Infection

Definition
- Pathogenic organism multiply and spread within body tissues
- Acute pyogenic - pus
- Chronic – granulation tissue

Principles of treatment
- Analgesia
- Relative rest
- Efffective antibiotics
- Surgical eradication

Laboratory Evaluation of Inflammation

Acute phase response

 consists of the systemic and inflammatory changes that occur after tissue injury or infection.
 Activated monocytes and macrophages secrete cytokines that alter the synthesis of acute phase proteins by
hepatocytes.
 Other acute phase phenomena include fever, anorexia and somnolence, and hormonal and metabolic changes.

Acute phase proteins

 defined as proteins whose concentration is increased or decreased by at least 25% during inflammatory disorders.
 The major positive acute phase proteins are CRP and serum amyloid A. Other important positive acute phase proteins
are haptoglobin, alpha-1-antitrypsin and fibrinogen.
 The major negative acute phase protein is albumin.
 The function of acute phase proteins is to potentiate the immune response, with potentially beneficial and harmful
results.

ESR
 The ESR measures the rate of sedimentation of a column of anticoagulated blood (rouleaux)
 Rouleaux formation is normally discouraged by the negative charge on the surface of red blood cells
 It is an indirect measure of the acute phase reaction and the level of fibrinogen synthesized in the liver in the blood –
excess fibrinogen neutralizes the –ve charge and decreases red cell repulsion = increased rouleaux formation =
aggregation = increased settling rates
 Rises 24-48hrs and takes 3weeks to settle
 The ESR is usually measured using the Westergren technique.
 The ESR is cheap, simple and widely available.
 It is a good screening test for the presence of active inflammation, however it is non-specific and there exists multiple
confounding factors, including anaemia, age and gender and RBC abnormalities such as poikilocytosis.
 Values in excess of 35mm/hr are considered abnormal and indicative of infection unless proved otherwise.
 Sensitivity of 0.82 and specificity of 0.85% in THR infection (Spangehl 1997)

CRP
 CRP is an 115kd pentameric protein encoded on chromosome 1, which has been highly conserved over millions of years
of evolution. It is synthesized by hepatocytes.
 It was discovered in 1930 and was so-called because it reacted with the C polysaccharide of Streptococcus pneumoniae.
 It has important recognition and activation capacities in acute inflammation; it can modulate neutrophil and monocyte
functions and is involved in the activation of complement.
 The CRP level is obtained by immunoturbometric assay, and is a direct rather than indirect measurement of one phase of
the acute phase response. It is normally found in trace levels in serum but undergoes rapid elevation (within 6 hours) in
response to acute inflammatory stimulus, and recovers quickly when that stimulus is removed. It reaches a peak at 50
hours post stimulus.
 The CRP value is unaffected by age, and is normally less than 5mg/ml – less confounders
 Rises with in 6hrs and takes 6-10days to settle in presence of infection – sensitive++
 Sensitivity of 0.96 and specificity of 0.92 in infected THR (Spangehl 1997).
 Has added significance over ESR (altered by physiological states) – increases before rises in ESR, and decreases sooner
 Declines after 4th day post op
CRP and ESR in clinical practice
 The major use is in monitoring the course of disease activity over time. CRP may be more valuable in this capacity
because it is less affected by other variables and has a more rapid rise and fall.

Orthopaedic manifestations of CRP (Aalto CORR 1984)

 40 patients undergoing THR
 Preop ESR elevated at 28 and CRP normal
 ESR peaked at 64mm/hr at day 6 and at three weeks the average level was 30. At one year post surgery the average
level was still 30.
 CRP peaked at 134mg/ml at D2 post surgery and was normalized by day 21.

Infection Common organisms Treatment

Cellulitis 1. Strep (Group A) Methicillin (diclox)
2. Staph aureus OR
Kefzol / Eryhtromycin / Amoxycillin
Necrotizing fasciitis 2 groups of infection : Debridement is mainstary
1. Group A Strep (-haemolytic) Antibiotics :
2. Polymicrobial – Aerobic + anaerobic  Penicillin + Clindamycin, OR
(clostridium + anaerobes)  Ceftriaxone
Gas gangrene Clostridium Penicillin + Clindamycin
Wound infection 1. Staph aureus  Flucloxacillin
2. Group A strep  MRSA  Vancomycin or Teicoplanin,
3. Enterobacter doxycycline
Bites 1. Human – Strep Viridans, Staph, Eikenella  Augmentin = Amoxycillin + clavulanate
 Augmentin
2. Cats – Psturella, Staph  Augmentin
3. Dogs - Pasturella, Strep  Ampicillin
4. Snake – Pseudomannas, enteropbacter,
staph, clostridium  Ceftriaxone
Osteomyelitis Newborn Newborns
1. S aureus  Dicloxacillin + Ceftriaxone
2. Group B strep
3. Gram negatives Children
 Dicloxacillin/Flucloxacillin +/ Ceftrtiaxone
Children OR
1. S aureus  Clindamycin +/- Ceftriaxone (GN present)
2. Group A Strep
3. Haemophilus – rare with immunisation Adults
4. Coliforms (rare)  Flucloxacillin +/- Vancomycin

Adults
1. Staph

Other
1. Sickle cell – Salmonella  Ciprofloxacin or
Ceftriaxone
2. IVDU – S aureus, S epidermidis,
Pseudomonnas  Flucloxacillin + Cirpo
Septic arthritis Newborns Newborns
1. S aureus  Dicloxacillin + Ceftriaxone
2. Group B Strep
3. GN – include Neiserria Children
 Dicloxacillin + ceftriaxone
Children
1. Staph Adolesecents and young adults
2. Styrep  Flucloxacillin + Ceftriaxone
3. Haemophilus - Flucloxa for gram positives
- Ceftriaxone for the Neiserria (more likely
Adolescents and young adults if the culture is negative)
1. S aureus Cipro can substitute for Ceftriaxone
2. Neiserria gonorrhoea

Foot puncture wound Pseudomonnas (or staph) 3rd gen cephalosporin or Cipro
Diabetic foot Acute – Staph  Cipro + Clindamycin
Chronic – Polymicrobial OR
1. Gram positives
2. Gram negatives * Timentin + Ampicillin
3. Anaerobes
Acute Osteomyelitis
- Infection of the bones - osteon (bone), myelo (marrow), it is (inflame)
- OM of less than 2/52 is essentially a disease of childhood
- infection of metaphysis of long bones - haematogenous spread most often, 2⁰
by direct spread (surgical/traumatic)
- Subacute osteomyelitis produces less severe constitutional changes and the
history is for more than 2 weeks. X-ray changes are seen at presentation.
-

Epidemiology
- Boys < girls
- Dist femur  prox tib  humerus  pelvis calcaneus  phalanx  radius

Organisms
- S. aureus 60-90%
- Strep sp eg pneumococcus
- Hib – declining with vaccination
- E.coli, pseudomonnas and other gram -ve's
o <4yo – 20% Hib (dec c vaccine)
o Infants – g-v & β haemolytic Strep

Presentation
- Unwell child
- Fever
- Localised bone tenderness
- Inflame – warmth, tenderness, erythema, swelling
- pseudoparaylsis

Neonates can have multifocal bone involvement

Pathogenesis
- most often haematogenous spread (but can be non-haematogenous – open # or penetrating injury)
- the area around the growth plate (metaphyseal-epiphyseal junction) has a plentiful blood supply
- Predilection for the metaphysis is due to
o ↑ blood flow at growing ends of long bones
o Endothelial gaps in the vessels in the metaphysis
o Hairpin arrangement of terminal vessels (=Trueta not favoured at present) before entering the large network of
sinusoidal veins
o Large cavernous sinuses with sluggish flow (relative vascular stasis as large) - deposition of blood borne bacteria
and poor white cell penetration
- In young infants in whom there is still a free anastamosis between metaphyseal and epiphyseal blood vessels, infection
can just as easily lodge in the epiphysis (still direct connection)
- ↑ infection = ↑ pressure = ↓ blood supply (vascular occlusion) = ischaemic bone necrosis (abscess)  local bone
destruction)  erosion of the cortex spreading infection to either 3 routes
o Into joint (if metaphysis is intracapsular)  septic arthritis (femur, humerus)
o Periosteum (if metaphysis is extracapsular)
o Into epiphysis (less likely)
- Brodie abscess forms (granulation tissue forms fibrous capsule)
Pathology
- Bacteria settle in metaphysis
o Local inflammation - vascular congestion, exudation of fluid and infiltration of PMN leukocytes
- Suppuration - 2nd to 3rd day pus forms within the bone and forces its way along the Volkmann canals to the surface where
is produces a subperiosteal abscess – pus then spreads across the shaft to re-enter the bone at another level and burst
into the surround soft tissues
- Pus forms resulting in bone necrosis and resorption
o Pus may track through Cortex to form a subperiosteal collection lifting the periosteum which lays down
new bone
 Sequestrum = Necrotic bone formed when cortex bone is deprived of its blood supply after
thrombosis of nutrient vessel and/or periosteal stripping and is detacted from living bone
 It remains dense and does not become demineralised unlike vital hyperaemic bone
 Involucrum = The periosteal new bone which forms over the Cortex surrounding the infected area
 Cloacae = The channels that form in the Cortex
 allowing free flow of pus and may communicate with the surface via sinus
 Sinus – communication bw a cavity & epithelial surface
 Fistula – abn communication bw 2 epithelial surfaces
 Necrosis – rising intraosseous pressure, vascular congestion, infective thrombosis and periosteal stripping increasing
compromise the blood supply, by the end of a week and is microscopic evidence of bone death
o Infants – growth disc and epiphysis may undergo irreparable damage (AVN)
o In growth of granulation tissue – boundary between dead and living bone becomes defined
 New bone formation – new bone forms from the deep layers of the stripped periosteum
o With time new bone thickens to form an involucrum enclosing the infected tissue and sequestra
o Persisting infection leads to discharge through tiny perforations (cloacae) in the involucrum
 Resolution and healing – bone around zone of infection is at first osteoporotic (due to hyperaemia)
o with healing there is fibros and appositional new bone formation – with periosteal reaction results in sclerosis
and thicking of the bone

Diagnosis
- blood cultures (+ve 50%)
Nil radiological bone changes for 7-10/7
- ↑WCC, ESR, CRP (best)
- Local aspirate (+ve 60-70%)
- XR (#, mal) – lag at least 2/52 behind
o Early - ? displacement of fat planes, show soft tissue swelling, and loss of normally defied tissue planes,
o 7-10 days - periosteal new bone formation
o 2 weeks – periosteal reaction evident - thickening, bone destruction, osteoporosis is a feature of metabolically
active and thus living bone (if the segment fails to become osteoporotic is metabolically inactive and possibly
dead), dead bone is whiter (more sclerotic)
- Bone scan – show site with ↑ uptake, 90% sensitive, if –ve doesn’t rule out (not a good test)
- US – to guide effusion aspiration, also will show subperiosteal reaction/collections before apparent radiologically
- MRI – most sensitive, best test for localised osteomyelitis (T1) – reduced intensity
- CT – sequestra in chronic OM
Need 50-75% of bone matrix destroyed to see lytic
DDx radiological changes
- Septic arthritis
- Tumours - Ewings
- Sickle cell crisis
- Others
o cellulitis
o Streptoccal necritisung myositis
 group a beta haemolytic strept invade muscles which in early stages may be mistaken for cellulitis
or OM
 rapidily can spiral out of control – death
 intense pain and board like swelling with fever and general malaise
 surgical debridement and IV abx
o Gauchers disease

Treatment
- IV Antibiotics (empiric aimed at Stap, Strept) to prevent discharging sinus, limb deformity, amyloidosis, bone necrosis,
chronic infection. IV's till afebrile for 24/24. PO at least 3/52 if acute and early response, ? go for 6/52 – depends on
clinical response & bloods
o Di/flucloxacillin 2g (50mg/kg up to 2 g) IV 6 hourly PLUS Intraarticular physis
o Ceftriaxone 2g (50mg/kg up to 2 g) IV daily (if gram –ve) - radial head
- Splintage – for analgesia, not improve outcomes though - hip + distal femur
- Surgical drainage if unresponsive to antibiotics - shoulder
o If failing to settle after 48hrs - distal fibula
o If abscess
o Idea is to allow pus to drain = OM  septic arthritis
o Incise periosteum only if pus below periosteum no need to window bone
o If not draining then oval window in bone

- Arthrotomy, arthroscopic washout with GA (septic arthritis)

Complications
- metastatic infection – can spread to multiple sites or actually have started in multiple site
- suppurative arthritis – young children with physis = no impenetrable barrier, where the metaphysis is intracapsular, from
metastatic infection
- premature growth plate arrest
- chronic OM
- pathological fracture
- septicaemia

Chronic OM
- Uncommon in kids as sequelae to acute OM
- Most common is 2ndary to open # or surgery

Classification
1. non specific
a. sequel to acute OM
b. chronic unifocal OM
c. chronic recurrent multifocal OM
2. specific
a. mycobacteria
b. mycoses
c. salmonella
d. other organisms

Pathology
- prescense of necrotic bone, formation of new bone, exudates of PMN leuks joined by large number of lymphocyts,
histiocytes and plasma cells
o involurcrum – encasing sheath of live bone encasing the dead bone under the periosteum
- is destroyed or devitalised in a discrete area at tge focus of infection of more diffusely along the surface of a foreign
implant
- Cavities containing pus and pieces of dead bone (sequestra) are surrounded by vascular tissue, and beyond that by areas
of sclerosis – the result of chronic reactive new bone formation
- The sequestra act as subtrates for bacterial adhesion in much the same way as foreign implants, ensuring the persistence
of infection until they are removed or discharge through draining sinuses
- Histology – one of chronic inflammatory cell infiltration around areas of cellular bone or microscopic sequestra

Radiology
May see
- Sequestrum
- Involucrum
- Cloacae

Organisms
- S.aureus 30-50%
- Mixed organims 25%
- Gram -ve, anaerobes, S.epidermidis and Strep

Management
- Usually conservative
o Bed rest
o Back slab
o IX
o AB's
o There is doubt about ability of AB's to eradicate organisms in chronic OM
o Bugs persist in 30% of cases
o Sinuses dressed regularly
- Operative – indications = abscess or Sequestrum. Options = Aim of operative treatment is
o Saucerisation - Dead bone debridement
- Reconstruction of bone defects and dead space
o Debridement with or without muscle flaps - Anti biotic therapy
o Bone grafting - Bone stabilisation
o AB impregnated PMMA beads - Soft tissue coverage
o Excision of infected bone and bone transport
o VAC devices
o Amputation

Lethal complications of chronic osteomyelitis

1. Amyloidosis
a. Causes death through renal failure
2. Marjolin’s ulcer
a. Squamous cell cancer in a site of chronic infection
b. This grows slowly initially and metastasizes late, because of scarring of the local lymphatics. Once it reaches
normal tissue it spreads at a normal rate.

Post operative OM

Classification
- Early infection - <1 month– superficial, deep, deep and superficial
- Intermediate – between 1month and 1 year
- Late infection - > 1yr – following early infection, covert infection appearing later, following a long period of normality

Notes
- CRP in absence of infection will return to normal in about 6/52
- Radionuclide imaging after arthoplasty - -ve PV88%

Prevention
- avoid operation on immune depressed patient
- eliminating focus of infection before operating
- insisting on optimal surgical sterility
- prophylactic antibiotics
- handling tissues gently
- high quality implant material
- ensure close fit and s3cure fixation of the implant
- preventing or counteracting later intercurrent infection
Charnley
- invented space suits – significant decrease in wound infection post total hip
- I/O cephalosporin + 2 post Abx
- Addition of above infection post hip < 0.2% (lidwell 1986)

Treatment
Infection following joint replacement – stability of prostheses rather than the presence of bacteria that dictates treatment, if
stable and no pain = no indication for operation
- Medically fit = revision arthoplasty
- Frank abscess = two stages
- Unfit = cross fingers and Abx

Subacute haematogenous OM (chronic unifocal OM)

- pathology – well defined cavity in cancellous bone, containing fluid, the cavity is lined by granulation tissue, bone
trabeculae are often thickened
- clinical features – pain near larger joints for several weeks or months
- imaging – tibial or femoral metaphysis, cavity well defined, if cavity has halo of sclerosis = Brodies Abscess
- Dx – may resemble osteoid osteoma, occ resemble malignant bone tumour

Garres (1893) sclerosing OM

- Rare form of non-suppurative OM (no necrosis of purulent exudate and little granulomatous tissue) characterised by
marked sclerosis and cortical thickening (i.e. intense proliferation of periosteum), only a diffuse enlargement of the bone
at the affected site (i.e. bony deposition)
- Children and young adults
- avg age 16yrs
- Aetiology unclear
- Anaerobe - Propionibacterium acnes implicated
- Common site is shaft of long bones, mandible also seen
- Symptoms recur at intervals of for several yrs and then subsides
- XR – increased bone density and cortical thickening, some case marrow cavity is completely obliterated, no abscess
cavity
- Dx – difficult
- Rx – not satisfactory Rx, Abx don’t change course, decompression may give symptomatic relief

Subacute recurrent multifocal OM

- Mainly children and adolescents
- Recurrent attacks of pain, swelling and tenderness around long bones metaphysis (distal femur or tibia) and clavicle – ie
in different areas at different times
- XR – characteristic, small lytic lesion in the metaphysis, usually adjacent to the physis, cavities surrounded by sclerosis,
others show varying stages of healing
- Biopsy – typical features of acute or subacute inflam, chronic inflam = lymphocytic infiltration
- Treatment – palliative, Abx no effects on disease, eventually heal without complication

Sterno-costo-clavicular hyperostosis
- Forties and fifties
- Changes to sternum, Vc and adjacent bones
- XR – hyperostosis of the medial ends of the clavicle, the adjacent sternum and the anterior ends of the upper ribs, as will
as ossification of the sternoclavicular and costoclavicular ligaments
- Sclerosis of individual Vbs, ossification of the anterior longitudinal ligament, anterior IV bridging, end plate erosion, disc
space narrowing and vertebral collapse
- Rx – protracted course with flares, no effective RX, may get ankylosis of jts

Caffey’s Disease
- Infantile cortical hyperostosis is a rare disease of infants and young children
- Rare disease affecting the mandible, scapula, clavicles, ribs and long bones
- Starts first few months of life with painful swelling occur the tubular bones and/or the mandible
- XR –There is irregular periosteal elevation of affected bone, with extensive cortical thickening. Normally the bones
remodel to their normal shape
- There is no treatment.
- Exclude other causes of hyperostosis – scurvy/ OM
- Unknown cause - ? viral
Post traumatic OM
- After open fractures due to combination of tissue injury vascular damage, oedema, haematoma, dead bone fragments
and an open pathway to the atmosphere must invite bacterial invasion even if the wound in not contaminated with
particulate dirt
- Rx – debridement and laavge, immobilisation and Abx

Brodie’s Abscess
- Brodie in 1836 described " Certain localised radiolucencies in the tibia, developing silently without any systemic signs and
without previous febrile illness"
- Manifestation of subacute OM

Gledhill Class
- I. Solitary metaphyseal lesion walled off lucent lesion surrounded by reactive sclerotic bone
- II. Lucent lesion in metaphysis not surrounded by reactive sclerotic bone but with adjacent loss of the Cx
- III. A diaphyseal lesion assoc with cortical hypertrophy and periosteal or endosteal new bone
o Radiolucent zones in Cx seen on CT or tomogram
- IV. Lesion assoc with layers of subperiosteal new bone formation --> onion skinning as in Ewings

- Pain and local tenderness +/-swelling

- Usually >8yrs
- Pain may fluctuate on background of mild ache
- Usually well with mild or abscent fever

Radiology
- Circumscribed area of bone destruction 0.5-5cm
- Variable degree of surrounding sclerosis but this is well demarcated and often extensive
- 40% show periosteal new bone
- 20% have a sequestrum often only seen on CT
- MRI demonstrates any cloacae
- May look like osteoid osteoma

Management
- Usually settles with rest +/- immobilisation and AB's
- Recurrent episodes treated with removal of abscess wall, curettage and removal of abscess wall

- AB's continued for 6/52

- En Bloc resection is alternative to curettage
 Routes of Infection
- haematogenous
- extension of OM
Acute suppurative arthritis o I/A physis
A joint can become infection by o Via trans-physeal
- direct invasion through a penetrating wound, intra-articular injection or arthroscopy
vessels
- direct spread from an adjacent bone abscess
o Haversian and
- blood spread from a distant site
Volkman canals in
children
Bugs - usually staph aureus, infants H influenxa (ie same bugs as OM)
- Penetrating wound/injury
Pathology
- usual trigger is a haematogenous infection which settles in the synovial membrane
- acute inflam reaction with a serous or seropurulent exudate and an increase in synovial fluid
- as pus appears in the joint, articular cartilage is eroded and destroyed by
o proteolytic enzymes (from bacteria and synovium)
o increased intra-articular pressure
o lack of movement
o spread of granulation tissue over cartilage
- infants – epiphysis may be damaged
- older children – vascular occlusion may lead to necrosis of the epiphyseal bone (AVN)
- adults – usually confined to articular cartilage

With healing there may be

- complete resolution and return to normal
- partial loss of articular cartilage and fibrosis of the joint
- loss of articular cartilage and bony ankylosis
- bone destruction and permanent deformity of the joint

Clinical features
- newborns – septicaemia, irritable, not eating, fever, tachycardia
- children – pain in large joint, reluctance to move (pseudoparesis)
- adults – often more superficial joint, movements are restricted

Imaging
XR – early on it is normal, late = joint space irregularities, E. coli sometimes gas in the joint

Investigations – joint aspirate plus normal stuff (50% diagnostic)

DDx
- acute OM
- trauma
- irritable joint
- haemophilic bleed
- RF
- Gout and pseudogout
- Gauchers disease

Treatment
- Septic joints should always be washed out
o To obtain Dx
Drainage Hip
o To release pus and irrigate the joint to prevent articular cartilage degradation
Anterior vs posterior
- Other care pts approach
o supportive care – analgesia and IVF - anterior sparing to
o splintage vascularature
o abx - posterior allows
natural gravity
Complications – bone destruction, cartilage destruction, growth disturbance dependent drainage

Gonococcal Arthritis
- Neisseria gonorrhoea is the commonest cause of septic arthritis in adults
- Need to examine for genito-urinary infection

Others – spirohaetal infection, tertiary syphilis, yaws

PATHOLOGY Of Joint Destruction
- Synovium oedematous & hyperaemic
- Inc cloudy synovial fluid
- > 2/7 frank pus
o Cartilage destruction
- Starts at areas of joint contact
- Synovial membrane replaced by granulation tissue
- Adhesions wall off pockets of pus
o Fibrous ankylosis

Cartilage Destruction
1. Proteolytic Enzymes
o Lysosomal >> PG
o Collagenases
o From WC/ Bugs / Cartilage itself
o Staphylokinase activates plasmin
2. Raised intra-articular Pressure
o Degrades cartilage
o AVN
o Dislocation
o Hip is held ABD 45°/ FLEX 15°/ ER 15°
o Knee FLEX 20°
3. Mechanical
o Immobilization = Lack of nutrition
o End result = cartilage fragmentation
GRANULOMATOUS INFECTIONS
- Fungal
- Syphilis
- TB

FUNGAL
Blastomycosis
- From lung portal
- Epiphyses and metaph long bones
- also hands and feet
- Rx amphoteracin

Coccidiomycosis
- As above

Actinomycosis
- Mandible and facial bones
- As introduced orally
- Bone involvement secondary to soft tissue infection
- Form granulomas
- Penicillin G 6/52 IV then 12/12 orally

Cryptococcosis
- In immunocompromised
- HIV, Leukemia/lymphoma, DM
- Produce radiolucent lesions with no periosteal raxtn
- Following meningitis
- Amphotericin B

Mycetomas
- 2 bugs Actinomyces(aerobic bact)
- Eumycetes -true fungi
- Form cutaneous tumoral enlargements which can erode into bone and soft tissues

SYPHILIS OF BONES
- Congenital or acquired
- Treponema pallidum - spirochete
- Infection is localised to metaph and diaphysis
- Doesn't cross into jt

Congenital Syphilis
- Irritable and restless
- Large, tender swelling around jt
- Limb immobile
- Cutaneous signs of syphilis may be present- skin lesions, mucous patches, keratits

X-rays
Two major findings are
- 1. Metaphysitis - Show widening of metaphysis with marginal density and an indentation on its epiphyseal border
- 2. periostitis – diffuse  With layers of new bone formation
- Affected bone takes on a spindle shape with loss of metaph

- Serological markers not +ve for 3/12 in neonate

- Spirochete can be demonstrated on histol
Responds well to AB's

Late Stage = 2-3yrs

- Characterised by osteoblastic activity
- A condensing osteitis
- Mainly tib, femur and skull
- Subperiosteal bone formation produces characteristic prominent ant tibia with out bowing = Sabre tibia
Clutton's jts
- Late stage of congenital syphilis
- 8-18yrs
- Recurrent bilat, painless effusions of knees
- aspirate shows high monomorph infiltrate

Syphilis in Adults
- Late or tertiary disease
- Painless nontender swelling of long bone or skull
- May be diffuse sclerotic rxtn resembling Paget's
- Charcot's jts
- Gummas apparent in soft tissues – Abx no longer work, need OT if path # or gumma breaks down

TB
Skeletal manifestations are seen chiefly in the large joints and the spine, but the infection may appear in any bone

Pathology
- Mycobacterium TB enters the body via the lung or the gut or rarely through the skin – causes a granulomatous reaction
which is associated with tissue necrosis and causation
- Primary complex – is the initial lesion in lung, pharynx or gut with lymphatic spread to regional lymph nodes
- No clinical illness but two important sequels
o within nodes which are apparently healed or even calcified, bacilli’s may survive for many years, so that a
reservoirs exists
o the body has been sensitised to the toxin and should re-infection occur, the response is quite different, the
lesion being a destructive one which spreads by contiguity
- Secondary complex – widespread dissemination via the blood stream  military tb or meningitis
- Tertiary spread – affected in 5% of tb patients – predilection for the vertebral bodies and the large synovial jts
- Multiple lesions in 1/3 of patients
- Tb granuloma – epitheloid and multinucleated giant cells surrounding an area of necrosis with round cells (lymphocytes)
around the periphery