RESUMEN
BACKGROUND: The typical clinical manifestation of an infection with the obligate anaerobic, gram-negative, rod-shaped bacteria Fusobacterium necrophorum is the Lemierre syndrome. As the cause of osteomyelitis and mastoiditis factors of the normal bacteria flora are more likely to be found than Fusobacterium necrophorum. Nevertheless, Necrobacillosis is an important differential diagnosis of complicated courses of mastoiditis. MATERIAL AND METHODS: Because the clinical courses of mastoiditis with osteomyelitis may differ a lot, making the appropriate diagnosis more difficult, consistently and flawless detection of the pathogens is important. Therefore a correct specimen collection, transportation and the subsequent cultivation of the pathogens is essential. RESULTS: The genus Fusobacterium is an obligate anaerobic, gram-negative rod-shaped bacteria. Infections involving the genus Fusobacterium are usually formed endogenously. They are characterized by subacute to chronic, purulent gangrenous necrotizing inflammations. CONCLUSION: As a differential diagnosis, infections with Streptococcus spp., Haemophilus influenzae, Branhamella catarrhalis and Staphylococcus aureus are more likely to cause mastoiditis and osteomyelitis than an infection with Fusobacterium necrophorum. However, the infection with this fusiform bacillus is possible under pathological circumstances e.g. deficiency syndroms, so that when observing a prolonged disease course of mastoiditis an infection with Fusobacterium necrophorum should be considered .
Asunto(s)
Infecciones por Fusobacterium/diagnóstico , Fusobacterium necrophorum , Mastoiditis/diagnóstico , Osteomielitis/diagnóstico , Base del Cráneo , Hueso Temporal , Trastornos de la Articulación Temporomandibular/diagnóstico , Antibacterianos/uso terapéutico , Técnicas Bacteriológicas , Terapia Combinada , Desbridamiento , Diagnóstico Diferencial , Infecciones por Fusobacterium/terapia , Humanos , Síndrome de Lemierre/diagnóstico , Síndrome de Lemierre/terapia , Mastoiditis/terapia , Pruebas de Sensibilidad Microbiana , Osteomielitis/terapia , Otitis Media/diagnóstico , Otitis Media/terapia , Trastornos de la Articulación Temporomandibular/terapia , Tomografía Computarizada por Rayos XRESUMEN
AIMS: Recent studies have shown that most Dutch families with atypical multiple-mole melanoma (FAMMM) have a 19-bp deletion (p16-Leiden) in exon 2 of the p16 gene. Apart from reports on metachronous pancreatic tumors, other cancer types have never been described in such families. Due to heterozygous p16-Leiden constitution, our proband with multiple head and neck carcinomas was a suitable model for studying the type of p16 inactivation according to the Knudson-two-hit model. METHODS: p16 mutations in exons 1 and 2 were determined using PCR-SSCP-Sequencing analysis. p16 methylation was assessed by methylation-specific PCR. RESULTS: All three metachronous (larynx, pharynx, oral cavity) tumors had a methylated p16 promotor. The p16 protein loss detected by immunohistochemistry clearly confirmed a complete loss of p16 tumor suppressor function. Thus, all three tumors exhibited biallelic inactivation of p16, caused by aberrant methylation of the p16 promotor. CONCLUSIONS: This is the first report on p16-Leiden mutation in head and neck cancer. We provide evidence that the somatic methylation of p16 promotor is associated with the germline transmission of p16-Leiden mutation. This is an example for the rare event of in which aberrant methylation acting as the 'second hit' in a familial cancer syndrome. Our results show that this epigenetic event is equivalent to genetic alterations (mutation/LOH) confirming the Knudson's hypothesis for tumor suppressor gene inactivation.