Meet Peter Steyger: The man behind breakthrough research into hearing loss
Peter Steyger underwent speech therapy in 1968 at the University of Manchester with Gordon Campbell and his mother, Peggy Steyger.
As a child, Peter Steyger, Ph.D. was cured of meningitis, but the drug that saved him also caused his hearing loss.
Now a neuroscience researcher, Dr. Steyger recently found that patients stricken with dangerous bacterial infections are at greater risk of hearing loss than previously recognized.
We sat down with Dr. Steyger to learn some more about his research and what comes next.
That’s a great photo of you and your mom with your speech therapist. Can you tell us a little more about it and how your own experiences shaped your research?
The photo was taken of me with my mother, Peggy Steyger, and Gordon Campbell, a speech therapist and coach for my mother, who was to teach me how to listen and talk. Gordon Campbell was at the University of Manchester (UK) at the time, where my mother and I would attend sessions with him to improve our own daily speech therapy sessions.
At the time of the photo, I was about six years old, and had been receiving speech therapy for close to three years. This speech training allowed me to be mainstreamed and obtain a regular grammar school education.
I was in speech therapy because I had lost my hearing though meningitis, streptomycin treatment (an aminoglycoside like gentamicin or kanamycin) and as the recent manuscript showed, the combination of infection-induced inflammation likely potentiated the ototoxic effect of these aminoglycosides.
My own experience has informed my research, primarily through the realization that most ototoxicity experiments are done in healthy pre-clinical models, and yet aminoglycosides are only given to very sick patients to save their lives.
What’s been the most interesting development in your area in the last two years?
One of the most interesting developments in auditory neuroscience that has affected our research in ototoxicity is the realization that the cochlea is not an immunologically-privileged site, and that in fact the cochlea and inner ear does in fact respond to vascular and immunological activation.
Lower power image of the cochlear coils, containing hair cells
This has been characterized by our colleague, Dennis Trune, who established that the cochlea is immunologically activated by middle ear infections, and this could alter auditory function. More importantly, these inner ear changes may alter auditory function.
What’s next for you? What projects are you currently working on/looking forward to?
To follow up on our existing data and determine if other sources of inflammation (e.g., viral, fungal) can also potentiate aminoglycoside-induced hearing loss, i.e., establish whether it is inflammation in general that potentiates drug-induced hearing loss, or if there is something specific about bacterial-induced inflammation that potentiates drug-induced hearing loss.
We also want to determine if individuals with bacterial infection and inflammation have a greater prevalence of hearing loss, and does that hearing loss occur to a greater extent than in other individuals treated with aminoglycosides without systemic inflammation (i.e., prophylactically).
What is the most important aspect of support that OHSU provides to you currently and how would you like this or other support to grow in the future?
Peter Steyger, Ph.D.
OHSU has a vast array of research expertise in a wide variety of areas that are surprisingly (to me) integrated when it comes to translating bench science into bedside practice.
I have found our basic and clinical colleagues to be very collegial, collaborative and supportive. This is further enhanced by the seed-funding of newly-innovative ideas (acorns) into thriving translational and clinical research projects by OCTRI (oaktrees; the Oregon Clinical and Translational Research Institute) that support our communities statewide and globally.
