Yellow Fever 1793
Yellow Fever Attacks Philadelphia 1793
The summer of 1793 was unusually hot and dry. Insects infested every corner in the streets, and Philadelphia was the busiest port in the U.S. Workers paced back and forth, carrying goods in and shipping goods out. In the midst of July, a ship of Caribbean refugees came to port. With them, they carried the yellow fever virus. The virus traveled slowly at first; with just a few fatalities in the first week, numbers grew steadily over time. No one suspected it was the aedes aegypti mosquito, retrieving the blood of an infected victim and transferring it to another healthy individual. The city’s leading physician Dr. Benjamin Rush had never seen anything like it before.[3] Three to six days after being infected with the virus, the victim would begin to show symptoms such as headaches, muscle and joint aches, a fever, flushing, loss of appetite, vomiting and jaundice. Jaundice makes the eyes and skin look yellow, hence the name yellow fever. [1] In the second stage, the symptoms would falsely leave after three days; at this time, most people would recover. Others could get worse within 24 hours. [1] The yellow fever virus is a dormant, single strand of RNA, packaged in a lipoprotein envelope. The transmissions occur through bites of infected aedes aegypti or haemagogus mosquitoes. Human and nonhuman primates are the main reservoirs of the virus. Traveling through a lytic life cycle, the virus first enters the host and is phagocytosed by a macrophage. The virus then sheds its envelope to keep from being further digested. The macrophage continues with the virus to the lymph nodes where the virus begins its replication. The virus leaves the host macrophage and then goes out to infect others. As the lymph nodes carry the virus through the bloodstream, it enters the liver. Inside the liver, it infects the Kupffer cells that line the blood vessels. The cells are macrophages that are needed to clean cellular debris and
The summer of 1793 was unusually hot and dry. Insects infested every corner in the streets, and Philadelphia was the busiest port in the U.S. Workers paced back and forth, carrying goods in and shipping goods out. In the midst of July, a ship of Caribbean refugees came to port. With them, they carried the yellow fever virus. The virus traveled slowly at first; with just a few fatalities in the first week, numbers grew steadily over time. No one suspected it was the aedes aegypti mosquito, retrieving the blood of an infected victim and transferring it to another healthy individual. The city’s leading physician Dr. Benjamin Rush had never seen anything like it before.[3] Three to six days after being infected with the virus, the victim would begin to show symptoms such as headaches, muscle and joint aches, a fever, flushing, loss of appetite, vomiting and jaundice. Jaundice makes the eyes and skin look yellow, hence the name yellow fever. [1] In the second stage, the symptoms would falsely leave after three days; at this time, most people would recover. Others could get worse within 24 hours. [1] The yellow fever virus is a dormant, single strand of RNA, packaged in a lipoprotein envelope. The transmissions occur through bites of infected aedes aegypti or haemagogus mosquitoes. Human and nonhuman primates are the main reservoirs of the virus. Traveling through a lytic life cycle, the virus first enters the host and is phagocytosed by a macrophage. The virus then sheds its envelope to keep from being further digested. The macrophage continues with the virus to the lymph nodes where the virus begins its replication. The virus leaves the host macrophage and then goes out to infect others. As the lymph nodes carry the virus through the bloodstream, it enters the liver. Inside the liver, it infects the Kupffer cells that line the blood vessels. The cells are macrophages that are needed to clean cellular debris and