wild animals every day, largely without ill consequences. But Jeremy’s encounter with this particular bat would be quite different.
In the CDC report that would document Jeremy’s case, the next events were described with clinical efficiency. On August 21 Jeremy complained of headache and neck pain. Then a day or so later his right arm became numb and he developed a slight fever. Perhaps of greater concern, he also developed diplopia, or double vision, and a constant, queasy confusion. Three days later he was taken to the local hospital’s emergency room but was discharged with the incorrect diagnosis of “muscle strain.” The next day he was back in the emergency room, this time with a fever of 102°F. He had the same symptoms, but now his speech was slurred, he had a stiff neck, and difficulty swallowing.
At this point, Jeremy was transferred to a local children’s hospital. By August 26 he could no longer breathe or think normally. He was also producing copious amounts of saliva. Highly agitated to the point of being combative, Jeremy was sedated and put on life support. His mental status deteriorated rapidly and by the next morning he was completely unresponsive. On August 31 Jeremy was pronounced brain-dead and, following the withdrawal of life support, he died of bat-borne rabies.
Jeremy’s family did not know that bats could carry rabies, much less transmit it to humans. They did not remember him complaining of a bite, although that’s exactly what must have happened while he carried the bat home from his fishing excursion. They probably did not know that the incubation period for rabies is generally three to seven weeks, well within the range of the time between his exposure to the bat and the first symptoms he experienced. Detailed studies of the virus that killed Jeremy revealed evidence of a variety of rabies found in silver-haired and eastern pipistrelle bats common in Tennessee.
Rabies is a terrible way to die. It’s a disease that devastates the families of its victims, with patients becoming virtual zombies in the days before death. It is among the small number of viruses that kill virtually all of the individuals they infect. But as tragic as it is that the doctors at the local Franklin County emergency room sent Jeremy home with a diagnosis of muscle strain, the reality is that it was already too late to help the boy at that point. Without rapid postexposure prophylaxis after infection, the boy was destined to die.
* * *
If we take a different view, the virus that causes rabies is not only a deadly menace but also a truly amazing feat of nature. This virus, shaped like a bullet, is a meager 180 nanometers long and 75 nanometers across. If you stacked rabies viruses one on top of the next, you would need more than a thousand of them to reach the thickness of a single human hair. Rabies has an almost trivial genome, with only twelve thousand bits of genetic information for a meager five proteins. It’s simple, tiny, and incredibly powerful.
While diminutive, the virus accomplishes remarkably sophisticated tasks. In addition to the standard viral work of invading cells, releasing genes, making new viruses, and spreading, it has some unique tricks. From the point of entry, the virus travels preferentially along neural pathways, making its way into the central nervous system. It accumulates selectively in the saliva. The virus particles that infect the central nervous system modify the host’s behavior, increasing aggression, interfering with swallowing, and creating a profound fear of water. When put together, a rabies infection leads to an aggressive host literally foaming at the mouth with virus. A host that lacks the capacity to drink or swallow further increases the probability of delivering a successful bite—a bite that gives this particular virus the ability to advance from one individual to the next.
Hospitalized human rabies victim in restraints. ( Courtesy of the Centers
In the CDC report that would document Jeremy’s case, the next events were described with clinical efficiency. On August 21 Jeremy complained of headache and neck pain. Then a day or so later his right arm became numb and he developed a slight fever. Perhaps of greater concern, he also developed diplopia, or double vision, and a constant, queasy confusion. Three days later he was taken to the local hospital’s emergency room but was discharged with the incorrect diagnosis of “muscle strain.” The next day he was back in the emergency room, this time with a fever of 102°F. He had the same symptoms, but now his speech was slurred, he had a stiff neck, and difficulty swallowing.
At this point, Jeremy was transferred to a local children’s hospital. By August 26 he could no longer breathe or think normally. He was also producing copious amounts of saliva. Highly agitated to the point of being combative, Jeremy was sedated and put on life support. His mental status deteriorated rapidly and by the next morning he was completely unresponsive. On August 31 Jeremy was pronounced brain-dead and, following the withdrawal of life support, he died of bat-borne rabies.
Jeremy’s family did not know that bats could carry rabies, much less transmit it to humans. They did not remember him complaining of a bite, although that’s exactly what must have happened while he carried the bat home from his fishing excursion. They probably did not know that the incubation period for rabies is generally three to seven weeks, well within the range of the time between his exposure to the bat and the first symptoms he experienced. Detailed studies of the virus that killed Jeremy revealed evidence of a variety of rabies found in silver-haired and eastern pipistrelle bats common in Tennessee.
Rabies is a terrible way to die. It’s a disease that devastates the families of its victims, with patients becoming virtual zombies in the days before death. It is among the small number of viruses that kill virtually all of the individuals they infect. But as tragic as it is that the doctors at the local Franklin County emergency room sent Jeremy home with a diagnosis of muscle strain, the reality is that it was already too late to help the boy at that point. Without rapid postexposure prophylaxis after infection, the boy was destined to die.
* * *
If we take a different view, the virus that causes rabies is not only a deadly menace but also a truly amazing feat of nature. This virus, shaped like a bullet, is a meager 180 nanometers long and 75 nanometers across. If you stacked rabies viruses one on top of the next, you would need more than a thousand of them to reach the thickness of a single human hair. Rabies has an almost trivial genome, with only twelve thousand bits of genetic information for a meager five proteins. It’s simple, tiny, and incredibly powerful.
While diminutive, the virus accomplishes remarkably sophisticated tasks. In addition to the standard viral work of invading cells, releasing genes, making new viruses, and spreading, it has some unique tricks. From the point of entry, the virus travels preferentially along neural pathways, making its way into the central nervous system. It accumulates selectively in the saliva. The virus particles that infect the central nervous system modify the host’s behavior, increasing aggression, interfering with swallowing, and creating a profound fear of water. When put together, a rabies infection leads to an aggressive host literally foaming at the mouth with virus. A host that lacks the capacity to drink or swallow further increases the probability of delivering a successful bite—a bite that gives this particular virus the ability to advance from one individual to the next.
Hospitalized human rabies victim in restraints. ( Courtesy of the Centers
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