows may define a paravertebral

abscess

Investigations ESR usually increased & there may be a relative

lymphocytosis.

Mantoux (tuberculin sensitivity test) or heaf test will be positive

(a sensitive but not specific tests).

Cloudy, increased protein concentration, elevated white cell

count & acid-fast bacilli are identified in 10-20% of cases in

aspirated synovial fluid.

Synovial biopsy for histological examination is more reliable,

sections will show the characteristic histologic features & acid-

fast bacilli maybe identified.

Cultures are positive in about 80% of patient who have not

received antimicrobial treatment.

Diagnosis

Diagnosis is often delayed simply because the diseases is not suspected,

except in areas where tuberculosis is common.

Features that should trigger more active investigation are:

Long history of pain & swelling

Involvement of only one joint

Marked synovial thickening

Severe muscle wasting

Enlarged regional lymph nodes

Peri-articular osteoporosis on X-ray

Positive Mantoux test (tuberculin sensitivity test)

Joint TB must be differentiated from the

following:

Transient synovitis, at first it seems no different from

any other low-grade inflammatory arthritis & always

settles down after a few weeks rest in bed. (common

in children)

Mono-articular rheumatoid arthritis, starts in a single

large joint (indistinguishable from tuberculosis) &

diagnosis have to wait the results of synovial biopsy.

Subacute arthritis

Hemorrhagic arthritis, the physical signs of blood in a

joint may resemble tuberculous arthritis.

Pyogenic arthritis

Treatment

Rest

Chemotherapy

Operation

Long ago TB should be treated by rest

through splintage of the joint and traction to

overcome muscle spasm & prevent collapse

of the articular surface.

Those who are diagnosed & treated early are

kept in bed only until pain and systemic

symptoms subsides, thereafter are allowed

restricted activity until joint changes resolve

(usually 6 months to a year).

Those with progressive joint destruction need

longer period of rest & splintage to prevent

ankylosis in bed position.

The most effective treatment is a combination

of anti-tuberculous drugs that should always

include rifampicin & isoniazid.

During the last decade drug resistance has

increased & this has led to addition of

potentiating drugs.

Operative drainage or clearance of

tuberculous focus is necessary nowadays.

Once the condition is controlled & arthritis

has completely subsided, normal activity can

be resumed & the patient must report any

renewed symptoms.

If joint is painful & articular surface is

destroyed, arthrodesis or replacement

arthroplasty may be considered.

It’s essential to give chemotherapy for 3

months before & after the operation.

If there is any question feel free to contact

Alan Graham Apley but unfortunately he’s

dead !!!

Instead, you can ask our awesome doctor

!

Je vous remercie