Pat Shaw, 77, was enjoying retired life with her high school sweetheart, Jerry Shaw, when she came down with a cold in the middle of August. Pat felt mostly normal at first—all she had was a small headache. She would still join Jerry at their kitchen table to read the paper over coffee every morning. After breakfast, they’d feed their seven guinea pigs and play with their dog, Bennie. In the afternoon, Pat and Jerry might swim in their pool, go for a walk, or spend a couple of hours in the garden outside their home in East Lyme, Connecticut. “We just enjoyed doing things together—being together,” said Jerry.
After about a week, Pat’s headaches got worse. She went to bed early, feeling exhausted. Overnight, she developed a 103-degree fever. “She got up in the morning and looked at me and said, ‘Oh, you’re growing a beard. I like it,’” Jerry remembered. “I’ve had a beard for fifty years.” He knew that his beloved wife wasn’t herself.
Jerry hurried Pat to the emergency room at their local hospital, where her doctors thought she was having a stroke, though her brain showed no signs of bleeding or damage. The doctors stuck a needle into Pat’s back to take fluid for testing. According to Jerry, her blood pressure skyrocketed, and her doctors were worried. They sent a heavily-sedated Pat to Yale-New Haven Hospital by helicopter.
Soon after she arrived at the hospital, Pat became unresponsive. She couldn’t breathe or eat without the help of machines. Her three sons and their daughters stood by her hospital bed, begging her to wake up, but MRIs showed worsening damage to her brain as August turned to September.
For two weeks, no one knew what was wrong. “Everything came back negative,” said Jerry. The doctors sent Pat’s spinal fluid to the Centers for Disease Control in Colorado. In mid-September, a scary diagnosis came back.
Pat had developed a viral infection from a mosquito that probably bit her when she was in her backyard. She had Eastern Equine Encephalitis—EEE for short. EEE is a rare, poorly understood virus that attacks the brain. “Who would have thought it would be one of us?” Jerry said.
Pat’s EEE was part of an outbreak that swept across the United States this summer. In 2019, the virus killed fifteen Americans. The number of people infected nationwide swelled to 38, more than five times the average over the past ten years. Diagnosis of EEE is difficult, and treatment is often futile. Its rise this year is a sign of what’s to come. A warming climate will generate a more favorable environment for mosquitoes, allowing more of them to carry and transmit the virus for longer each year. More people will get sick across New England, and no one is prepared.
Mosquitoes in the tropics can carry EEE year round because of consistently warm weather. Migrating birds fly to the tropics for the winter. There, they pick up EEE from mosquito bites. Birds don’t get sick or show symptoms from EEE, but they carry the virus back to North America.
When spring comes to New England, EEE-infected birds return. Upon arriving, many look for food along the Connecticut-Rhode Island border in swamps filled with large trees. The swampy water at the roots of these trees is a perfect breeding habitat for Culiseta melanura, the main mosquito species that carries EEE. C. melanura feeds almost exclusively on birds.
When the migrating birds reach the swamps, C. melanura mosquitoes first pick up the virus by biting them. Birds and mosquitoes then pass the virus back and forth in a game of hot potato. “If more birds get infected, more mosquitoes get infected,” says Leonard Munstermann, an epidemiologist at the Yale School of Public Health.
Munstermann focuses on insect-borne illnesses like EEE. He finds striking how quickly C. melanura can spread the virus. “For some reason, it is able to go through them like a hot knife through butter,” says Munstermann.
The knife is the hottest under the warm summer sun. During the summer, levels of EEE in C. melanura reach a high point.
When the adult mosquitoes die at the end of each year, their offspring somehow carry the virus into the next spring. Scientists don’t know how the virus manages to overwinter. But experts suspect that larvae spend the winter nestled in their forested wetlands, harboring the virus. In the spring and summer, mature mosquitoes can once again infect humans. Not only do birds bring EEE to New England anew each year—it also rolls over from the year before.
The virus spills out of the bird-mosquito exchange to infect humans during the rare instance when C. melanura bites a person. Although EEE does not affect birds, it causes severe brain damage and kills a third of the people it infects. Though EEE does not mean certain death, the disease is always life-altering and debilitating. Children and the elderly are especially susceptible to infection.
Philip Armstrong has watched the summertime risk of EEE infection in New England slowly rise over the past two decades. During that time, he has been the scientist in charge of Connecticut’s mosquito trapping and testing program. Armstrong studies EEE for a living, but the mention of it makes him shake his head in dismay. “I never wish EEE on my worst enemy. It’s devastating.”
Armstrong is a tall, skinny man with ginger hair graying at the temples. His lab is teeming with mosquitoes of all kinds. Dead ones sit piled in glass containers near microscopes. On the walls of the lab, there are illustrated comics and larger-than-life mosquito posters. Armstrong approaches a fridge-sized incubator along one of the walls, where he keeps live mosquitoes for experiments. He opens the door to reveal a tower of Tupperware containers full of mosquito larvae that look like grains of rice floating around in murky water. Armstrong bypasses the Tupperware, turning instead to a basketball-sized box covered in cloth.
Armstrong carefully removes the box from the incubator. He gingerly places it on a table in the middle of the room, lifting the cloth that covers it. Underneath, there’s a metal mesh cage. A small cloud of mosquitoes convulses inside.
Armstrong peers into the cage, running his hands over the mesh. He chuckles when the mosquitoes inside won’t bite him. “They don’t seem too interested. These are C. melanura,” he says. The buzzing cloud is made from the bird-biting mosquitoes that can carry EEE.
These mosquitoes aren’t infected, but running experiments on them could help scientists learn more about the ones that are. The experiments are only possible here. Armstrong’s lab is the only one in the country to have its own colony of C. melanura.
Armstrong and his team collect wild mosquitoes from almost 100 locations across Connecticut each week. They identify each individual mosquito according to species. Then they check whether the mosquitoes were carrying diseases. “We really need to know what species we’re looking at and what viruses they’re carrying, which gives us a more informed assessment of the risk,” says Armstrong. He and his team trapped, identified, and tested almost a quarter of a million mosquitoes in 2019 alone.
Starting in June, Armstrong noticed a concerning pattern: “One species in particular, C. melanura, had numbers way above the historical average.” With more potential carriers of EEE, Armstrong worried about an outbreak. Sure enough, he and his team found lots of C. melanura infected with EEE in Connecticut during August. The largest number of infected mosquitoes came from their typical swamp habitat near the Rhode Island border. More C. melanura carrying EEE wound up in traps along Connecticut’s southeast shoreline, close to where the Shaws live in East Lyme.
In response, Armstrong worked closely with the Department of Public Health to develop suggested courses of action for towns in these areas. “The goal is to figure out how to best protect the public in a way that’s acceptable to the public and doesn’t disrupt people’s lives too much,” he said. Twenty-one local governments in high-risk areas heeded Armstrong’s recommendations. They urged people to stay inside after dark, or to wear insect repellent if they ventured outside. Schools cancelled afternoon activities.
But no matter how much care people take during the summer to prevent bug bites, one unlucky bite from the wrong mosquito could mean big trouble. This year, the Shaws spent their 45th summer together in their blue-gray house nestled in the woods of East Lyme. Pat and Jerry had been aware of the risk of EEE during the late summer and early fall, so they never went outside without putting on bug spray. They burned citronella by their pool to keep the mosquitoes away. “But obviously, there was one time that it didn’t work,” said Jerry, with tears in his eyes.
When a mosquito carrying EEE bites a person like Pat, the virus slips into the body along with the mosquito’s saliva. It then finds its way into the skin tissue surrounding the bite, infecting nearby cells. These infected cells move to nearby lymphoid tissues, part of the body’s control center for fighting infection. There, the virus hijacks cell machinery in order to replicate itself. Leaving the lymphoid tissue, the virus travels through the bloodstream in increased abundance, winding up in the brain.
When EEE reaches the brain, chaos reigns. The virus attacks neurons, the cells our brains use to send signals throughout the body. “They tend to target gray matter, the parts of our brains where there are neuron cell bodies,” says Firas Kaddouh, a neurologist at Yale-New Haven Hospital. The virus overwhelms the gray matter parts of the brain, its attack leaving behind neurons damaged beyond repair. As these cells die, fluid builds up in the brain and blood vessels swell up. A domino effect of inflammation follows from the buildup of fluid and dead neurons. Collateral damage ensues. Inflammation of the brain in this fashion is called encephalitis.
About a day after EEE makes it to a person’s brain, they may appear disoriented and even lose consciousness. When people with EEE lose consciousness, they may never wake up. And if they do, the damage to their brain is catastrophic. Though the heart is still pumping blood to the rest of the body, the brain damage approaches destruction.
When Kaddouh was taking care of Pat, he and his colleagues knew that some sort of encephalitis was at play. From scans of Pat’s brain, they saw that there was severe damage to gray matter on both the surface and the deep interior of the brain. But it took them weeks to figure out what was causing the damage.
Initially, doctors suspected herpes simplex virus, a common—and treatable—cause of encephalitis. “If you’re dealing with herpes, you’ll start to wake up,” said Merceditas Villanueva, an infectious disease specialist who took care of Pat at Yale-New Haven. Pat wasn’t waking up, and the test for herpes came back negative.
Her doctors ordered tests for about fifteen different diseases, including a preliminary test for EEE. All of the tests at Yale came back negative, so Villanueva and her colleagues sent Pat’s spinal fluid to the CDC in Colorado for more extensive testing.
Despite so many negative tests at first, Pat’s doctors were confident that some kind of virus was causing inflammation in her brain. After she had been at Yale-New Haven for about ten days, they gave her treatment to prop up her failing immune system. This treatment is called intravenous immunoglobulin—IVIg for short. The goal with IVIg is to contain a virus at its point of attack in the brain.
Had the doctors started Pat on IVIg even sooner, it might have made a difference. “It’s expensive, but it’s the only treatment that can be offered for EEE,” said Kaddouh. IVIg has stemmed the tide of EEE infection in other patients. Three years ago, a man from Massachusetts on the brink of death made a full recovery. He had been nearly comatose from developing encephalitis from a mosquito bite. He received early IVIg treatment, and his condition improved rapidly. Within months, he was home again with his family. Because of IVIg, he had his life back.
The timing of the treatment is a key difference between Pat and the man who recovered. On September 15th, positive test results for EEE came from Colorado. Pat finally had a definitive diagnosis. “By the time the EEE test came back positive, it was too late,” said Villanueva.
Early treatment is a source of hope in the fight against EEE, but the difficulty of diagnosis makes it hard to achieve. More effective testing for EEE could help. There were four confirmed cases of EEE in Connecticut this year, and they all ended up at Yale-New Haven Hospital. In all four of these cases, the quicker, preliminary test for EEE was negative. The CDC’s more complicated test was consistently positive.
No one knows exactly why the preliminary test for EEE has fallen short. Testing for viruses is a complicated process. Doctors have guessed that the test may have trouble detecting some recent evolutionary change to the strain of EEE virus in Connecticut.
The CDC’s more complicated test works, though it requires both a higher degree of safety and more time than the preliminary test. The EEE virus grows in cells for two days. The state government sends samples to the CDC, where they join a national queue. It may take days or weeks to receive a diagnosis. It’s possible that those days or weeks could mean the difference between receiving IVIg treatment and dying.
Kaddouh argues that doctors should use IVIg earlier on to treat people with even the slightest possibility of EEE infection. “If it’s in the season, one can get a spinal fluid sample, send it to be tested, and start a patient on IVIg immediately,” he says. Doctors adopting Kaddouh’s approach could give patients a better chance.
As the first two weeks in September passed, Pat’s sickness persisted. She had been comatose for two weeks, but Jerry hadn’t given up hope. “I was hoping that the inevitable would not be what eventually took place,” he said.
On September 18th, Kaddouh sat down with the family to explain Pat’s situation. “When I heard, I knew what the outcome was going to be,” said Jerry. During the conversation with Kaddouh, the rest of Jerry’s family realized that their beloved Pat wasn’t going to wake up. She died peacefully the next day, surrounded by her family.
Jerry went home to a house full of memories, with his dog Bennie and his guinea pigs for company. Losing Pat has been hard. “You live with somebody for 55 years, and all of a sudden they’re not here? That leaves a big void in your life. A real empty spot in your heart,” he says.
To fill the emptiness, Bennie barks a lot more than usual. “He really misses my wife,”
Jerry says, seated on his living room couch. Pat’s smiling face presides over the room from the mantlepiece, where Jerry keeps two candles burning. Her past works of needlepoint adorn the yellow walls. The living room window overlooks a tall stand of trees growing in the middle of a swamp.
In all likelihood, Pat’s EEE came from a mosquito living in the swamp next to her house. A small brook used to flow through the woods in place of the swamp, but the landscape has changed in recent years, becoming muddier. A warming climate is bringing more changes to Connecticut and the rest of New England, where it will increase the prevalence of EEE.
Right now, cold temperatures are the only natural way to kill adult mosquitoes carrying EEE. “You really need temperatures 28 degrees and below,” says Armstrong. “That’s what you need to shut down mosquito activity completely.” With the first frost, adult C. melanura mosquitoes die, and infected larvae hunker down in swamps for the winter—out of commission, but possibly harboring the virus. In most years, adult mosquitoes are gone for the season come October. In 2019, the summer was hotter than normal. Armstrong and his team were trapping mosquitoes well into November.
“They’ve been active later in the season, thriving longer than they have been in the past. Our concept of seasonality is changing,” said Villanueva. With changing seasonality and longer-lasting summers, spending time outside is already becoming risky for longer.
A hotter planet will also mean higher rates of evaporation, so more water from the Earth’s surface will wind up in the clouds. “There’s more water cycling through the atmosphere,” says Armstrong. Rainfall will become more plentiful as time passes, so groundwater will accumulate. With more water on the ground, swamps will grow in size, just like Pat and Jerry’s brook-turned-swamp. More available swamp habitat will bring more C. melanura to Connecticut and the rest of New England. Mosquitoes will stay around longer, biting more birds and humans. More people will get sick with EEE.
EEE isn’t the only disease on the rise because of climate change.“We’re seeing a trend towards greater instances of mosquito- and tick-borne diseases,” says Armstrong. Most people think of the tropics as a hotbed for viruses like Zika, dengue, and malaria. Different, deadly infections are coming to backyards in the Northeast in larger numbers: EEE, West Nile and Powassan all infected people in New England in 2019.
There’s not much we can do to keep EEE and other diseases out of New England. They’re already here. “We’re trying to do what we can to mitigate them. We’re never going to get rid of them,” says Armstrong. But with improvements to testing and treatment strategies, New England—and the rest of the nation—could be better prepared.
Doctors are already taking 2019 as a warning and starting to prepare for the future. Kaddouh and some of his colleagues at Yale-New Haven have agreed on a standard way to take care of patients who could have EEE. The formula is simple and aims to give patients the best chance possible: administer IVIg early and get the right testing done.
The lack of preparation for EEE showed in 2019, as the virus killed more people in the United States than it has in decades. Regardless of whether doctors agree on the best way to test and treat the virus, both testing and treatments are still far from perfect. The yearly number of deaths due to EEE is likely to rise barring rapid advancements.
Armstrong thinks EEE will be back in 2020, whether we’re ready or not. “I don’t think it’ll be as bad,” he says. “It’s a long-term and ongoing challenge.” Though infections this year might not reach the outbreak levels of 2019, any EEE news is bad news. As long as the virus is around, everyone is at risk.
“You hear about the potential threat of EEE in New England,” says Jerry, turning away from the window that overlooks his and Pat’s backyard. “I hope you never have to deal with anything like this.”
Pat Shaw, 77, was enjoying retired life with her high school sweetheart, Jerry Shaw, when she came down with a cold in the middle of August. Pat felt mostly normal at first—all she had was a small headache. She would still join Jerry at their kitchen table to read the paper over coffee every morning. After breakfast, they’d feed their seven guinea pigs and play with their dog, Bennie. In the afternoon, Pat and Jerry might swim in their pool, go for a walk, or spend a couple of hours in the garden outside their home in East Lyme, Connecticut. “We just enjoyed doing things together—being together,” said Jerry.
After about a week, Pat’s headaches got worse. She went to bed early, feeling exhausted. Overnight, she developed a 103-degree fever. “She got up in the morning and looked at me and said, ‘Oh, you’re growing a beard. I like it,’” Jerry remembered. “I’ve had a beard for fifty years.” He knew that his beloved wife wasn’t herself.
Jerry hurried Pat to the emergency room at their local hospital, where her doctors thought she was having a stroke, though her brain showed no signs of bleeding or damage. The doctors stuck a needle into Pat’s back to take fluid for testing. According to Jerry, her blood pressure skyrocketed, and her doctors were worried. They sent a heavily-sedated Pat to Yale-New Haven Hospital by helicopter.
Soon after she arrived at the hospital, Pat became unresponsive. She couldn’t breathe or eat without the help of machines. Her three sons and their daughters stood by her hospital bed, begging her to wake up, but MRIs showed worsening damage to her brain as August turned to September.
For two weeks, no one knew what was wrong. “Everything came back negative,” said Jerry. The doctors sent Pat’s spinal fluid to the Centers for Disease Control in Colorado. In mid-September, a scary diagnosis came back.
Pat had developed a viral infection from a mosquito that probably bit her when she was in her backyard. She had Eastern Equine Encephalitis—EEE for short. EEE is a rare, poorly understood virus that attacks the brain. “Who would have thought it would be one of us?” Jerry said.
Pat’s EEE was part of an outbreak that swept across the United States this summer. In 2019, the virus killed fifteen Americans. The number of people infected nationwide swelled to 38, more than five times the average over the past ten years. Diagnosis of EEE is difficult, and treatment is often futile. Its rise this year is a sign of what’s to come. A warming climate will generate a more favorable environment for mosquitoes, allowing more of them to carry and transmit the virus for longer each year. More people will get sick across New England, and no one is prepared.
Mosquitoes in the tropics can carry EEE year round because of consistently warm weather. Migrating birds fly to the tropics for the winter. There, they pick up EEE from mosquito bites. Birds don’t get sick or show symptoms from EEE, but they carry the virus back to North America.
When spring comes to New England, EEE-infected birds return. Upon arriving, many look for food along the Connecticut-Rhode Island border in swamps filled with large trees. The swampy water at the roots of these trees is a perfect breeding habitat for Culiseta melanura, the main mosquito species that carries EEE. C. melanura feeds almost exclusively on birds.
When the migrating birds reach the swamps, C. melanura mosquitoes first pick up the virus by biting them. Birds and mosquitoes then pass the virus back and forth in a game of hot potato. “If more birds get infected, more mosquitoes get infected,” says Leonard Munstermann, an epidemiologist at the Yale School of Public Health.
Munstermann focuses on insect-borne illnesses like EEE. He finds striking how quickly C. melanura can spread the virus. “For some reason, it is able to go through them like a hot knife through butter,” says Munstermann.
The knife is the hottest under the warm summer sun. During the summer, levels of EEE in C. melanura reach a high point.
When the adult mosquitoes die at the end of each year, their offspring somehow carry the virus into the next spring. Scientists don’t know how the virus manages to overwinter. But experts suspect that larvae spend the winter nestled in their forested wetlands, harboring the virus. In the spring and summer, mature mosquitoes can once again infect humans. Not only do birds bring EEE to New England anew each year—it also rolls over from the year before.
The virus spills out of the bird-mosquito exchange to infect humans during the rare instance when C. melanura bites a person. Although EEE does not affect birds, it causes severe brain damage and kills a third of the people it infects. Though EEE does not mean certain death, the disease is always life-altering and debilitating. Children and the elderly are especially susceptible to infection.
Philip Armstrong has watched the summertime risk of EEE infection in New England slowly rise over the past two decades. During that time, he has been the scientist in charge of Connecticut’s mosquito trapping and testing program. Armstrong studies EEE for a living, but the mention of it makes him shake his head in dismay. “I never wish EEE on my worst enemy. It’s devastating.”
Armstrong is a tall, skinny man with ginger hair graying at the temples. His lab is teeming with mosquitoes of all kinds. Dead ones sit piled in glass containers near microscopes. On the walls of the lab, there are illustrated comics and larger-than-life mosquito posters. Armstrong approaches a fridge-sized incubator along one of the walls, where he keeps live mosquitoes for experiments. He opens the door to reveal a tower of Tupperware containers full of mosquito larvae that look like grains of rice floating around in murky water. Armstrong bypasses the Tupperware, turning instead to a basketball-sized box covered in cloth.
Armstrong carefully removes the box from the incubator. He gingerly places it on a table in the middle of the room, lifting the cloth that covers it. Underneath, there’s a metal mesh cage. A small cloud of mosquitoes convulses inside.
Armstrong peers into the cage, running his hands over the mesh. He chuckles when the mosquitoes inside won’t bite him. “They don’t seem too interested. These are C. melanura,” he says. The buzzing cloud is made from the bird-biting mosquitoes that can carry EEE.
These mosquitoes aren’t infected, but running experiments on them could help scientists learn more about the ones that are. The experiments are only possible here. Armstrong’s lab is the only one in the country to have its own colony of C. melanura.
Armstrong and his team collect wild mosquitoes from almost 100 locations across Connecticut each week. They identify each individual mosquito according to species. Then they check whether the mosquitoes were carrying diseases. “We really need to know what species we’re looking at and what viruses they’re carrying, which gives us a more informed assessment of the risk,” says Armstrong. He and his team trapped, identified, and tested almost a quarter of a million mosquitoes in 2019 alone.
Starting in June, Armstrong noticed a concerning pattern: “One species in particular, C. melanura, had numbers way above the historical average.” With more potential carriers of EEE, Armstrong worried about an outbreak. Sure enough, he and his team found lots of C. melanura infected with EEE in Connecticut during August. The largest number of infected mosquitoes came from their typical swamp habitat near the Rhode Island border. More C. melanura carrying EEE wound up in traps along Connecticut’s southeast shoreline, close to where the Shaws live in East Lyme.
In response, Armstrong worked closely with the Department of Public Health to develop suggested courses of action for towns in these areas. “The goal is to figure out how to best protect the public in a way that’s acceptable to the public and doesn’t disrupt people’s lives too much,” he said. Twenty-one local governments in high-risk areas heeded Armstrong’s recommendations. They urged people to stay inside after dark, or to wear insect repellent if they ventured outside. Schools cancelled afternoon activities.
But no matter how much care people take during the summer to prevent bug bites, one unlucky bite from the wrong mosquito could mean big trouble. This year, the Shaws spent their 45th summer together in their blue-gray house nestled in the woods of East Lyme. Pat and Jerry had been aware of the risk of EEE during the late summer and early fall, so they never went outside without putting on bug spray. They burned citronella by their pool to keep the mosquitoes away. “But obviously, there was one time that it didn’t work,” said Jerry, with tears in his eyes.
When a mosquito carrying EEE bites a person like Pat, the virus slips into the body along with the mosquito’s saliva. It then finds its way into the skin tissue surrounding the bite, infecting nearby cells. These infected cells move to nearby lymphoid tissues, part of the body’s control center for fighting infection. There, the virus hijacks cell machinery in order to replicate itself. Leaving the lymphoid tissue, the virus travels through the bloodstream in increased abundance, winding up in the brain.
When EEE reaches the brain, chaos reigns. The virus attacks neurons, the cells our brains use to send signals throughout the body. “They tend to target gray matter, the parts of our brains where there are neuron cell bodies,” says Firas Kaddouh, a neurologist at Yale-New Haven Hospital. The virus overwhelms the gray matter parts of the brain, its attack leaving behind neurons damaged beyond repair. As these cells die, fluid builds up in the brain and blood vessels swell up. A domino effect of inflammation follows from the buildup of fluid and dead neurons. Collateral damage ensues. Inflammation of the brain in this fashion is called encephalitis.
About a day after EEE makes it to a person’s brain, they may appear disoriented and even lose consciousness. When people with EEE lose consciousness, they may never wake up. And if they do, the damage to their brain is catastrophic. Though the heart is still pumping blood to the rest of the body, the brain damage approaches destruction.
When Kaddouh was taking care of Pat, he and his colleagues knew that some sort of encephalitis was at play. From scans of Pat’s brain, they saw that there was severe damage to gray matter on both the surface and the deep interior of the brain. But it took them weeks to figure out what was causing the damage.
Initially, doctors suspected herpes simplex virus, a common—and treatable—cause of encephalitis. “If you’re dealing with herpes, you’ll start to wake up,” said Merceditas Villanueva, an infectious disease specialist who took care of Pat at Yale-New Haven. Pat wasn’t waking up, and the test for herpes came back negative.
Her doctors ordered tests for about fifteen different diseases, including a preliminary test for EEE. All of the tests at Yale came back negative, so Villanueva and her colleagues sent Pat’s spinal fluid to the CDC in Colorado for more extensive testing.
Despite so many negative tests at first, Pat’s doctors were confident that some kind of virus was causing inflammation in her brain. After she had been at Yale-New Haven for about ten days, they gave her treatment to prop up her failing immune system. This treatment is called intravenous immunoglobulin—IVIg for short. The goal with IVIg is to contain a virus at its point of attack in the brain.
Had the doctors started Pat on IVIg even sooner, it might have made a difference. “It’s expensive, but it’s the only treatment that can be offered for EEE,” said Kaddouh. IVIg has stemmed the tide of EEE infection in other patients. Three years ago, a man from Massachusetts on the brink of death made a full recovery. He had been nearly comatose from developing encephalitis from a mosquito bite. He received early IVIg treatment, and his condition improved rapidly. Within months, he was home again with his family. Because of IVIg, he had his life back.
The timing of the treatment is a key difference between Pat and the man who recovered. On September 15th, positive test results for EEE came from Colorado. Pat finally had a definitive diagnosis. “By the time the EEE test came back positive, it was too late,” said Villanueva.
Early treatment is a source of hope in the fight against EEE, but the difficulty of diagnosis makes it hard to achieve. More effective testing for EEE could help. There were four confirmed cases of EEE in Connecticut this year, and they all ended up at Yale-New Haven Hospital. In all four of these cases, the quicker, preliminary test for EEE was negative. The CDC’s more complicated test was consistently positive.
No one knows exactly why the preliminary test for EEE has fallen short. Testing for viruses is a complicated process. Doctors have guessed that the test may have trouble detecting some recent evolutionary change to the strain of EEE virus in Connecticut.
The CDC’s more complicated test works, though it requires both a higher degree of safety and more time than the preliminary test. The EEE virus grows in cells for two days. The state government sends samples to the CDC, where they join a national queue. It may take days or weeks to receive a diagnosis. It’s possible that those days or weeks could mean the difference between receiving IVIg treatment and dying.
Kaddouh argues that doctors should use IVIg earlier on to treat people with even the slightest possibility of EEE infection. “If it’s in the season, one can get a spinal fluid sample, send it to be tested, and start a patient on IVIg immediately,” he says. Doctors adopting Kaddouh’s approach could give patients a better chance.
As the first two weeks in September passed, Pat’s sickness persisted. She had been comatose for two weeks, but Jerry hadn’t given up hope. “I was hoping that the inevitable would not be what eventually took place,” he said.
On September 18th, Kaddouh sat down with the family to explain Pat’s situation. “When I heard, I knew what the outcome was going to be,” said Jerry. During the conversation with Kaddouh, the rest of Jerry’s family realized that their beloved Pat wasn’t going to wake up. She died peacefully the next day, surrounded by her family.
Jerry went home to a house full of memories, with his dog Bennie and his guinea pigs for company. Losing Pat has been hard. “You live with somebody for 55 years, and all of a sudden they’re not here? That leaves a big void in your life. A real empty spot in your heart,” he says.
To fill the emptiness, Bennie barks a lot more than usual. “He really misses my wife,”
Jerry says, seated on his living room couch. Pat’s smiling face presides over the room from the mantlepiece, where Jerry keeps two candles burning. Her past works of needlepoint adorn the yellow walls. The living room window overlooks a tall stand of trees growing in the middle of a swamp.
In all likelihood, Pat’s EEE came from a mosquito living in the swamp next to her house. A small brook used to flow through the woods in place of the swamp, but the landscape has changed in recent years, becoming muddier. A warming climate is bringing more changes to Connecticut and the rest of New England, where it will increase the prevalence of EEE.
Right now, cold temperatures are the only natural way to kill adult mosquitoes carrying EEE. “You really need temperatures 28 degrees and below,” says Armstrong. “That’s what you need to shut down mosquito activity completely.” With the first frost, adult C. melanura mosquitoes die, and infected larvae hunker down in swamps for the winter—out of commission, but possibly harboring the virus. In most years, adult mosquitoes are gone for the season come October. In 2019, the summer was hotter than normal. Armstrong and his team were trapping mosquitoes well into November.
“They’ve been active later in the season, thriving longer than they have been in the past. Our concept of seasonality is changing,” said Villanueva. With changing seasonality and longer-lasting summers, spending time outside is already becoming risky for longer.
A hotter planet will also mean higher rates of evaporation, so more water from the Earth’s surface will wind up in the clouds. “There’s more water cycling through the atmosphere,” says Armstrong. Rainfall will become more plentiful as time passes, so groundwater will accumulate. With more water on the ground, swamps will grow in size, just like Pat and Jerry’s brook-turned-swamp. More available swamp habitat will bring more C. melanura to Connecticut and the rest of New England. Mosquitoes will stay around longer, biting more birds and humans. More people will get sick with EEE.
EEE isn’t the only disease on the rise because of climate change.“We’re seeing a trend towards greater instances of mosquito- and tick-borne diseases,” says Armstrong. Most people think of the tropics as a hotbed for viruses like Zika, dengue, and malaria. Different, deadly infections are coming to backyards in the Northeast in larger numbers: EEE, West Nile and Powassan all infected people in New England in 2019.
There’s not much we can do to keep EEE and other diseases out of New England. They’re already here. “We’re trying to do what we can to mitigate them. We’re never going to get rid of them,” says Armstrong. But with improvements to testing and treatment strategies, New England—and the rest of the nation—could be better prepared.
Doctors are already taking 2019 as a warning and starting to prepare for the future. Kaddouh and some of his colleagues at Yale-New Haven have agreed on a standard way to take care of patients who could have EEE. The formula is simple and aims to give patients the best chance possible: administer IVIg early and get the right testing done.
The lack of preparation for EEE showed in 2019, as the virus killed more people in the United States than it has in decades. Regardless of whether doctors agree on the best way to test and treat the virus, both testing and treatments are still far from perfect. The yearly number of deaths due to EEE is likely to rise barring rapid advancements.
Armstrong thinks EEE will be back in 2020, whether we’re ready or not. “I don’t think it’ll be as bad,” he says. “It’s a long-term and ongoing challenge.” Though infections this year might not reach the outbreak levels of 2019, any EEE news is bad news. As long as the virus is around, everyone is at risk.
“You hear about the potential threat of EEE in New England,” says Jerry, turning away from the window that overlooks his and Pat’s backyard. “I hope you never have to deal with anything like this.”
