Hydatid disease of bones is uncommon, and the spine is involved in ~ 50% of these cases. It is a rare occurrence, even in rural areas where echinococcus is endemic, but it is the most serious. Primary infestation of the spine occurs through the porto-vertebral shunts, and the center of the vertebral body is the first site to get involved. When larva penetrates cancellous bone in the vertebrae, it causes a multivesicular and diffuse infiltration [7]. In bony HD, pericyst formation does not occur, thus allowing aggressive proliferation along the line of least resistance, particularly the bony canals [4]. Eventually, daughter vesicles invade the bone and replace the medullary cavity and the disease reaches the cortex and destroys it with subsequent spread of the disease to surrounding tissues [8]. They may grow to very large sizes and may remain asymptomatic for years. While extraosseous hydatids often calcify, intraosseous hydatids rarely do so [9]. In majority of the cases, the disease is confined to the bone and the epidural space [10]. Intradural extramedullary disease has been reported only in 9% of the cases [11, 12]. Neurological complications arise as a result of compressive myelopathy or neuropathy secondary to intradural and extradural disease component.

On radiograph, the disease may mimic non-specific osteomyelitis in its initial phase because of medullary infiltration by the larvae. Bony erosion, osteolysis and destruction occur with progression of time, and in later stages, a multiloculated cystic appearance may be seen [13]. Some typical imaging features of spinal HD include lack of osteoporosis or sclerosis in involved bone, lack of intervertebral disk space involvement and subperiosteal, subligamentous or paraspinal extension of the disease [8]. CT may contribute in better demarcation of the lesion showing bony expansion with honeycomb-like appearance of the spine and may even demonstrate rim calcification [13]. MRI is superior in assessing the lesion extent and neural involvement and can help in ruling out other differentials. The lesions show intermediate to low-signal intensities on T1-weighted and high-signal intensity on T2-weighted images with multilocularity being a key feature [14]. Hyperintensity on T2WI suggests viable cysts, whereas isointense signal to muscle on both T1 and T2WI or T2 hypointense signals and T1 hypointense signals represent dying or dead cysts. Though efficacy of albendazole for primary bony hydatid treatment is questionable, postoperative albendazole therapy seems only way to prevent recurrence [15]. All of our patients received albendazole (15 mg/kg) in divided doses daily for 3 months, and there was no recurrence in any of our cases till latest follow-up. Because of poor bony penetration of albendazole, radical excisional surgery of primary disease should be done at earliest. The aim of surgery should be removal of all cysts along with involved bone and soft tissues. We were able to get good surgical clearance in all our cases. We irrigated the surgical field with hypertonic saline to prevent local recurrence (16). Though there was a theoretical risk of chemical injury, we did not encounter any such problem. The strength of our study is that it confirms the role of diagnostic imaging and radical excision in the management of these rare lesions, and only possible limitation is short-term follow-up to conclude complete remission.

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