11.2 Miscellaneous orthopaedic infections

Leprosy is one of the oldest diseases known, and there are currently estimated to be 12–15 million cases worldwide.

The causative organism is Mycobacterium leprae. It is of very low virulence, and the incubation period varies from 3–5 years for tuberculoid leprosy and 9–11 years for lepromatous leprosy. Human beings are the only significant reservoir of the bacterium, and transmission is mainly by droplet spread and human contact via broken skin and nodules.

M. leprae selectively invades nerves. The extent of damage depends on the cell-mediated immunologic response of the patient. If immunity is high, bacterial multiplication is arrested early and a localized form of the disease results (tuberculoid type). An active granulomatous response occurs with destruction of axons and early neurological deficit results. If immunity is low, a severe and generalized form of the disease results (lepromatous type) with no immune response and no neural damage. These two types form the ends of the clinical spectrum of the disease, with intermediate types being described, and clinical presentation is varied.

Mixed nerve trunks are usually involved, at subcutaneous sites, often close to tight osteofascial canals or joints where the inflamed and swollen nerves are prone to further damage by joint motion and external trauma (Figure 11.2.1). The nerves involved are, in order of frequency, the ulnar nerve above the elbow (high ulnar type) or at the wrist (low ulnar type), the median nerve at the wrist, the common peroneal nerve at the fibular neck, the facial nerve, and the radial nerve.

The neurological deficit in leprosy is often apparent as a claw hand. The commonest combination of deficit is a high ulnar and a low median nerve paralysis. Radial nerve involvement is less common and only occurs in combination with involvement of the other two nerves.

Corrective surgery may be performed after there is a good clinical response to leprosy treatment, with no tenderness over the nerve trunks and no history of neuritis during the preceding 6 months. Surgical procedures are designed to restore grasp and pinch.

Foot drop is the commonest deformity, resulting from involvement of the common peroneal nerve as it crosses the fibular neck. Rarely, tibial nerve involvement at the level of the ankle joint produces complete intrinsic muscle paralysis of the foot resulting in clawing of the toes. The development of a neuropathic foot leads to secondary deformities in untreated cases.

Ulcers are common in the anaesthetic foot, particularly in the presence of deformity, and occur particularly over pressure points. Skeletal deformities must be appropriately corrected so that high pressure zones are removed, and prevention depends on education in the importance of proper care of the foot.

Treatment in the acute situation may involve irrigation, drainage, and antibiotics. In the case of a chronic ulcer, thorough cleaning and debridement of all necrotic and infected tissues is performed, with elevation and daily dressings. The leg is then protected in a well-moulded below-knee walking cast.

Various strains of Brucella can affect the joints and cause osteomyelitis. The lumbar spine or sacroiliac joints are commonly involved (Figure 11.2.2). Brucellosis may cause a monoarticular arthritis with isolation of the pathogen, or a polyarticular reactive arthritis where no organism is isolated. Differentiation from tuberculosis can be difficult, but characteristically brucellosis produces a combination of lytic and blastic lesions. X-rays show early bone repair with dense sclerosis and syndesmophytes. The characteristic radiological feature is erosion of the anterosuperior margin of the vertebral body (Pons sign) with rounding of the corner and decrease in the disc space. Doxycycline alone, or combined with streptomycin or gentamicin is usually effective.

Syphilis is caused by the spirochete Treponema pallidum and is sexually transmitted. The blood-borne organism lodges in the vascular metaphysis and produces a low-grade inflammatory response. In patients with inadequate host-defences, extensive necrosis of periosteum and bone occur with a yellowish gummatous sticky exudate (gumma). Beyond the central area of necrosis, an osteoblastic reaction is characteristic.

In the child, infection of the metaphysis interferes with endochondral ossification, with granulation tissue invading the zone of calcified cartilage. The long bones are particularly involved, especially the tibia, and the skull and nasal bones. The child with early congenital syphilis presents with a large tender swelling and reluctance to move the limb. Radiographs are typical, showing lucency of the metaphysis with sclerosis at the epiphyseal border. A fracture of the epiphysis may occur. Treatment usually produces rapid recovery with little subsequent interference with growth.

In late congenital syphilis, osteoblastic changes around the tibia, femur, and skull are seen. Asymmetric periosteal bone formation in the tibia produces bowing (saber shin). The phalanges and metacarpals appear spindle-shaped. Painless effusions of the knee may be seen in the second decade (Clutton’s joints). Little residual damage is usually seen, and the child remains well.

In an adult, bone and joint lesions occur many decades after the primary stage, and are characterized by thickening of skull and long bones without pain or inflammation. Extensive necrosis of bone occasionally leads to a draining sinus. Joints are involved only secondarily by direct extension. Peripheral neuropathic changes produce Charcot joints.

T. pallidum is highly sensitive to penicillin and the disease is completely curable.

Hydatid disease is caused by the parasitic tapeworm, Echinococcus, and is transmitted in the faeces of hosts such as dogs. Skeletal hydatidosis is rare (0.5–4%). There is a latent period of many years or decades before symptoms manifest, so that it is only seen in the second to fourth decades.

The vertebrae, long bones, the pelvis, skull, and ribs are affected in descending order of frequency. Extension of the cyst occurs along the medullary canal, but once the cortex is breached, the cyst expands into adjacent soft tissues. Cysts elsewhere are usual (liver and lung). Clinical presentation is usually with a pathological fracture or pressure over a neurovascular structure.

Radiographs show lucent areas with thinned out cortices and expansion of the bone. Resorption of bone without a periosteal or sclerotic reaction is characteristic (Figure 11.2.3). Calcification within soft tissue shadows is reported to be an important diagnostic sign of hydatid disease.

In the spine, the lower thoracic and lumbar vertebrae are most commonly involved. The trabeculae are eroded but the vertebrae maintain their shape until late, and the discs are relatively resistant. Large cysts form in paravertebral areas. Extension into the spinal canal often leads to neurological symptoms. Patients present with localized back pain with or without radicular pain, with paraparesis in more than 50% of cases. It is often confused with tuberculosis.

Treatment requires complete excision of the involved tissues and graft reconstruction, although this is rarely possible. Recurrence is therefore common. Drug treatment may occasionally be successful in eradicating the disease.

Mycetoma is a fungal infection of the foot causing painless swelling, induration, and sinus formation with discharge of fungal grains (Figure 11.2.4). It is common in the tropics. Infection is usually via inoculation by a thorn prick; hence it is common in agricultural workers and barefoot walkers. It is caused by two main groups of organisms: the true fungi (infections termed eumycetoma) and actinomycetes (infections called actinomycetoma).

Radiographs show erosions of bone in eumycotic infections, and small cavities with sclerosis in actinomyctoic disease (Figure 11.2.5). Streptomycin or co-trimoxazole may be successful in the treatment of actinomycetoma, although eumycetomas are more resistant to chemotherapy. Surgical excision of the affected area (usually below-knee amputation) may be required in late or resistant cases.

Salmonella typhi and S. paratyphi can cause metastatic bone and joint infections by haematogenous spread. The long bones, chondrosternal junction, and the spine are common sites of involvement. Predisposing factors include sickle cell anaemia, young children, diabetes mellitus, and steroid therapy.

Osteomyelitis is the common mode of presentation, although septic arthritis can occur, either as direct extension from adjacent bone, or by haematogenous infection. Knee, shoulder, hip, and sacroiliac joints are commonly involved.

Salmonella gastroenteritis can also be accompanied by a reactive polyarthritis, presenting about 10 days following the gastrointestinal episode. Knees, ankles, and wrist joints are most commonly affected.

Radiographs show numerous punched out lytic lesions in the metaphysis extending into the diaphysis. Irregular sclerosis with subperiosteal bone formation is seen.

Salmonellae are highly sensitive to third-generation cephalosporins.

Panton–Valentine leucocidin (PVL) is a bacterial exotoxin that is usually associated with skin and soft tissue infections and necrotizing pneumonia. However, in the last few years, an increasing number of musculoskeletal infections have been reported.

PVL can be secreted by methicillin-sensitive or methicillin-resistant strains of Staphylococcus aureus, and in Britain is secreted by 1–2% of Staph. aureus isolates. It produces a particularly virulent infection via leucocyte destruction, thereby impairing the immune response, and tissue necrosis. Deep venous thrombosis, septic emboli, and coagulopathy are common. In bones, intravascular coagulation means that pus rapidly becomes loculated, glutinous, and difficult to drain, and the true extent of bony and soft tissue involvement is often more extensive than suggested clinically.

Patients usually present with extremity pain with or without swelling, which may not be marked initially and may be misdiagnosed as minor trauma. If not treated appropriately and with a high index of suspicion, deterioration is rapid, with septic shock common. Full intensive care support with ventilation and inotropes may be required. Early magnetic resonance imaging (MRI) is vital to reveal the presence and extent of bone and joint involvement and guide appropriate surgery. Diagnosis requires identification of the PVL from the causative organism.

A recent case series has emphasized the importance of early surgical intervention to debride poorly vascularized areas of infection. Joints must be aggressively and repeatedly washed out, with bones drilled and debrided thoroughly. Surgical eradication of all infected material is of paramount importance, and often requires repeated surgery. Clindamycin and rifampicin are usually advised as anti-staphylococcal medication, and need to be continued for many months. Decolonization therapy in affected patients and close relatives may also be required.

The incidence of musculoskeletal complications following these severe infections is high. There should therefore be a high index of suspicion for all staphylococcal bone and joint infections, with routine requesting of the PVL status of every staphylococcal infection, early MRI scanning and aggressive surgery in positive cases.

An acute viral infection causing neural damage to the anterior horn grey matter of the spinal cord resulting in an asymmetrical lower motor neuron palsy. The motor neuron cells are irreparably damaged or rendered temporarily functionless. Immunization has almost eradicated polio from many developed countries but it still remains prevalent in others—in India up to 150 000 new cases a year have been reported.

The lower limb is most frequently affected. Muscle imbalance results in deformity, the most common example is equinus due to paralysis of tibialis anterior with sparing of the triceps surae. Gait is affected with weakness in knee extension. Patients will walk with their hand on their affected knee preventing collapse in stance due to quadriceps weakness (Figure 11.2.6).

Progressive deformity will occur in the skeletally immature. Lack of stretch will produce a slower rate of growth of the affected muscle resulting in further contracture and possible bone deformity.

During the acute stage, appropriate splinting and limb posturing to avoid contractures. Passive range of motion exercises to minimize deformity due to muscle imbalance.

Tuberculosis (TB) continues to be a cause of death and disability in many parts of the world. Most commonly seen in underdeveloped countries, it is being increasingly seen in developed countries, attributed to global travel and immigration as well as increasing elderly populations and more people with suppressed immune systems—seen in patients taking immunosuppressive drugs and AIDS patients. The cause is mycobacterium, predominantly Mycobacterium tuberculosis (human type) although there are other types such as M. bovis, M. africanum (restricted to African countries), M. canetti, and M. microti.

Mycobacterium tuberculosis is an aerobic bacteria spread through air when affected patients cough, sneeze, or spit. It is a small rod-like bacillus and is classified as an acid-fast bacillus (AFB). The Ziehl–Neelsen stain dyes the AFB bright red. It does not grow on ordinary culture medium, requiring an enriched albumin base. There is a very slow growth rate with colonies only seen 2–4 weeks after inoculation.

Pulmonary TB accounts for 75% of cases; skeletal tuberculosis is uncommon, involving 3–5% in total. Spinal involvement represents almost half of these cases (see Chapter 3.18). Haematogenous spread from a primary focus reaches the skeletal system by arterial vessels except the spine where spread via Batson’s plexus of veins can also occur.

Systemic symptoms (Box 11.2.4) include fever, chills, night sweats, appetite loss, weight loss, and fatigue. Skeletal infection is usually mono-osseous or monoarticular. Localized symptoms characteristically involve pain and loss of function. With progression of disease, joints become deformed by destruction and assumption of a comfortable position. Joint involvement is seen to pass through characteristic stages—initial synovitis with soft tissue swelling, slight reduction in joint movement, and little pain. Early arthritis with decrease in joint space leads to advanced arthritic changes, significant restriction in movement, and increasing pain. Eventual joint destruction with minimal movement and severe pain on movement can lead to fibrous ankylosis.

Diagnosis is made with identification of the causative organism following biopsy. A high index of suspicion is often warranted in cases with minimal symptoms at presentation. A history of travel or recent immigration must be noted. The tuberculin skin test indicates exposure to the bacteria but does not indicate active disease and therefore may not be relied upon to make a diagnosis.

Combination chemotherapy is mandatory, operative intervention is an adjunct to medical therapy. The choice of drug is dependant on sensitivity to the organism and must include one which is bactericidal. Multiple therapies are performed in an attempt to avoid bacterial resistance. Prolonged therapy, of several months, is necessary to eliminate small groups of ‘persistent’ bacilli. An initial intensive phase of three or four drugs is followed by a continuation phase of two drugs.

Surgical intervention due to the success of the chemotherapeutic drugs has a limited indication. Emergency decompression in tuberculosis paraplegia aside, abscess drainage may be conducted dependent on symptoms and functional loss and may not be required. Joint involvement requires drainage and potential debridement. Immobilization in a functional position can lead to a functional ankylosis. In the cases of joint instability, formal arthrodesis may be required. Joint arthroplasty can be considered but prolonged disease inactivity prior to surgery with 3 months of chemotherapy prior to joint replacement followed by several months of therapy postoperatively is advised.