- Retrospective multicentre, 24 dogs
- Onset typically acute <48hrs,
- Otitis media/interna commonly implicated
- Survival to dischagre 83%
- Long term neuro deficits can occur
- Clinical signs variable, negative cultures occured and need to perform cytology for intracellular bacteria
- SRMA cases typically younger, sporting breeds/hounds, pyrexia more common (83%) and TNCC typically lower
In cases of bacterial meningitis or meningoencephalitis without empyema, what is the most commonly identified source of infection?
a. Otitis media/interna
b. Bacteriuria
c. Penetrating injury
d. Septic arthritis
A
Background: Congenital insensitivity to pain (CIP) and hereditary sensory and auto-nomic neuropathies (HSANs) are a rare group of genetic disorders causing inability to feel pain. SCN9A gene encodes alpha subunit of NaV1.7 voltage gated sodium channel. Mutations in this gene have been associated with insenitivity to pain in humans
Population: 2x mixed breed dogs from same litter with fractures and thermal skin lesions. Compared to 926 control dogs.
Results: Presence of SCN9A variant in a homozygous state in both cases. Argenine to cysteine substitution. No automutilation or other neurological deficits in these dogs (which is often present)
Conclusion: Variant in SCN9A gene has been reported to cause congenital insensitivity to pain (CIP) closely resembling human phenotype
Variation in what gene has been reported to cause congenital insensitivity to pain in 2 mixed-breed dogs
a) SLC2A9
b) COMMD1
c) SCN9A
d) SLC3A1
c) SCN9A
