This document discusses the history and pathogenesis of tuberculosis, with a focus on skeletal tuberculosis. It details how Robert Koch discovered the bacterial cause of tuberculosis in 1882. It then explains the typical progression of skeletal tuberculosis, including how the bacteria spreads hematogenously and causes formation of epithelioid cells, Langhans' giant cells, and caseating granulomas. The document also outlines treatments for skeletal tuberculosis including rest, nutrition, drug therapy, surgery, and discusses diagnostic tools such as imaging and labs.

2.  Discovered that anthrax was caused by bacteria
 Discovered how to grow bacteria in cultures for study
and how to add stain in order to see them
 Proved that most diseases are caused by a particular
type bacteria
 Discovered the tubercle bacillus in 1882 where one in
seven deaths in Europe was due to TB

3.  Samhitha of Charaka and Susrutha ( 1000- 600BC) called
this disease as YAKSHAMA
 Greek- roman
PHTHISIS or CONSUMPTION
 Egyptian mummied – lesions were recorded
 Laennec (1781-1826)
French physician described the TUBERCLE

4.  20 % of AIDS patients have TB
 50 % of young adults with TB
have AIDS

8.  Skeletal tuberculosis is a chronic infectious
disease caused by Mycobacterium
tuberculosis.

9.  Predisposing factors
 Poor diet and sanitation
 Direct injury
 Reactive disease
 Measles and chicken pox

10.  Skeletal TB always secondary
 Hematogenous spread

11.  Initial response
in reticulo-endothelial skeletal tissue
polymorphs replaced by mononuclear cells
highly phagocytic – bacilli phagocytosed and broken down
lipid dispersed in cytoplasm of mononuclear cells – EPITHELIOD CELLS

12.  EPITHELOID CELLS
characteristic of TB
large and pale with large vesicular nucleus
abundant cytoplasm, indistinct margins

13.  LANGHAN’S GIANT CELLS
fusion of many epithelioid cells
peripheral nuclei
often contains TB bacilli
seen only in caseation necrosis
digest and remove dead tissue

14.  After 1 week
lymphocytes appear
form a ring around the lesion
mass of newly fromed cells
translucent nodule- TUBERCLE
several tubercles fuse to a larger one

15.  During 2 week
caseating necrosis
liberation of protein fraction of bacilli
caseation is diagnostic

16.  Local destruction of the joint, marked demineralization with surrounding lytic
areas (PHEMISTER TRIAD)
 Extension of the granulation tissue from the synovium on to the bone , at the
periphery of the articular cartilage the granulation tissue forms a ring (PANNUS)
which grows ion the subchondral region

17.  RICE BODIES: flakes of loose sheets of necrotized articular cartilage and
fibrinous material in the synovial fluid

18.  Cold abscess is formed by a collection of products of liquefaction and t reactive
exudation.
 Mostly composed of serum, leukocytes, caseous material, bone debris and tubercle
bacilli
 Penetrates the ligaments and migrates in various direction following the fascial
planes and along the vessels and nerves
 Feels warm
 May burst into form a sinus or ulcer
 Walls of abscess , sinus or ulcer are covered with tuberculous granulation

20.  Cord compression
quadri/paraplegia
 Tense paravertebral abscess with or without neurological symptoms

21.  Pus produced at the site of pathology may stay at
the same vertebral level
 May track down the paths of least resistance
along the fascial planes , vessels or nerves
 Present as a cold abscess in different regions far
away from the site of pathology

22.  Cervical and upper dorsal abscess track
down upto D4
retropharyngeal abscess
posterior mediastinal mass

23.  From D4 – D10 lesions present on either side of the
vertebral body contained in a thick walled sac leading to a
bird’s nest abscess
 May track along the
intercostal nerves
midaxillary
parsternal

24.  Below D11 lesions
 May present as late as then psoas
sheath can accommodate lot of pus
 May track behind the medial arcuate
ligament of the diaphragm along the
sheath up to its insertion into LT
 Present as groin swelling pushing
forward the femoral artery

25.  May track down behind lateral arcuate ligament between lumbodorsal fascia and
quadratus lumborum
 May remain kidney
 May track along three nerves
subcostal
ilioinguinal
iliohypogastric

26.  May present in
anterior abdominal wall
petit’s triangle
ischiorectal fossa
femoral canal
gluteal region
popliteal fossa

28.  Osseous destruction by lysis of bone
 Necrosis- ischemic infarction of a segment due to endarteritis
 Softening leads to yielding – gravity and muscle action
 Bone compression, collapse and deformity
 Sequestration – coarse sand
 Rarely large sequestrum

30.  Granular
synovial
osseous
 Exudative
synovial
osseous

31. Constitutional
 Low grade fever
 Anorexia
 Loss of weight
 Lassitude
 Night sweats
 Tachycardia


32.  Local symptoms
 Pain
 Night cries
 limitation of movements
 Effusion and swelling
 Muscle wasting
 Regional lymphadenitis

33. Xray
 localized osteoporosis – first sign
 Art margin and cortex – haziness
 Osteolysis
 Soft tissue swelling
 Narrowing of joint space
 Collapse of bone , subluxation , dislocation
 Irregular growth – premature fusion of epiphysis
 Increased longitudinal growth- hyperemia

39.  Leukocytosis
 Relative lymphocytosis
 Low HB
 Raised ESR

40.  Positive – present or past infection
 Negative – generally rules out disease
 False negative
severe and disseminated diseas3e
high fever
exanthemata
post viral vaccination
steroid treatment
immune incompentent

42. Microscopic examination of tubercle
 Granulation tissue
 Synovium
 Bone
 Lymph node

43.  Leukocytosis
 Glucose decreased
 Protein elevated

44.  Positive scan localizes suspicious lesions
 Technicium-99
 Gallium 67
 indium 111

45.  Picks up early lesions
 Difficult area
CV junction
cervico-dorsal
LS region
ribs, sternum

46.  Confirms plain Xray/ CT finding
 Pre destructive lesions
 Encroachment of vertebral canal
 Displacement of Dural sheath
 Localised tuberculoma

47.  Detection of soft tissue abscess
 Behaviour to treatment

48.  Pyogenic spinal osteomyelitis: severe pain, spasm, hyperextension, early disc
destruction
 Typhoid spine: follows enteric fever
 Brucellosis: undulant fever
 Mycotic infection: sinuses and typical discharge

49.  Benign
hemangioma: coarse vertical trabeculae
giant cell and ABD
 PRIMARY MALIGNANT: Ewings’s sarcoma, lymphoma, chordoma,
chondrosarcoma, fibrosarcoma, multiple myeloma
 secondaries

51.  General rest
 Anti anemic drugs
 Multivitamins
 High protein diet

52.  TRACTION:
 Relieves spasm
 Prevents deformity
 Maintains joint space and avoids subluxation and minimizes migrating acetabulum
 Active and assited movements at hip and knee are started after pain and muscel
spasm comes down

60.  Gamma interferons
 Alpha TNF
 IL -2, 12

61.  If response to conservative treatment is not favorable
 Failure to achieve acceptable outcome

62.  SYNOVECTOMY and joint debridement
 Osteotomy
 Arthrodesis
 Girdlestone excision arthroplasty
fibrous ankkylosis
 Total hip replacement

63.  Pott’s spine indications for surgery
 Quadriplegia/ paraplegia
 Active disease with severe pain
 Progression of kyphotic deformity
 Impairment of pulmonary function
 Resistance to chemotherapy

64.  Drainage of cold abscess
 Costotransversectromy
 Anterolateral decompresiion
 Laminectomy
 Posterior spinal fusion