Tyzzers disease is an acute epizootic bacterial disease found in rodents, rabbits, dogs, cats, birds, pandas, deer, foals, cattle, and other mammals including gerbils  and spinifex hopping-mice (Notomys alexis) . It is caused by the spore-forming bacterium Clostridium piliforme, formerly known as Bacillus piliformis. It is an infectious disease characterized by necrotic lesions on the liver, is usually fatal, and is present worldwide. Animals with the disease become infected through oral ingestion of the bacterial spores and usually die within a matter of days. Animals most commonly affected include young, stressed animals in laboratory environments, such as immature rodents and rabbits. Most commonly affected wild animals include muskrats (Ondatra zibethicus) and occasionally cottontail rabbits (Sylvilagus spp.). Even today, much remains unknown about Tyzzers disease, including how and why it occurs. Distribution
Although Tyzzers disease is commonly found in laboratory animals worldwide, infected wild animal populations have been identified in North America and Australia. Specific locations where the disease has been reported in the United States include Connecticut, Idaho, Iowa, Maryland, Michigan, Montana, Ohio, Wisconsin, and Wyoming. In Canada, it has been reported in British Columbia, Manitoba, Ontario, and Saskatchewan. Outbreaks in these locations are primarily attributed to muskrat populations; however infected cottontail rabbits  have been discovered in Maryland. Transmission
Tyzzers disease is transmitted horizontally through the fecal-oral route. Bacterial spores within infected fecal matter can contaminate soil or feed and become orally ingested by a viable host.
Antacids administered in a peptic ulcer regimen may decrease the AUC of a single dose of phenytoin. Patients should be cautioned against concomitant use of antacids and phenytoin. "Warfarin and trimethoprim increase serum phenytoin levels and prolong the serum half-life of phenytoin by inhibiting its metabolism. Consider using other options if possible. Pharmacology
Mechanism of action
Phenytoin is believed to protect against seizures by causing voltage-dependent block of voltage gated sodium channels. This blocks sustained high frequency repetitive firing of action potentials. This is accomplished by reducing the amplitude of sodium-dependent action potentials through enhancing steady-state inactivation. Sodium channels exist in three main conformations: the resting state, the open state, and the inactive state. Phenytoin binds preferentially to the inactive form of the sodium channel. Because it takes time for the bound drug to dissociate from the inactive channel, there is a time-dependent block of the channel. Since the fraction of inactive channels is increased by membrane depolarization as well as by repetitive firing, the binding to the inactive state by phenytoin sodium can produce voltage-dependent, use-dependent and time-dependent block of sodium-dependent action potentials.The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, phenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of post-tetanic potentiation at synapses which prevents cortical seizure foci from detonating adjacent cortical areas.