*Department of Oto-Rhino-Laryngology, Head and Neck Surgery, University Hospital, Rigshospitalet/Gentofte, Copenhagen; †Department of Infectious Diseases, Copenhagen University Hospital Hvidovre; ‡Department of Clinical Microbiology, Copenhagen University Hospital Hvidovre, Hvidovre; and §The Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen Denmark.
Otol Neurotol. 2014 Jun;35(5):e178-86. doi: 10.1097/MAO.0000000000000305.
To examine the pathways of bacterial invasion and subsequent spreading in the inner ear during pneumococcal meningitis.
A well-established adult rat model of Streptococcus pneumoniae meningitis was used.
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.
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.
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.
研究肺炎链球菌性脑膜炎时细菌入侵内耳及随后扩散的途径。
采用已建立的成年大鼠肺炎链球菌性脑膜炎模型。
30 只大鼠经蛛网膜下腔接种血清型 1、3 或 9V 肺炎链球菌，不进行其他治疗。当达到疾病终末期或第 7 天，处死大鼠并进行连续切片，行 PAS-Alcian 蓝染色，行光镜检查。
接种后最初几天，细菌通过耳蜗导水管侵入内耳，进入耳蜗的鼓阶（外淋巴间隙）。从这里，细菌向耳蜗的螺旋孔顶部扩散，随后向底部通过前庭阶，向前庭和前庭系统扩散。当细菌在第 5 至 6 天到达耳蜗底转的前庭阶时，发生血源性播散至螺旋韧带并进入耳蜗内淋巴，随后进入前庭内淋巴。我们没有发现细菌在内耳中有其他入侵途径的证据。在内耳中发现了几个阻止细菌扩散的内部屏障。细菌的消除被证明是通过内耳内的巨噬细胞吞噬。
脑膜炎链球菌在感染的最初几天通过耳蜗导水管侵入内耳，而血源性通过螺旋韧带毛细血管床的入侵发生在后期。尽管内耳内存在内部屏障，但细菌的扩散是通过液体腔的自然途径发生的。细菌的消除是通过局部巨噬细胞的吞噬作用实现的。
