The significance of this approach is that, if the white blood cells in the small intestine have been exposed to Trichinella antigens (through vaccination), when an individual does get infected, the immune system will respond to expel the worms from the small intestine fast enough to prevent the female worms from releasing their larvae. A DNA vaccine tested on mice "induced a muscle larva burden reduction in BALB/c mice by 29% in response to T. spiralis infection". Epidemiology
About 11 million humans are infected with Trichinella; T. spiralis is the species responsible for most of these infections. Infection was once very common, but this disease is now rare in the developed world, but two known outbreaks occurred in 2015. In the first outbreak, around 40 people were infected in Liguria, Italy, during a New Years Eve celebration. The second outbreak in France was associated with pork sausages from Corsica, which were eaten raw, affecting 14 people in total. The incidence of trichinosis in the U.S. has decreased dramatically in the past century from an average of 400 cases per year mid-20th century down to an annual average of 20 cases per year (2008–10). The number of cases has decreased because of legislation prohibiting the feeding of raw meat garbage to hogs, increased commercial and home freezing of pork, and the public awareness of the danger of eating raw or undercooked pork products.China reports around 10,000 cases every year, so is the country with the highest number of cases.
Age may also be a significant factor. Some psychoactive drugs such as LSD, methaqualone, or phencyclidine can cause hyperacusis. An antibiotic, ciprofloxacin, has also been seen to be a cause, known as ciprofloxacin-related hyperacusis. Benzodiazepine withdrawal syndrome is also a possible cause. Neurophysiological mechanisms
As one important mechanism, adaptation processes in the auditory brain that influence the dynamic range of neural responses, are assumed to be distorted by irregular input from the inner ear. This is mainly caused by hearing loss related damage in the inner ear. The mechanism behind hyperacusis is not currently known, but it is suspected to be caused by damage to the inner ear and cochlea. It is theorized that type II afferent fibers become excited after damage to hair cells and synapses, triggering  a release of ATP in response. This release of ATP results in pain, sound sensitivity, and cochlear inflammation. Diagnosis
The basic diagnostic test is similar to a normal audiogram. The difference is that additionally to the hearing threshold at each test frequency also the lowest uncomfortable sound level is measured. This level is called loudness discomfort level (LDL), uncomfortable listening level (UCL), or uncomfortable loudness level (ULL). In patients with hyperacusis this level is considerably lower than in normal subjects, and usually across most parts of the auditory spectrum.