In 2018, 51 children in the United States died in hot cars, more than the previous high of 49 in 2010.Dogs are even more susceptible than humans to heat stroke in cars, as they cannot produce whole-body sweat to cool themselves. Leaving the dog at home with plenty of water on hot days is recommended instead, or, if a dog must be brought along, it can be tied up in the shade outside the destination and provided with a full water bowl. Pathophysiology
The pathophysiology of heat stroke involves an intense heat overload followed by a failure of the bodys thermoregulatory mechanisms. More specifically, heat stroke leads to inflammatory and coagulation responses that can damage the vascular endothelium and result in numerous platelet complications, including decreased platelet counts, platelet clumping, and suppressed platelet release from bone marrow.Growing evidence also suggests the existence of a second pathway underlying heat stroke that involves heat and exercise-driven endotoxemia. Although its exact mechanism is not yet fully understood, this model theorizes that extreme exercise and heat disrupt the intestinal barrier by making it more permeable and allowing lipopolysaccharides (LPS) from gram-negative bacteria within the gut to move into the circulatory system. High blood LPS levels can then trigger a systemic inflammatory response and eventually lead to sepsis and related consequences like blood coagulation, multi-organ failure, necrosis, and central nervous system dysfunction.
A total of 231 cases of vCJD have been reported since it was first discovered. These cases have been found in a total of 12 countries with 178 in the United Kingdom, 27 in France, five in Spain, four in Ireland, four in the United States, three in the Netherlands, three in Italy, two in Portugal, two in Canada, and one each in Japan, Saudi Arabia, and Taiwan. History
In the 5th century BCE, Hippocrates described a disease like TSE in cattle and sheep, which he believed also occurred in man. Publius Flavius Vegetius Renatus records cases of a disease with similar characteristics in the 4th and 5th centuries AD. In 1755, an outbreak of scrapie was discussed in the British House of Commons and may have been present in Britain for some time before that. Although there were unsupported claims in 1759 that the disease was contagious, in general it was thought to be due to inbreeding and countermeasures appeared to be successful. Early-20th-century experiments failed to show transmission of scrapie between animals, until extraordinary measures were taken such as the intra-ocular injection of infected nervous tissue. No direct link between scrapie and disease in man was suspected then or has been found since. TSE was first described in man by Alfons Maria Jakob in 1921. Daniel Carleton Gajduseks discovery that Kuru was transmitted by cannibalism accompanied by the finding of scrapie-like lesions in the brains of Kuru victims strongly suggested an infectious basis to TSE.