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Seeding of a cavernous angioma with Mycoplasma hominis: case report.

To the Editor: We have read with great interest the article by House et al. (4). We agree that static or slow venous flow within a preexisting cavernous angioma (CA) contributed to focal bacterial deposition and abscess formation in this particular patient. The finding of a disproportionate cerebral edema surrounding the malformation is a good clue, as suggested by the authors, of a secondary infection that should be carefully checked at operation. However, in general, the problem may be more intriguing, and not only “superinfection” but also direct promotion (de novo or growth) of the malformation should be considered. Fender et al. (3) described a de novo genesis of two CAs after bacterial meningitis and subdural empyema. They suggested that thrombophlebitis of small veins and ensuing venous hypertension could be initiating factors promoting a capillary proliferation evolving into a CA. This is a sort of “convergent” disease leading to the formation of a de novo malformation (9). The origin of CAs is multifactorial: genetic causes, irradiation, and infection (viral or bacterial) have been implicated and may be variably connected (2). Viruses may be significant cofactors for angiogenic processes and activation of cerebrovascular malformations. We are particularly interested in infective pathogenesis of CAs (7). The main issue is whether the infection might be involved directly, and not through an indirect mechanism, in the formation of the angioma. The polyoma virus, a member of the papovavirus family, is associated with the induction of multiple CAs in immunodeficient rats (2). It is probably not coincidental that some de novo CAs occur in children irradiated for leukemia and lymphomas (5, 6). We found the deoxyribonucleic acid of cytomegalovirus, a member of the herpesvirus family, by in situ hybridization in the intercavernous matrix of some CAs (7); it is noteworthy that the cytomegalovirus infection of fibroblasts may induce an endothelial cell growth factor and promote angiogenesis (1). This may partly correlate with the expression of angiogenic factors observed by several authors in CAs (8). Strong angiogenic activity of the human immunodeficiency virus was recently suggested in an arteriovenous malformation (10). The activity of basic fibroblast growth factor and vascular endothelial growth factors is augmented in human immunodeficiency virus-infected patients, and antiretroviral therapy may inhibit the virusinduced angiogenic stimulation (10). In conclusion, cerebrovascular malformations, and CAs in particular, may be a target of infection that may interfere with the development of the lesion: this issue has scarcely been investigated but constitutes a promising field of study and research.