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Year : 1985 | Volume
: 31
| Issue : 4 | Page : 223-5 |
Cervicofacial actinomycosis with upper cervical vertebral involvement and fatal meningitis (a case report).
Deshpande RB, Rao AA
How to cite this article: Deshpande R B, Rao A A. Cervicofacial actinomycosis with upper cervical vertebral involvement and fatal meningitis (a case report). J Postgrad Med 1985;31:223 |
How to cite this URL: Deshpande R B, Rao A A. Cervicofacial actinomycosis with upper cervical vertebral involvement and fatal meningitis (a case report). J Postgrad Med [serial online] 1985 [cited 2023 Sep 21];31:223. Available from: https://www.jpgmonline.com/text.asp?1985/31/4/223/5377 |
Vertebral involvement in actinomycosis is uncommon. No such case was found in the study of 181 subjects suffering from actinomycosis by Brown.[1]Cope,[2]in 1951, reviewed the literature, and could count only 66 cases including four of his own. Since then only a few more have been added to the list.[4],[5],[6],[7]However, atlanto-axial involvement has not yet been recorded. Actinomycosis, in all its forms, may be mistaken for tuberculosis. We are reporting this case to re-emphasise the subtle radiological changes which may help to distinguish the two diseases.
A fifty-five year old farmer presented with pain stiffness of neck of three months duration and a discharging sinus with a swelling on the right side of the neck of 7 months' duration. He denied any history of fall, lifting weights or fever. He was emaciated, and had torticollis with chin to the left. All the cervical movements were severely restricted and accompanied by muscle spasm. There was no neurological deficit. Two mobile, discrete lymph nodes were palpable in the right cervical region. Investigations revealed hemoglobin of 9 gm% and a total white cell count of 6,600/cmm with a differential count P:80%, and L:20; E.S.R. was 125 mm at the end of first hour. Radiological features were interpreted as tuberculosis and the patient was put on Halter traction with antitubercular drugs. While still on traction, his general condition worsened, gradually progressing to coma, and he finally died on the 14th day of admission. Autopsy revealed dense fibrocollagenous tissue on the right side of the neck with a sinus tract extending on to the skin. The inflammatory process extended posteriorly to the pre and paravertebral soft tissue with marked destruction of the first, second and part of the third cervical vertebrae. Necrotic and yellowish brown granular material was present in the destroyed vertebral bones. The exudate had spread on to the dura producing a pachy meningitis, with purulent exudate around the spinal cord, which extended upwards to the lower end of medulla oblongata. There were yellowish brown granules on the under surface of the dura at the level of the foramen magnum. The cerebral hemispheres and cerebellum were free of any exudate or abscess. Histologically, there was fibrocollagenous tissue diffusely infiltrated with histiocytes, plasma cells and many lymphocytes, forming local aggregates at places. Multiple granules of 'ray fungus' were seen surrounded by dense polymorphonuclear aggregates. There was a partial destruction of the vertebral bodies with evidence of new bone formation. The 'ray fungus' showed centrally dense basophilic material and a lightly stained peripheral portion with characteristic radiating clubs. On closer examination, they revealed colonies of actinomyces comprised of Gram positive, nonacid fast, slender, branching and beaded organisms.[5] The enlarged lymph nodes revealed no evidence of actinomycosis. However, the peripheral lymphoid tissue was replaced by dense hyaline nodules. The lungs showed evidence of aspiration pneumonia, but no evidence of actinomycosis. All other organs were unremarkable. The radiological features were reviewed again, and, the features that were overlooked at first appeared obvious now. The lateral view of the cervical spine showed a total obliteration of lordosis. Rarefaction was noted in the upper cervical spine, especially in the region of the second and third cervical vertebrae. The odontoid process showed a mottled appearance with sclerosis and lytic areas interspersed. The cortices of second and third vertebrae showed destruction, and diminution of joint space. No sequestrae were seen. The rest of the cervical vertebrae showed spondylotic changes (See[Fig. 1]on page 222B). The open mouth view showed the odontoid process tilted to the right side, with lytic areas in the right lateral mass of atlas. The axis showed new bone formation in this view. The mandible and maxillae were normal (See[Fig. 2]on page 222B). The chest X-ray was within normal limits.
Vertebral involvement occurs invariably by direct continuous extension of the infection from a primary site, initially setting up a pre-or paraverebral phlegmon. As the bone is eroded there is initially periostitis with subperiostial new bone formation. In a slowly progressing disease the new bone formation may be extensive, rarely, forming bony tumourous growth. However in an aggressive process the new bone formation may be scant and inconspicuous. This new bone formation appears to be a defence mechanism on the part of the bone.[2],[7] As the disease progresses, the initial erosions become deeper causing destruction of the cancellous bone of the vertebrae with secondary ostiomyelitis, and abscess formation resulting in multiple intercommunicating cystic spaces. Along with the bony destruction there invariably occurs new bone formation around the cystic cavities giving a mottled or lattice like appearance on X-ray. Sequestrae formation does not occur. One or several successive vertebrae may be involved. While in tuberculosis, the initial focus starts by haematogenous spread to the cortex of the bone, actinomycosis invariably reaches the bone by continuous, direct spread. Actinomycosis usually spares the discs, but unlike tuberculosis invariably affects the adjacent pedicles, transverse processes and corresponding heads of the ribs.[7]As a result of the abundant new bone formation, vertebral collapse and angular deformities are uncommon.[2],[7]However, in an aggressive disease process, where new bone formation is minimal, such collapse and deformities may occur.[7] Actinomycosis is known to respond well to penicillin therapy. Complete recovery following treatment with penicillin in a case of spinal meningitis secondary to cervicofacial actinomycosis has been reported.[3]
1. | Brown, J. R.: Human actinomycosis: a study of 181 subjects. Hum. Pathol. 4: 319-330, 1973. |
2. | Cope, V. Z.: Actinomycosis of bone with special reference to infection of vertebral column. J. Bone and Joint Surg., 33-B: 205-214, 1951. |
3. | Intile, J. A. and Richert, J. H.: Cervicofacial actinomycosis complicated by meningitis. J. Amer. Med. Assoc., 181: 724-726, 1962. |
4. | Nathan, M. H., Paul Radman, W. and Barton, H. L.: Osseous actinomycosis of the head and neck. Amer. J. Roentgenol., 87: 1048 1053, 1962. |
5. | Robboy, S. J. and Vickery, A. L. Jr.: Tinctorial and morphologic properties distinguishing actinomycosis and nochardiosis. New Engl. J. Med., 282: 593-596, 1970. |
6. | Simpson, W. M. and McIntosh, C. A.: Actinomycosis of the vertebrae (Actinomycotic Pott's disease). Report of 4 cases. Arch. Surg., 14: 1166-1186, 1927. |
7. | Young, W. B.: Actinomycosis with involvement of the vertebral column: Case report and review of the literature. Clin. Radiol., 11: 175-182, 1960. |
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