The level of control that one has over the crying, anger or other emotional displays in PBA is minimal or nonexistent, whereas for those with depression, the emotional expression (typically crying) can be modulated by the situation. Similarly, the trigger for episodes of crying in patients with PBA may be nonspecific, minimal or inappropriate to the situation, but in depression the stimulus is specific to the mood-related condition. These differences are outlined in the adjacent Table. In some cases, depressed mood and PBA may co-exist. Since depression is one of the most common emotional changes in patients with neurodegenerative disease or post-stroke sequelae, it is often comorbid with PBA. Comorbidity implies that depression is distinct from PBA and is not necessary for, nor does it exclude, a diagnosis of PBA. Causes
The specific pathophysiology involved in this frequently debilitating condition is still under investigation; the primary pathogenic mechanisms of PBA remain controversial. One hypothesis, established by early researchers such as Wilson and Oppenheim, placed emphasis on the role of the corticobulbar pathways in modulating emotional expression in a top-down model, and theorized that PBA occurs when bilateral lesions in the descending corticobulbar tract cause failure of voluntary control of emotion, which leads to the disinhibition, or release, of laughing/crying centers in the brainstem. Other theories implicate the prefrontal cortex. Secondary condition
PBA is a condition that occurs secondary to neurological disease or brain injury, and is thought to result from disruptions of neural networks that control the generation and regulation of motor output of emotions.
Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations. Treatment and Control
Currently, antibiotic drugs such as penicillin or tetracycline are the only effective methods for disease treatment. Within wild populations, disease control consists of reducing the amount of bacterial spores present in the environment. This can be done by removing contaminated carcasses and scat. History
Tyzzers disease was first discovered by parasitologist Ernest Tyzzer in 1917 when his entire colony of Japanese waltzing mice suddenly died. Upon closer observation, Tyzzer discovered necrotic lesions and spore-forming bacillus in the livers of the deceased mice. This led Tyzzer to name the bacteria Bacillus piliformis and deem it the cause of this new disease. Later on, B. piliformis was renamed C. piliforme. In the 1940s, a biologist named Paul Errington found a fatal condition in Iowa muskrat populations that he believed to be a new disease. Dead muskrats were found with blood around their anus and internal bleeding, therefore Errington called this new condition “hemorrhagic disease”. Upon necropsy, lesions were found on the liver of the deceased muskrats. While hemorrhagic disease was identified in dead muskrats across North America, the causative agent remained undetermined. After Erringtons death, the name “hemorrhagic disease” was changed to “Errington’s disease”. It was not until 1971 that the two diseases were discovered to be the same, upon which the name was reverted to “Tyzzer’s disease”. == References ==