Acute Streptococcus pneumoniae Meningogenic Labyrinthitis: An Experimental Guinea Pig Model and Literature Review

Blank, Andrew L.; Davis, Gustave L.; VanDeWater, Thomas R.; Ruben, Robert J.

doi:10.1001/archotol.1994.01880360040008

Cited by 29 publications

(13 citation statements)

References 25 publications

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“…On the other hand, earlier studies of acute otitis media identified inner ear osteoneogenesis in a chinchilla model 8 . This was, however, associated with spreading of the infection from the middle to the inner ear and evidence of active labyrinthitis, which experimentally is known to induce inner ear osteoneogenesis 25 . No signs of inner ear infection were found in the present study.…”

Section: Discussioncontrasting

confidence: 79%

Bone modeling dynamics in acute otitis media

Cayé‐Thomasen¹,

Hermansson²,

Tos³

et al. 1999

The Laryngoscope

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These findings may support the existence of a perilymphatic barrier of specialized bone and suggest that even a single episode of acute infection may alter properties of ossicular chain conduction. The authors conclude that acute otitis media is accompanied by massive and progressing net osteoneogenesis, already evident at 3 days and peaking 3 months after inoculation, followed by some degree of normalization. This is conceivably in support of the environmental theory of mastoid pneumatization, claiming inflammatory disease as the cause of a sclerotic mastoid.

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Section: Discussioncontrasting

confidence: 79%

Bone modeling dynamics in acute otitis media

Cayé‐Thomasen¹,

Hermansson²,

Tos³

et al. 1999

The Laryngoscope

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“…The underlying pathophysiology has been studied in several animal models (39,40,45,244,421,477) Cochlear involvement may result from direct spread of pneumococcal infection from the meninges, CSF, and cochlear perilymphatic system (40,227,244). Alternatively, a hematogenous route may occur following bacteremia or sepsis (227,244).…”

Section: Cochlear Damage and Hearing Lossmentioning

confidence: 99%

Pathogenesis and Pathophysiology of Pneumococcal Meningitis

et al. 2011

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SUMMARY Pneumococcal meningitis continues to be associated with high rates of mortality and long-term neurological sequelae. The most common route of infection starts by nasopharyngeal colonization by Streptococcus pneumoniae , which must avoid mucosal entrapment and evade the host immune system after local activation. During invasive disease, pneumococcal epithelial adhesion is followed by bloodstream invasion and activation of the complement and coagulation systems. The release of inflammatory mediators facilitates pneumococcal crossing of the blood-brain barrier into the brain, where the bacteria multiply freely and trigger activation of circulating antigen-presenting cells and resident microglial cells. The resulting massive inflammation leads to further neutrophil recruitment and inflammation, resulting in the well-known features of bacterial meningitis, including cerebrospinal fluid pleocytosis, cochlear damage, cerebral edema, hydrocephalus, and cerebrovascular complications. Experimental animal models continue to further our understanding of the pathophysiology of pneumococcal meningitis and provide the platform for the development of new adjuvant treatments and antimicrobial therapy. This review discusses the most recent views on the pathophysiology of pneumococcal meningitis, as well as potential targets for (adjunctive) therapy.

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“…Blank et al used the guinea pig to create an experimental model of Streptococcus pneumoniae type 3 meningogenic labyrinthitis (Blank et al, 1994). The virulence of S. pneumoniae D39 strain 2 and its potential to induce meningitis in the guinea pig after intracisternal infection have been shown by Winter et al (Winter et al, 1997).…”

Section: Discussionmentioning

confidence: 99%