Actinomycotic mastoiditis complicated by sigmoid sinus thrombosis and labyrinthine fistula.

Actinomyces is a rare pathogen that can be the cause of infections in the digestive and urinary tracts, skin, genitalia, and lungs, which generally have an indolent clinical course. However, in some cases these can be locally destructive and become generalized infections. Actinomyces has been previously implicated in infections of the middle ear, nasopharynx, and sinuses, occasionally causing complications such as chronic mastoiditis. Here we describe the case of a 10-year-old-male presenting with nausea, vomiting, and headache who developed intracranial complications of actinomycotic mastoiditis.

Bacterial invasion of the inner ear in association with pneumococcal meningitis.

OBJECTIVE: To examine the pathways of bacterial invasion and subsequent spreading in the inner ear during pneumococcal meningitis. STUDY DESIGN: A well-established adult rat model of Streptococcus pneumoniae meningitis was used. METHODS: Thirty rats were inoculated intrathecally with S. pneumoniae serotype 1, 3 or 9 V and received no additional treatment. The rats were sacrificed when reaching terminal illness or on Day 7 and then prepared for serial sectioning and PAS-Alcian blue staining for light microscopy. RESULTS: During the first few days after inoculation, bacteria invade the inner ear through the cochlear aqueduct, into the scala tympani of the cochlea (perilymphatic space). From here, bacteria spreads apically toward the helicotrema and subsequently basally through the scala vestibuli, toward the vestibule and the vestibular system. When the bacteria after 5 to 6 days had reached scala vestibuli of the basal turn of the cochlea, hematogenous spreading occurred to the spiral ligament and into the cochlear endolymph, subsequently to the vestibular endolymph. We found no evidence of alternative routes for bacterial invasion in the inner ear. Several internal barriers to bacterial spreading were found within the inner ear. Bacterial elimination was evidenced by engulfment by macrophages within the inner ear. CONCLUSION: From the meninges, pneumococci invade the inner ear through the cochlear aqueduct during the first days of infection, whereas hematogenous invasion via the spiral ligament capillary bed occur at later stages. Although internal barriers exist within the inner ear, the spreading of bacteria occurs via the natural pathways of the fluid compartments. Bacterial elimination occurs by local macrophage engulfment.

Managing chronic otitis media with cholesteatoma report of 223 patients seen in a 5-year period.

BACKGROUND: To assess the clinical features, diagnosis, and treatment of patients having chronic otitis media (COM) with cholesteatoma seen in the ENT/Head and Neck Surgery Clinic at the University Clinical Center, Prishtina, Kosovo. METHOD: A systematic review of the medical records of all patients admitted to the ENT clinic having COM with cholesteatoma between January 1999 and December 2003. RESULTS: During this period, 223 patients suffering from COM with cholesteatoma underwent surgical treatment. There were 123 (55%) male and 100 (45%) female patients. Their mean age was 30.7 years, ranging from youngest patient (7-year-old girl) to oldest (73-year-old lady). Thirty-three patients developed complications: 17 patients extracranial complications (EC) and 16 intracranial complications (IC). Leading pathogens in this series were Proteus mirabilis in 52% of cases, Proteus vulgaris in 14% and Staphylococcus aureus in 12%. All patients underwent surgical treatment: 10 patients (4.5%) a canal-wall up (CWU) procedure and 213 (95.5%) a canal-wall down (CWD) procedure. No deaths occurred in this series. CONCLUSION: Because of possibility of developing life-threatening complications, patients with COM with cholestatoma must diagnosed in time and followed as soon as possible to the center that performs ear surgery, as only adequate treatment option for these patients.

Actinomycosis of the temporal bone with labyrinthine and facial nerve involvement.

OBJECTIVES: To demonstrate the clinical, radiologic, and pathologic findings of actinomycosis of the temporal bone. STUDY DESIGN: Case report and literature review. METHODS: Analysis of a case through medical records and literature review. RESULTS: Actinomycosis is a rare cause of subacute-chronic suppurative infection of the temporal bone. We present an 11-year-old male with a history of ciliary dyskinesia presenting with a 6-week history of right-sided otorrhea, otalgia, and a 1-week history of progressive facial weakness. Final histopathology revealed a diagnosis of actinomycosis. A review of the literature showed 25 cases of temporal bone actinomycosis. This is the first reported case of actinomycosis causing facial nerve palsy and labyrinthine invasion. Effective treatment includes aggressive surgical debridement followed by long-term administration of appropriate antibiotic. CONCLUSIONS: Actinomycosis can be a cause for bone erosive lesions of the temporal bone and can result in significant morbidities. Prompt tissue diagnosis with suspicion for nonmalignant causes of bone erosive disease can help in implementing appropriate treatment.

Typical and atypical Cogan's syndrome: 32 cases and review of the literature.

OBJECTIVE: To report our experience on a multicentre series of 32 patients with either typical or atypical Cogan's syndrome, to combine our results with a detailed review of the literature, and to compare the clinical manifestations of typical and atypical Cogan's syndrome. METHODS: Patients were identified from a survey conducted with physicians affiliated to the French National Society for Internal Medicine, and were classified into typical or atypical Cogan's syndrome according to the Haynes criteria. Clinical data were collected in a standardized manner. A comprehensive literature review using the Medline database and the reference lists of identified articles was performed. RESULTS: Seventeen patients had typical Cogan's syndrome and 15 had atypical Cogan's syndrome. Apart from non-syphilitic interstitial keratitis, the ocular manifestations of patients with atypical Cogan's syndrome were mainly uveitis and episcleritis. All but one patient presented with Ménière-like syndrome, and at the end of follow-up 11 were deaf and 19 additional patients had developed a significant decrease in auditory acuity. Twenty-five patients (78%) developed systemic manifestations, including aortitis in four. Comparison of typical and atypical Cogan's syndrome showed that some systemic manifestations were more common in atypical Cogan's syndrome, but these differences may be explained by reporting bias in the literature. CONCLUSION: Differences regarding the associated systemic manifestations of typical and atypical Cogan's syndrome may reflect reporting bias in the literature. However, the diversity of the ocular and audiovestibular manifestations and the acceptable lengthy delay between the two types of involvement in atypical Cogan's syndrome should make one cautious before accepting this diagnosis as the diagnosis may mimic various other systemic diseases.

Differential diagnosis of virus-like particles in the human inner ear.

The entire endolymphatic duct and sac as well as the vestibular epithelia were obtained from four patients with Meniere's disease during translabyrinthine (TL) eighth nerve section and from 12 patients undergoing TL resection of acoustic schwannomas. After these specimens were processed for routine transmission electron microscopy (TEM), they were studied for morphologic evidence of viral infection. Although no virus particles were identified, numerous regularly occurring cell components and artifacts were found to morphologically mimic viruses. An atlas of these structures is presented.

[Viral origin of postnatally acquired inner ear damage]. / Zur viralen Genese postnatal erworbener Innenohrschäden.

Experimental and clinical data exist which point at a possible role of herpes virus infections in postnatally acquired inner ear disturbances. The presence of viral DNA in the inner ear and vestibular organ of experimentally infected mice and pigs suggests that not only primary infections but also the reactivation of latent herpes viruses can cause severe inner ear damage. Serological examinations are presented and therapeutic considerations discussed.

Otosyphilis: a practical guide to diagnosis and treatment.

The diagnosis and management of patients with suspected treponemal infection of the temporal bone pose some challenges. The following points deserve emphasis: 1) the MHA-TP or FTA-Abs is recommended over the reagin serologic tests (VDRL, RPR); 2) one should regard this process as an attempt to define a subgroup of patients with sensorineural hearing loss who will benefit from a combination of antibiotics and steroid therapy rather than explicitly diagnosing infection of the temporal bone. The response rate to therapy is limited; but, otosyphilis, as one of the few treatable causes of sensorineural hearing loss, must be suspected in the differential diagnosis of a wide range of otologic patients.

The role of acute and latent virus infections in the pathogenesis of inner ear disturbances.

The possible role of herpesviral infections of the inner ear in suddenly appearing inner ear disturbances was investigated. Experimental pseudorabies virus (PRV, Herpes sui 1) infection of mice and swine was used as a model system. Infected mice represented the productive cycle of PRV infection (acute phase), whereas the latent phase of infection could be tested in swine. From the acutely infected mice the virus could be reisolated from perilymphatic fluid and various parts of the brain. Massive histopathologic alterations and signs of total cell damage to the organ of Corti and the vestibular organ were found. Accordingly, in all of the cells of the inner ear multiple copies of the PRV genome could be demonstrated. We therefore suggest that the disturbances of the inner ear were induced by the acute virus infection. In two latently infected swine (sixty weeks after infection), PRV could not be recovered either from the perilymphatic fluid or from a variety of different neural and extraneural tissues. However, histopathologic changes similar to those found in the acutely infected mice were observed. The presence of viral DNA could be demonstrated by in situ cytohybridization in both sensory and supportive cells of the inner ear and vestibular organ, but not in the corresponding nerve fibers, which is in contrast to the acutely infected mice. The distribution of the viral genome was further analyzed in adjacent areas of the central nervous system. An involvement of acute and latent herpes virus infection in inner ear dysfunction including sudden deafness and vestibular neuronitis in man, might be suggested from the results described. The presented animal model system, PRV-infected swine, should permit further studies on a possible role of herpetic recurrences, particularly with regard to inner ear disturbances.

Detection of pseudorabies virus DNA in the inner ear of intranasally infected BALB/c mice with nucleic acid hybridization in situ.

Evidence for the pathogenicity of pseudorabies virus for the auditory and vestibular organs of experimentally infected mice is presented. We demonstrate viral genomes in cells of the peripheral sensory organs, the nerve structures, and the affected areas of the brain in single sections from an entire cranium of an adult mouse. The data were obtained by an in situ hybridization technique adapted for use with fixed, plastic-embedded materials. In contrast to conventional methods which use frozen sections, we were able to analyze cartilaginous and bony materials with high resolution.

[Cochleo-vestibular attacks of viral origin]. / Les atteintes cochléo-vestibulaires d'origine virale.

The viral etiology of some cochlear or vestibular lesions is well documented. Concerning the cochlear congenital lesions, the cytomegalovirus is becoming the main etiologic factor, while the rubella vaccination has shown its efficiency in the United States. The acquired hearing or vestibular diseases were briefly reviewed as well as the pathology and their therapeutic considerations.

[Nasal infection of the domestic cat with feline herpesvirus as an animal model of experimental viral labyrinthitis]. / Nasale Infektion der Hauskatze mit felinem Herpesvirus als Tierversuchsmodell der experimentellen viralen Labyrinthitis.

Looking for a suitable animal model of experimental labyrinthitis we performed in vivo infections of the domestic cat with feline rhinotracheitis virus. After instillation of the virus suspension into the nose of the anaesthetized cat we could find the complete virus particles in so-called virus factories in the nasal mucosa four days later by means of electron-microscopy. The adjacent ganglia of the olfactory nerve were stained by immunohistochemical methods and showed positive viral antigen. After embedding of the cochlea for electron microscopy virus particles could be demonstrated in the inflammatory cell material in the scala tympani. Our experimental model seems to be suitable for further studies of the rhinogenic way of infection in experimental viral labyrinthitis.

Circling syndrome and inner ear disease in mice infected intraperitoneally or intravenously with Coccidioides immitis spherule-endospore phase cultures.

Infection was studied in mice with varying doses of spherule-endospore phase cultures of Coccidioides immitis, administered intraperitoneally, intravenously and intranasally. Stain 46 was compared with strain Silveira. The first of these is relatively avirulent in the mycelial phase, the second, rather virulent. Animals were observed for acute death and for circling. Gross and microscopic pathology was studied in mice sacrificed at appropriate intervals after infection. Numbers of fungi were assayed in spleen, lung, kidney, liver, blood, brain, and ear tissue. Strain 46 endospores administered intraperitoneally in doses from 9 X 10(6) to 2.5 X 10(7) produced a high incidence of 'circling syndrome' ataxia attributable to inner ear disease.

Experimental infection of the guinea pig inner ear with Toxoplasma gondii.

Based on the question whether toxoplasma gondii is a potential pathogenetic factor in sudden deafness and vertigo (especially in the acquired form of Toxoplasmosis) we started a series of investigations, dealing with direct, local, hematogenous, and intracisternal infection of the guinea pig cochlea with toxoplasma gondii. Three of ten directly inoculated and one of five hematogenously infected guinea pigs showed a severe labyrinthitis in electron and light microscopy. Thus, we could demonstrate that toxoplasma gondii is a potent pathogenetic factor in acute inner ear disturbances in laboratory animals. Toxoplasmosis should always be considered in cases with sudden deafness and vertigo without obvious other cause. With a specific therapy the labyrinthine disturbances can apparently be successfully treated.

Viral labyrinthitis -- an experimental study.

Summary--An attempt was made to produce viral labyrinthitis in the rhesus monkey. Rhesus monkeys are susceptible to the mumps virus. Nine animals were used. After removal of the stapes, the left oval windows were plugged with Gelfoam soaked in a culture of live mumps virus; right oval windows were plugged with Gelfoam soaked in killed cultures. Animals were sacrificed at different time intervals, postinfection. In eight of the nine animals there was seroconversion from negative to positive; however, none of the animals developed the histologic changes of viral labyrinthitis.