On reviewing our cases of hydatid disease seen over a period of 20 years (1978-1998), we encountered a number of unusual radiological appearances and sites, which are demonstrated in this pictorial review. We briefly discuss the pathology of hydatid disease and its complications.
Twenty‐two patients with brucella spondylitis and neurobrucellosis were studied during a 2‐year period. The diagnosis was based on history of exposure, compatible signs and symptoms, high antibody titre and/or positive culture of a clinical specimen(s). Spondylitis was confirmed by plain radiographs, bone scan, CT and in some cases by histology. Neurobrucellosis was confirmed by CSF examination and culture, myelography, NCV, EMG and CT head. The spondylitis was early in 4 cases, chronic active in 12, smouldering “partially healed”in 3 and healed in 3 cases. Of these, 15 patients (68%) had neurological complications of various types. Plain radiographs were not a good index of activity of spondylitis. Tc99 bone scan was not specific and it remained positive long after the completion of therapy. CT was superior in revealing details of bone destruction, soft tissue swelling and entrapment of nerve roots and cord. The 3 modalities were complementary. Spondylitis is commonly associated with neurobrucellosis and symptoms of one may over shadow those of the other and in some cases neurobrucellosis may be subclinical. In all cases of spondylitis, a thorough search for neurobrucellosis should be made and vice versa. Prolonged treatment with a combination of 3 antibrucella drugs is recommended and prolonged follow‐up is necessary.
Of 65 cases presenting with neuropsychiatric manifestations of brucellosis (CNS-brucellosis), 9(13.8%) had CT-detected basal ganglia calcification (BGC). Of these, 5 had meningitis and 4 had psychiatric manifestations as presenting features. The diagnosis of brucellosis was made by the finding of consistent history and physical findings and the presence of significantly elevated antibody titres and/or positive culture in the blood and/or CSF. In all the cases, BGC was in the form of punctate hyperdense non-enhancing shadows with average density 44.5-58.4 and maximum density 49-64HU. The calcification was unilateral in 3 cases, bilateral and symmetrical in 4 and bilateral but asymmetrical in 2. None of the cases had other predisposing conditions to BGC and in one of the cases did specific anti-brucella treatment effect a detectable change in the BGC. The finding of CT-detected BGC in patients coming from areas endemic for brucellosis should alert physicians to the possibility of underlying brucellar infection.
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