BILATERAL VESTIBULAR LOSS AS A COMPLICATI ON OF YERSINIOSIS

Background: Yersinia infections other than plaque are caused by Yersin ia pseudotuberculosis and Yersinia enterocolitica. Food and water cont amination as well as animal-to-person and person-to-person contact are common pathways of transmission. Clinical manifestations include ente ritis, enterocolitis, acute appendicitis, inflammation of the terminal ileum, and mesenteric adenitis. Y. enterocolitica may cause bacteremi a with subsequent septicemia predominantely in patients with underlyin g illnesses such as diabetes mellitus or malignancy. More frequently e nteritis is followed by immunological post-infectious syndromes such a s arthritis and erythema nodosum. The present case report discusses bi lateral vestibular loss possibly caused by an infection with Y. entero colitica. Patients: A 27-year-old caucasian woman initially presented with the otologic symptom of spinning vertigo accompanied by nausea an d vomiting, Results: physical exam revealed spontaneous nystagmus to t he left. Bithermal caloric responses were absent. Pure tone audiometry showed a bilateral symmetric high-frequency sensorineural hearing los s. Neurologic exams did not reveal involvement of the central vestibul ar system. Perilymphatic fistula on the left side was excluded by tymp anoscopy. Serology for rheumatoid factors and HLA B27 was negative. Le ad or mercury intoxication was also excluded, In her medical history t he patient reported intermittent watery diarrhea and stress dependent arthralgia that had commenced during a stay in Argentina three years a go. Serology was positive, revealing elevated titers for Y. enterocoli tica type 3 (1:200) and type 9 (1:400). Discussion: Bilateral vestibul ar loss is rare. The main cause is aminoglycoside ototoxicity or menin gitis. Yersina infections have not yet been described as inducing dise ase of the labyrinth. Present pathophysiologic knowledge of yersinia i nfections is described as follows: After peroral infection, gastrointe stinal permeability is increased. Low-molecular-weight substances may enter the bloodstream and stimulate the formation of circulating immun ecomplexes. These are held responsible for extraintestinal manifestati ons of yersinosis. Whether these circulating immune complexes and anti bodies against Y. enterocolitica have an effect on the inner ear remai ns unclear. Conclusion: Because the coincidence of yersiniosis and a b ilateral vestibular loss with no other identified cause, a postinfecti ous immune response is suggested as possible pathogenic mechanism.