Tropical diseases

Skeletal and soft tissue diseases

 

Osteomyelitis

There is a wide variety of osteomyelitis found throughout the tropics and bone infection is probably more common than in many temperate climates. Osteomyelitis due to typhoid and salmonella should also be considered, especially in patients with sickle cell disease. The use of ultrasound in the early diagnosis of any acute bone infection is important in children. Needle aspiration guided by ultrasound will not only decompress the abscess, but allow identification of the organism and accurate antibiotic therapy. Healing will be quicker and the skeletal deformity will be less. Tuberculosis can affect the skeleton in a wide variety of ways, resembling an acute osteomyelitis, a cyst in a long bone, an acute or chronic arthritis, a severe periosteal reaction, or a destructive lesion. Think of tuberculosis in any tropical bone disease, but remember typhoid, klebsiella and syphilis also: then worry about more common organisms!

Tropical ulcer

A tropical ulcer is an acute specific, localised necrosis of skin and soft tissues, followed by a chronic ulcer involving the entire skin and subcutaneous tissues. It usually occurs in the front of the lower leg or on the foot. The acute organism is Bacillus fusiformis, with secondary infection inevitably following. Tropical ulcer must not be confused with the sores due to cutaneous Leishmaniasis. After the acute phase, the surrounding oedema and granulation tissue persist, and in many patients the ulcer spreads to involve the deep fascia, the tendons and the underlying bone. When this occurs there is a characteristic radiological change, almost always first in the tibia but involving the fibula also. A localized periosteal re action, usually fusiform and linear but sometimes with spiculation, develops under the soft tissue ulcer (Fig. 36). This eventually results in a

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Figure 36. Tropical ulcer. Four different patterns of bone reaction beneath tropical ulcers. a) A laminated periosteal reaction on the tibia. (Nigeria) b) An "osteoma" on the anterior edge of the tibia. (Nigeria) c) AP and lateral views of a large tibial "osteoma ". (Nigeria) d) A very irregular hypertrophic postero-Iateral "osteoma" on the fibula, with minimal cortical thickening on the tibia. (Kenya). All these reactions are smooth and there are no changes which might suggest malignancy.

thick sclerotic layer of bone, which may be as much as 2.5 cm in thickness and resembles (and has been called) an ivory osteoma. At this stage the original layered periosteal reaction will have disappeared. The reaction can spread around the whole bone, above and below the site of the soft tissue ulcer. It varies in width and length, and may be followed by superficial sequestration in a localized area. There is loss of the overlying soft tissue, with underlying osteoporosis, followed by expansion of the medullary cavity, with considerable remodelling into a cancellous osteoma. This residual deformity may have to be removed surgically before the ulcer can be properly treated. Secondary infection of the ulcer with further bone reaction can occur.
The tissues around tropical ulcers may undergo malignant change, but usually after a period of some years. There will then be soft tissue and

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Figure 37. Malignant tropical ulcer. a) Ulceration in the upper third of the lower leg with bone destruction. (Nigeria) b) More advanced ulceration in the lower half of the leg with destruction of more than two thirds of the tibia. (Nigeria)

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Figure 38. Ainhum. a) The typical soft tissue band around the fifth toe, constricting the middle and proximal phalanges. (Nigeria) b) A much less common, but similar appearance in the hand. The distal half of the middle finger has been auto-amputated and there is another tight band constricting the middle phalanx of the indexfinger. (Nigeria)

bony destruction which spreads, involves the cortex and the medullary cavity and may lead to pathological fracture (Fig. 37). Systemic tumour dissemination and metastatic spread is possible, but is not common. The whole chronic destructive process can be prevented if the initial skin wound is thoroughly washed with soap and water and kept dean.

Ainhum

This is an unusual afflication of one or more toes, usually in middle-aged black men who are otherwise healthy. A constricting, sometimes painful groove develops around the base of the toe which can lead to auto-amputation. It can occur, but is much less common in the fingers. The aetiology is unknown. The fifth toes, often bilaterally, are the most commonly affected, but other phalanges may be involved. Clinically, the disease is obvious, easy to diagnose, and appears trivial. However, it can be painful and crippling. The radiological changes are similarly characteristic (Fig. 38). The fibrous groove around the toe can be seen in the soft tissues and there will be underlying localized osteoporosis, usually of the proximal phalanx. The cortex becomes absorbed and the affected phalanx is concentricaly thinned and asymmetrically tapered. If there is infection, there may be a small cortical reaction. Eventually, there is angulation of the digit, a pathological fracture which can be very painful, and auto-amputation. Fortunately, treatment is seldom necessary, but surgery may be helpful to ease the pain or the lymphoedema which results from the tight constriction.

It is important for the radiologist to distinguish this benign process from leprosy. It is unusual for leprosy to affect only one bone and very seldom in leprosy is the only clinical abnormality in one toe, or even one toe of each foot. Unlike leprosy, there is no sensory loss in ainhum, no other soft tissue abnormality and very seldom any ulceration or infection. It is, clinically and radiologically very easy to recognise and there are very few complications. There is no indication for complex investigations to exclude some other disease. Ainhum is an entity in its own right.

Leprosy

This bacillary infection has been feared for centuries and there are still several million lepers in the world, with 650,000 new patients every year. It is a chronic and destructive infection due to M. leprae with many unanswered questions. As with many of the other tropical diseases, there can only be a brief summary here, but if suspected, reference to a more comprehensive description is strongly recommended.

Many of the clinical results of leprosy are in the soft tissues, and for the radiologist it is the effects of soft tissue infection, distorsion and denervation which are of importance. However, one result is absolutely diagnostic. Calcification of nerves occurs in leprosy and in no other condition. It may be linear, along the nerve, sometimes in flakes, or oval calcification may be the end-result of a perineural abscess. Contrast injection along the nerve sheeth has been suggested, to localise the calcification, but a clinical diagnosis of leprosy should be much easier! Except in the skeleton (particularly the extremities) there are no other significant imaging findings. Leprosy granulomas do occur in the liver, spleen and in many other organs, but are not reliably identifiable by any imaging method.

When primary bone changes in leprosy are recognised, they are medullary and destructive, with only a little bone response until healing occurs. The digits are the most frequently affected, showing localised osteoporosis, honeycombing and concentric bone absorption. There can be well-defined cystic lesions (from which M. leprae can be aspirated), but these are not necessarily related to the soft tissue changes. Microfractures are common, but heal with treatment, as do the cysts.

A periosteal reaction occurs in about one third of all leprosy patients, usually painless except in a minority who have severe pain and tenderness. The tibia and ulna are common sites. During the "lepra" stage bone destruction can be severe, usually in the vascular parts of bone.

The soft tissue changes are ulceration, atrophy and fibrosis, all modified by infection. There is often underlying osteoporosis, particularly during the "lepra" stage. Almost all the other skeletal changes in leprosy result from neurological and vascular deficits, which are superimposed on the changes caused by motor and sensory paralysis. Added complications are the soft tissue infection and ulceration, and sometimes secondary bone infection as well. To these must be added the results of trauma, often repeated, to limbs which have damaged sensory appreciation and poor motor control. This prolonged and sad sequence can be summarised:
- Localised osteoporosis
- Periosteal and subperiosteal reaction. Infection and sequestration
- Absorption of bone and formation of new bone, a combination of is chaemia and soft tissue contraction
- Fractures of the distal metatarsal shafts and absorption of the metatarsal heads (characteristic)
- Contraction of the soft tissues and bone absorption with resulting apparent gaps on the radiograph between the remaining bones
- Secondary bone infection, especially related to soft tissue ulceration, which is common and persistent
- Neurotrophic changes in the joints, usually in the small joints of the hands and feet, with subluxation. This is added to the ischaemic changes and hastened by weightbearing on the feet and hands (sticks and crutches will be needed eventually) when there is no protective sensation.

The end-results are major destructive bone loss with disorganised joints, most obviously in the digits and later in the tarsus, less often in the carpus (Fig. 39). Similar destructive changes can be seen in the nasal bones and occasionally elsewhere.

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Figure 39.Leprosy. a, b) The destructive process of leprosy in the foot and the hands. (India)

It must be re-emphasised that the diagnosis of leprosy is almost always made clinically. The task of the radiologist is to assess the damage which results. Reconstruction is often undertaken and requires cooperation between all concerned. There are special radiographic positioning techniques to aid this process.

Filariasis

Many different filaria infect millions of people around the world. Amongst them, the most important are Wuchereria bancrofti, Brugia malayi and B. timori. These filaria cause elephantiasis. Loa Loa causes "calabar swellings" and Onchocerca volvulus causes onchocerciasis or "river blindness". Each have a distinctive geographical distribution, but together infect millions of people. All are transmitted by insect bites.
The limbs of patients who have gross clinical elephantiasis do not have very specific radiological changes. There is loss of the soft tissue fat lines.

a	Figure 40. Filariasis. a) Multiple circular calcified nymphs of armillifer armillatus seen throughout the liver and spleen (an upper abdominal film taken during contrast urography). (Nigeria) b) Abdominal ultrasound showing similar calcified nymphs of armillifer armillatus. (Nigeria; courtesy of Dr. Marinho) c) The faintly calcified line which results from calcification of the dead filaria, Loa Loa, in the soft tissues of the hand. (Nigeria)
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c

The underlying limb bones may show marked periosteal and cortical thickening, which results from the soft tissue changes and is not an effect of the filaria on the bones. Contrast urography will show dilated renal lymphatics in patients with lymphuria. Lymphangiography is technically very difficult and only useful to exclude congenital lymphoedema (which is often unilateral).

Not all elephantiasis is due to filariasis. Any lymphatic obstruction, e.g. due to tuberculosis, Kaposi's sarcoma, or L.G.V., may be responsible. To make the differential diagnosis more difficult, filarial elephantiasis can be unilateral.

Figure 41.Tropical eosinophilia. Soft bilateral fluffy nodules throughout the lungs. There was a 67 % peripheral eosinophilia, which suggested the correct diagnosis: filariasis. (Nigeria)

Porocephalosis

Porocephalosis results from tongue worm infection, usually Armillifer armillatus or Porocephalus crotali. There are few clinical symptoms. The A. armillatus are acquired by eating snakes, or drinking water used by snakes.

Many of these small parasites calcify and may be recognized as fine strands of calcification in the soft tissue (Fig. 40). They are then de ad, but the filaria cannot be accurately identified. The fine calcified remnants must be distinguished from cysticercosis (usually oval and more numerous) and porocephalosis (multiple, crescentic or horseshoe calcifications in the abdomen or chest, but seldom elsewhere). (See also guinea worm page 63).

 

Philip E.S. Palmer, with Stanley P. Bohrer, Carlos Bruguera, Xing-Rong Chen, Mahmoud R. EImeligi, Hassen A. Gharbi, S.B. Lagundoye, M. W. Wachira