Inner ear and facial nerve complications of acute otitis media with focus on bacteriology and virology.

CONCLUSION: Among 20 patients with inner ear complications and/or peripheral facial palsy secondary to acute otitis media (AOM) a proven or probable bacteriological cause was found in 13 (65%). In seven patients (35%), a proven or probable viral cause was found. Only two of the patients (10%), with a proven bacterial AOM and a clinical picture of a purulent labyrinthitis in both, together with a facial palsy in one, had a substantial degree of dysfunction. Although the number of patients in this study is relatively low our findings show that inner ear complications and facial palsy due to AOM can be of both bacterial and viral origin. Severe sequelae were found only where a bacterial origin was proven. OBJECTIVES: Inner ear complications and/or peripheral facial palsy secondary to AOM are rare. The general understanding is that they are due to bacterial infections. However, in some of these patients there are no clinical or laboratory signs of bacterial infections and they have negative bacterial cultures. During recent years different viruses have been isolated from the middle ear or serologically proven in AOM patients and are thought to play a pathogenetic role. We suggest that in some cases of AOM complications from the inner ear and the facial nerve can be caused by viruses. The purpose of our study was to analyze infectious agents present in patients with inner ear complications and/or facial palsy arising from AOM. PATIENTS AND METHODS: The medical records of 20 patients who had inner ear complications and/or facial palsy following AOM ( unilateral in 18, bilateral in 2) between January 1989 and March 2003 were evaluated. Bacterial cultures were carried out for all patients. Sera from 12 of the patients were stored and tested for a battery of specific viral antibodies. In three patients, investigated between November 2002 and March 2003, viral cultures were also performed on samples from the middle ear and nasopharynx. RESULTS: Nineteen patients had inner ear symptoms. Eight of them had a unilateral sensorineural hearing loss and vertigo, three had vertigo as an isolated symptom and one, with bilateral AOM, had bilateral sensorineural hearing loss. Seven patients had a combination of facial palsy and inner ear symptoms (unilateral sensorineural hearing loss in three, unilateral sensorineural hearing loss and vertigo in two, bilateral sensorineural hearing loss and vertigo in one, with bilateral AOM, and vertigo alone in one). One patient had an isolated facial palsy. Healing was complete in 11 of the 20 patients. In seven patients a minor defect remained at follow-up (a sensorineural hearing loss at higher frequencies in all). Only two patients had obvious defects (a pronounced hearing loss in combination with a moderate to severe facial palsy (House-Brackman grade 4) in one, distinct vestibular symptoms and a total caloric loss in combination with a high-frequency loss in the other. Eight patients had positive bacteriological cultures from middle ear contents: Streptococcus pneumoniae in two, beta-hemolytic Streptococcus group A in two, beta-hemolytic Streptococcus group A together with Staphylococcus aureus in one, Staph. aureus alone in one and coagulase-negative staphylococci (interpreted as pathogens) in two. In the 12 patients with negative cultures, there was a probable bacteriological cause due to the outcome in SR/CRP and leukocyte count in five. In four patients serological testing showed a concomitant viral infection that was interpreted to be the cause (varicella zoster virus in two, herpes simplex virus in one and adenovirus in one.) In three there was a probable viral cause despite negative viral antibody test due to normal outcome in SR/CRP, normal leukocyte count, serous fluid at myringotomy and a relatively short pre-complication antibiotic treatment period.

[Detection of varicella-zoster virus DNA by polymerase chain reaction in patients with Hunt syndrome and clinical progression].

Varicella-zoster virus (VZV) is known to be associated with Hunt syndrome. In this study, the detection of VZV-DNA in peripheral blood, throat swabs, urine and crusts was performed, in 6 cases of Hunt syndrome, by the polymerase chain reaction (PCR) method. For DNA-extraction, glass-powder was used. As a primer, an oligonucleotide, which specifically amplifies 1201-1424 in the Sst-Ig region, was used. Amplification was performed by repeating 30 cycles of the following procedures: denaturing at 94 degrees C, annealing at 60 degrees C, and extension at 72 degrees C. In one case, VZV-DNA was detected in all samples, in another case it was detected in a throat swab, urine and crust, and in another case in peripheral blood, urine and crust. The other 3 cases showed VZV-DNA only in crusts. These results indicate that viremia might occur in Hunt syndrome, and that those patients in whom VZV-DNA was detected in peripheral blood and urine showed a tendency for slow recovery. The present results indicate that this method provides a valuable tool for the early diagnosis of Hunt syndrome and zoster sine herpes and that it is useful for predicting the progression of Hunt syndrome.

Detection of human alpha-herpesvirus DNA using consensus primers and specific probes.

A simple and rapid diagnostic assay system was developed for detecting and identifying human alpha-herpesviruses, such as herpes simplex virus types 1 and 2 and varicella-zoster virus, by polymerase chain reaction. This system was based on an amplification step, using primers that bind the DNA polymerase consensus sequence of alpha-human herpesviruses, and a detection step, using non-radioactive virus-specific probes. This method could be used to amplify any human alpha-herpesviruses, and each virus-specific probe was highly specific for identification of the amplified product. This system is readily applicable for implementation in the clinical laboratory.