MDedge Infectious Disease

The Food and Drug Administration on June 17 granted emergency use authorization (EUA) to the Moderna and Pfizer COVID-19 vaccines for use in children 6 months of age and older, one of the final steps in a long-awaited authorization process to extend protection to the youngest of Americans.

The agency’s move comes after a closely watched FDA advisory group vote earlier this week, which resulted in a unanimous vote in favor of the FDA authorizing both vaccines in this age group.

“The FDA’s evaluation and analysis of the safety, effectiveness, and manufacturing data of these vaccines was rigorous and comprehensive, supporting the EUAs,” the agency said in a news release.

The data show that the “known and potential benefits” of the vaccines outweigh any potential risks, the agency said.

The Moderna vaccine is authorized as a two-dose primary series in children 6 months to 17 years of age. The Pfizer vaccine is now authorized as a three-dose primary series in children 6 months up to 4 years of age. Pfizer’s vaccine was already authorized in children 5 years old and older.

Now all eyes are on the Centers for Disease Control and Prevention, which is expected to decide on the final regulatory hurdle at a meeting June 18. The CDC’s Advisory Committee on Immunization Practices has scheduled a vote on whether to give the vaccines the green light.

If ACIP gives the OK, CDC Director Rochelle Walensky, MD, MPH, is expected to issue recommendations for use shortly thereafter.

Following these final regulatory steps, parents could start bringing their children to pediatricians, family doctors, or local pharmacies for vaccination as early as June 20.

A version of this article first appeared on WebMD.com.

The Food and Drug Administration on June 17 granted emergency use authorization (EUA) to the Moderna and Pfizer COVID-19 vaccines for use in children 6 months of age and older, one of the final steps in a long-awaited authorization process to extend protection to the youngest of Americans.

The agency’s move comes after a closely watched FDA advisory group vote earlier this week, which resulted in a unanimous vote in favor of the FDA authorizing both vaccines in this age group.

“The FDA’s evaluation and analysis of the safety, effectiveness, and manufacturing data of these vaccines was rigorous and comprehensive, supporting the EUAs,” the agency said in a news release.

The data show that the “known and potential benefits” of the vaccines outweigh any potential risks, the agency said.

The Moderna vaccine is authorized as a two-dose primary series in children 6 months to 17 years of age. The Pfizer vaccine is now authorized as a three-dose primary series in children 6 months up to 4 years of age. Pfizer’s vaccine was already authorized in children 5 years old and older.

Now all eyes are on the Centers for Disease Control and Prevention, which is expected to decide on the final regulatory hurdle at a meeting June 18. The CDC’s Advisory Committee on Immunization Practices has scheduled a vote on whether to give the vaccines the green light.

If ACIP gives the OK, CDC Director Rochelle Walensky, MD, MPH, is expected to issue recommendations for use shortly thereafter.

Following these final regulatory steps, parents could start bringing their children to pediatricians, family doctors, or local pharmacies for vaccination as early as June 20.

A version of this article first appeared on WebMD.com.

The Food and Drug Administration on June 17 granted emergency use authorization (EUA) to the Moderna and Pfizer COVID-19 vaccines for use in children 6 months of age and older, one of the final steps in a long-awaited authorization process to extend protection to the youngest of Americans.

The agency’s move comes after a closely watched FDA advisory group vote earlier this week, which resulted in a unanimous vote in favor of the FDA authorizing both vaccines in this age group.

“The FDA’s evaluation and analysis of the safety, effectiveness, and manufacturing data of these vaccines was rigorous and comprehensive, supporting the EUAs,” the agency said in a news release.

The data show that the “known and potential benefits” of the vaccines outweigh any potential risks, the agency said.

The Moderna vaccine is authorized as a two-dose primary series in children 6 months to 17 years of age. The Pfizer vaccine is now authorized as a three-dose primary series in children 6 months up to 4 years of age. Pfizer’s vaccine was already authorized in children 5 years old and older.

Now all eyes are on the Centers for Disease Control and Prevention, which is expected to decide on the final regulatory hurdle at a meeting June 18. The CDC’s Advisory Committee on Immunization Practices has scheduled a vote on whether to give the vaccines the green light.

If ACIP gives the OK, CDC Director Rochelle Walensky, MD, MPH, is expected to issue recommendations for use shortly thereafter.

Following these final regulatory steps, parents could start bringing their children to pediatricians, family doctors, or local pharmacies for vaccination as early as June 20.

A version of this article first appeared on WebMD.com.

There may be a link between the recent unexplained cases of hepatitis in children and prior coronavirus infections, according to new research from Israel.

The study involves five children in Israel who had mild cases of COVID-19 who went on to develop hepatitis; two of these children required liver transplants. But clinicians are cautious about drawing conclusions from such a small study.

“All you can say is that these five cases seem to have proximity to COVID-19, and COVID-19 may be able to cause pediatric liver complications,” said Nancy Reau, MD, section chief of hepatology at Rush University in Chicago. She was not involved with the study.

While COVID-19 could be one explanation for these hepatitis cases, it is also possible that the two are unrelated, said William Balistreri, MD, director emeritus of the Pediatric Liver Care Center at Cincinnati Children’s Hospital Medical Center. He also is unaffiliated with the study.

Hepatitis is rare in children, and between 30% and 50% of these pediatric cases have no known cause, according to the CDC.

Since April 2022, children with hepatitis of an unexplained cause have garnered global attention. The United Kingdom now has 240 confirmed cases, the United States is investigating 290 cases, and Israel has reported 12 cases to the World Health Organization. Many investigators think that these liver problems could be related to adenovirus – a common infection in children that normally causes cold or flu-like symptoms – because more than half of global cases tested for the virus have been positive, according to the WHO. About 12% of children with unexplained hepatitis have tested positive for SARS-CoV-2, the virus that causes COVID-19, but investigators are considering the possibility that some cases may be related to prior infections.

The study documents five patients, 3-months to 13 years old, with prior  coronavirus infection who later developed hepatitis. All were treated at Schneider Children’s Medical Hospital in Petah Tikva, Israel, during 2021. The paper was published in the Journal of Pediatric Gastroenterology and Nutrition. Two patients, a 3-month-old and 5-month-old, needed liver transplants. The other three patients (two 8-year-olds and a 13-year-old) were treated with steroids. None of the five children had received any vaccinations against COVID-19. The time between COVID-19 infection and liver problems ranged from 21 to 130 days.

“It took time to be convinced that this could be COVID-related,” said senior study author Orith Waisbourd-Zinman, MD, director of pediatric liver disease service at Schneider Children’s Medical Hospital. “It’s something that wasn’t described.”

Sudden-onset hepatitis after COVID-19 has been recorded in adults, and the virus has been associated with multisystem inflammatory syndrome in children (MIS-C). The condition causes inflammation through the body, including the heart, lungs, and kidneys.

“We know that COVID can be mischievous, and children are no more exempt from that than adults,” Dr. Reau said.

Liver samples taken from these five patients did not test positive for COVID-19, similar to how liver samples have tested negative for adenovirus in more recent hepatitis cases around the world. Dr. Waisbourd-Zinman suggested that in these patients, hepatitis may have been brought on by an inflammatory response that was triggered by the virus. 

Still, there are notable differences between these five cases and current cases internationally. These five children became sick during the period of December 2020 to September 2021, whereas all current counted cases in the United Kingdom occurred after January 2022. The first cases in the United States took place in October 2021. It could be that there were similar hepatitis cases before that were not identified, Dr. Reau said.

The ages of the Israeli children with hepatitis also differ from the cases seen globally. More than three-fourths of these reported hepatitis cases occurred in children under 5, the WHO reports, though affected individuals have been as young as 1-month-old up to 16 years old. In the United Kingdom, which accounts for about a third of cases reported to the WHO, most children with unexplained hepatitis have been between 3 and 5 years old.

More research is needed to tease out any relationship between prior COVID-19 infection and liver inflammation, Dr. Balistreri said.

“I’m not sure what to make of any of it yet. We know that SARS-CoV-2 can alter immune responses ... so it wouldn’t surprise me,” if COVID-19 and these hepatitis cases were linked, he said. “It’s just that we need more information.”

A version of this article first appeared on WebMD.com.

There may be a link between the recent unexplained cases of hepatitis in children and prior coronavirus infections, according to new research from Israel.

The study involves five children in Israel who had mild cases of COVID-19 who went on to develop hepatitis; two of these children required liver transplants. But clinicians are cautious about drawing conclusions from such a small study.

“All you can say is that these five cases seem to have proximity to COVID-19, and COVID-19 may be able to cause pediatric liver complications,” said Nancy Reau, MD, section chief of hepatology at Rush University in Chicago. She was not involved with the study.

While COVID-19 could be one explanation for these hepatitis cases, it is also possible that the two are unrelated, said William Balistreri, MD, director emeritus of the Pediatric Liver Care Center at Cincinnati Children’s Hospital Medical Center. He also is unaffiliated with the study.

Hepatitis is rare in children, and between 30% and 50% of these pediatric cases have no known cause, according to the CDC.

Since April 2022, children with hepatitis of an unexplained cause have garnered global attention. The United Kingdom now has 240 confirmed cases, the United States is investigating 290 cases, and Israel has reported 12 cases to the World Health Organization. Many investigators think that these liver problems could be related to adenovirus – a common infection in children that normally causes cold or flu-like symptoms – because more than half of global cases tested for the virus have been positive, according to the WHO. About 12% of children with unexplained hepatitis have tested positive for SARS-CoV-2, the virus that causes COVID-19, but investigators are considering the possibility that some cases may be related to prior infections.

The study documents five patients, 3-months to 13 years old, with prior  coronavirus infection who later developed hepatitis. All were treated at Schneider Children’s Medical Hospital in Petah Tikva, Israel, during 2021. The paper was published in the Journal of Pediatric Gastroenterology and Nutrition. Two patients, a 3-month-old and 5-month-old, needed liver transplants. The other three patients (two 8-year-olds and a 13-year-old) were treated with steroids. None of the five children had received any vaccinations against COVID-19. The time between COVID-19 infection and liver problems ranged from 21 to 130 days.

“It took time to be convinced that this could be COVID-related,” said senior study author Orith Waisbourd-Zinman, MD, director of pediatric liver disease service at Schneider Children’s Medical Hospital. “It’s something that wasn’t described.”

Sudden-onset hepatitis after COVID-19 has been recorded in adults, and the virus has been associated with multisystem inflammatory syndrome in children (MIS-C). The condition causes inflammation through the body, including the heart, lungs, and kidneys.

“We know that COVID can be mischievous, and children are no more exempt from that than adults,” Dr. Reau said.

Liver samples taken from these five patients did not test positive for COVID-19, similar to how liver samples have tested negative for adenovirus in more recent hepatitis cases around the world. Dr. Waisbourd-Zinman suggested that in these patients, hepatitis may have been brought on by an inflammatory response that was triggered by the virus. 

Still, there are notable differences between these five cases and current cases internationally. These five children became sick during the period of December 2020 to September 2021, whereas all current counted cases in the United Kingdom occurred after January 2022. The first cases in the United States took place in October 2021. It could be that there were similar hepatitis cases before that were not identified, Dr. Reau said.

The ages of the Israeli children with hepatitis also differ from the cases seen globally. More than three-fourths of these reported hepatitis cases occurred in children under 5, the WHO reports, though affected individuals have been as young as 1-month-old up to 16 years old. In the United Kingdom, which accounts for about a third of cases reported to the WHO, most children with unexplained hepatitis have been between 3 and 5 years old.

More research is needed to tease out any relationship between prior COVID-19 infection and liver inflammation, Dr. Balistreri said.

“I’m not sure what to make of any of it yet. We know that SARS-CoV-2 can alter immune responses ... so it wouldn’t surprise me,” if COVID-19 and these hepatitis cases were linked, he said. “It’s just that we need more information.”

A version of this article first appeared on WebMD.com.

There may be a link between the recent unexplained cases of hepatitis in children and prior coronavirus infections, according to new research from Israel.

The study involves five children in Israel who had mild cases of COVID-19 who went on to develop hepatitis; two of these children required liver transplants. But clinicians are cautious about drawing conclusions from such a small study.

“All you can say is that these five cases seem to have proximity to COVID-19, and COVID-19 may be able to cause pediatric liver complications,” said Nancy Reau, MD, section chief of hepatology at Rush University in Chicago. She was not involved with the study.

While COVID-19 could be one explanation for these hepatitis cases, it is also possible that the two are unrelated, said William Balistreri, MD, director emeritus of the Pediatric Liver Care Center at Cincinnati Children’s Hospital Medical Center. He also is unaffiliated with the study.

Hepatitis is rare in children, and between 30% and 50% of these pediatric cases have no known cause, according to the CDC.

Since April 2022, children with hepatitis of an unexplained cause have garnered global attention. The United Kingdom now has 240 confirmed cases, the United States is investigating 290 cases, and Israel has reported 12 cases to the World Health Organization. Many investigators think that these liver problems could be related to adenovirus – a common infection in children that normally causes cold or flu-like symptoms – because more than half of global cases tested for the virus have been positive, according to the WHO. About 12% of children with unexplained hepatitis have tested positive for SARS-CoV-2, the virus that causes COVID-19, but investigators are considering the possibility that some cases may be related to prior infections.

The study documents five patients, 3-months to 13 years old, with prior  coronavirus infection who later developed hepatitis. All were treated at Schneider Children’s Medical Hospital in Petah Tikva, Israel, during 2021. The paper was published in the Journal of Pediatric Gastroenterology and Nutrition. Two patients, a 3-month-old and 5-month-old, needed liver transplants. The other three patients (two 8-year-olds and a 13-year-old) were treated with steroids. None of the five children had received any vaccinations against COVID-19. The time between COVID-19 infection and liver problems ranged from 21 to 130 days.

“It took time to be convinced that this could be COVID-related,” said senior study author Orith Waisbourd-Zinman, MD, director of pediatric liver disease service at Schneider Children’s Medical Hospital. “It’s something that wasn’t described.”

Sudden-onset hepatitis after COVID-19 has been recorded in adults, and the virus has been associated with multisystem inflammatory syndrome in children (MIS-C). The condition causes inflammation through the body, including the heart, lungs, and kidneys.

“We know that COVID can be mischievous, and children are no more exempt from that than adults,” Dr. Reau said.

Liver samples taken from these five patients did not test positive for COVID-19, similar to how liver samples have tested negative for adenovirus in more recent hepatitis cases around the world. Dr. Waisbourd-Zinman suggested that in these patients, hepatitis may have been brought on by an inflammatory response that was triggered by the virus. 

Still, there are notable differences between these five cases and current cases internationally. These five children became sick during the period of December 2020 to September 2021, whereas all current counted cases in the United Kingdom occurred after January 2022. The first cases in the United States took place in October 2021. It could be that there were similar hepatitis cases before that were not identified, Dr. Reau said.

The ages of the Israeli children with hepatitis also differ from the cases seen globally. More than three-fourths of these reported hepatitis cases occurred in children under 5, the WHO reports, though affected individuals have been as young as 1-month-old up to 16 years old. In the United Kingdom, which accounts for about a third of cases reported to the WHO, most children with unexplained hepatitis have been between 3 and 5 years old.

More research is needed to tease out any relationship between prior COVID-19 infection and liver inflammation, Dr. Balistreri said.

“I’m not sure what to make of any of it yet. We know that SARS-CoV-2 can alter immune responses ... so it wouldn’t surprise me,” if COVID-19 and these hepatitis cases were linked, he said. “It’s just that we need more information.”

A version of this article first appeared on WebMD.com.

The cupboard in Dr. Nicolás Rascovan’s microbial paleogenomics lab at Institut Pasteur in Paris is filled up with cardboard boxes that look as if they were shipped from an office supply store. Yet, instead of pencils and Post-it notes, the boxes are filled with ancient human remains from South America – several-thousand-year-old vertebrae, petrus bones (which protect inner ear structures), and teeth – all neatly packed in plastic bags. From these artifacts Dr. Rascovan hopes to retrieve DNA of ancient pathogens – which could help us better understand how microbes emerge and evolve and how pandemics spread. It could even, perhaps, rewrite history. “It’s a story of a continent in a closet,” Dr. Rascovan says.

Over the past decade, technologic advances in DNA recovery and sequencing have made it possible for scientists such as Dr. Rascovan, an Argentinian molecular biologist, to analyze ancient specimens relatively quickly and affordably. They’ve been hunting for – and finding – DNA of centuries-old microbes in various archeological samples: from smallpox variola virus and Mycobacterium tuberculosis in mummified tissues, to the Black Death bacteria, Yesinia pestis, in neolithic teeth, to Plasmodium falciparum preserved in historical blood stains.

The ultramodern Parisian offices of the microbial paleogenomics group, a team of five scientists led by Dr. Rascovan, clash with the logo they half-jokingly chose for themselves and plastered all over the lab’s walls: a Jurassic Park–inspired dinosaur baring its giant, ancient teeth, made to look like an image seen under a microscope. Ancient teeth are certainly central to the group’s work, because it’s there where ancient pathogens’ DNA is most likely to be preserved – after death, teeth act like tiny, sealed-up boxes for microbes. “If you have a pathogen that is circulating in the blood, it will sometimes get into the teeth, and when you die, the DNA will stay there,” Dr. Rascovan says.

To process ancient teeth, Dr. Rascovan enters a lab clad head to toe in protective gear. That’s not so much to save himself from potentially deadly disease as to save the samples from contamination, he says. According to Sebastian Duchene Garzon, a microbiologist at the University of Melbourne, “the likelihood of ancient pathogen DNA leading to infections at present is remote, although certainly not impossible, because of how degraded the DNA usually is and because it would still need all the molecular machinery to infect a modern host.”

To process ancient teeth in his lab, Dr. Rascovan starts with a thorough cleaning that involves bleach to remove any modern DNA contamination. Next, he cuts the tooth with a Dremel rotary tool to open it up and get into its pulp – which is not only very durable but also naturally sterile – a perfect place to find ancient pathogens. He then scrapes the pulp into a powder that can be poured into a tube for DNA extraction.

So far, Dr. Rascovan’s biggest breakthrough didn’t come from the teeth he cut up himself, though. It came from analyzing publicly available DNA data from studies of ancient human genomes. When such genomes are sequenced from fossil teeth or bones, scientists pick out the material they need for study of our ancestors’ evolutionary history. However, among the double helixes coding hominid genetic instructions often hide scraps of microbial DNA, which in the past were frequently simply discarded.

Dr. Rascovan downloaded data from published articles on ancient human DNA that had been found in teeth and reanalyzed them, searching for bacteria. One night, when he was alone in his office going through lines and lines of data, he spotted it: DNA of the plague-causing bacteria, Y. pestis. When Dr. Rascovan cross-checked to determine in which samples the bacteria’s DNA was found, his heart raced. “It was not supposed to be there,” he says. He had just discovered the most ancient case of plague in humans – which occurred 4,900 years ago in Sweden.

Scientists used to believe that plague pandemics came to Europe from the Eurasian Steppe. Yet here was the DNA of Y. pestis lodged in the teeth of two farmers, a woman and a man, who died in Scandinavia before the plague’s supposed arrival from the East. Their bodies were buried in an unusually large common grave – of itself a possible indication of an epidemic.

When Dr. Rascovan and his colleagues applied molecular-clock analyses of the phylogenetic tree of the plague bacteria and compared various strains to see which one was the most ancestral, they confirmed that the Swedish strain of Y. pestis, named Gok2, was indeed the oldest – the origin of the Steppe strains rather than its distant cousin. Plague, it seemed, wasn’t brought to Europe during mass migrations from the East. Instead, it might have originated there.

Such work is not simply about rewriting history. By updating our knowledge of ancient pandemics, we can learn how different factors influence each other in fostering outbreaks. For Dr. Rascovan, the Swedish plague story underscores the importance of our lifestyle and environment for the emergence and spread of dangerous pathogens. The Gok2 strain didn’t contain a gene that makes plague particularly virulent, called ymt, yet it might have played an important role in Bronze Age Europe. At that time, mega-settlements of 10,000 to 20,000 people existed in what is now Ukraine, Romania, and Moldova, yet those settlements were frequently burned to the ground and abandoned. According to Dr. Rascovan and his colleagues, that could fit with the plague pandemic story (although this remains very much a hypothesis).

In Mexico, environmental factors might have played an important role in the severity of the 16th century “cocoliztli” epidemic (the word means “pestilence” in a local language), considered one of the most devastating epidemics in New World history. The disease, which caused vomiting, red spots on the skin, and bleeding from various body orifices, didn’t have a known cause. Some hypothesized the bug might have been smallpox, judging by the severity of the outbreak. A 2018 study of a victim’s DNA showed it contained the genome of Salmonella enterica, a bacterium that causes enteric fever – a microbe generally milder than smallpox. The study’s authors argued that specific conditions may have been necessary at the onset of the epidemic for the S. enterica microbe to cause such devastating outcomes. A mix of severe draught, forced relocations of the local population by their Spanish rulers, and new subsistence farming practices all negatively affected hygienic conditions in the local settlements. According to Dr. Rascovan, such research can “place pandemics into their broader context” – with potential lessons for the future.

One of the microbes Dr. Rascovan and his team are hoping to find in the ancient teeth stocked in their lab’s closet is tuberculosis – a pathogen that kills 1.5 million people a year, yet whose evolutionary history remains largely a mystery. The focus of Dr. Rascovan and his colleagues remains on fossils shipped from South America, since we still know very little about microbes that were associated with pre-Columbian populations. South Americans have been isolated from the rest of the world for 20,000 years, making them particularly interesting candidates for the study of emergence, evolution, and spread of pathogens.

Dr. Rascovan believes that ancient microbial genomic data can help scientists better understand antibiotic resistance through comparisons of bacterial evolution before and after the discovery of antibiotics. In general, he says, by studying only current pathogens and the modern outbreaks they cause, we see only a narrow sample of something that is much more diverse and much larger. “We are missing an important part of information. Ancient samples can bring us a perspective,” he says.

A version of this article first appeared on Medscape.com.

The cupboard in Dr. Nicolás Rascovan’s microbial paleogenomics lab at Institut Pasteur in Paris is filled up with cardboard boxes that look as if they were shipped from an office supply store. Yet, instead of pencils and Post-it notes, the boxes are filled with ancient human remains from South America – several-thousand-year-old vertebrae, petrus bones (which protect inner ear structures), and teeth – all neatly packed in plastic bags. From these artifacts Dr. Rascovan hopes to retrieve DNA of ancient pathogens – which could help us better understand how microbes emerge and evolve and how pandemics spread. It could even, perhaps, rewrite history. “It’s a story of a continent in a closet,” Dr. Rascovan says.

Over the past decade, technologic advances in DNA recovery and sequencing have made it possible for scientists such as Dr. Rascovan, an Argentinian molecular biologist, to analyze ancient specimens relatively quickly and affordably. They’ve been hunting for – and finding – DNA of centuries-old microbes in various archeological samples: from smallpox variola virus and Mycobacterium tuberculosis in mummified tissues, to the Black Death bacteria, Yesinia pestis, in neolithic teeth, to Plasmodium falciparum preserved in historical blood stains.

The ultramodern Parisian offices of the microbial paleogenomics group, a team of five scientists led by Dr. Rascovan, clash with the logo they half-jokingly chose for themselves and plastered all over the lab’s walls: a Jurassic Park–inspired dinosaur baring its giant, ancient teeth, made to look like an image seen under a microscope. Ancient teeth are certainly central to the group’s work, because it’s there where ancient pathogens’ DNA is most likely to be preserved – after death, teeth act like tiny, sealed-up boxes for microbes. “If you have a pathogen that is circulating in the blood, it will sometimes get into the teeth, and when you die, the DNA will stay there,” Dr. Rascovan says.

To process ancient teeth, Dr. Rascovan enters a lab clad head to toe in protective gear. That’s not so much to save himself from potentially deadly disease as to save the samples from contamination, he says. According to Sebastian Duchene Garzon, a microbiologist at the University of Melbourne, “the likelihood of ancient pathogen DNA leading to infections at present is remote, although certainly not impossible, because of how degraded the DNA usually is and because it would still need all the molecular machinery to infect a modern host.”

To process ancient teeth in his lab, Dr. Rascovan starts with a thorough cleaning that involves bleach to remove any modern DNA contamination. Next, he cuts the tooth with a Dremel rotary tool to open it up and get into its pulp – which is not only very durable but also naturally sterile – a perfect place to find ancient pathogens. He then scrapes the pulp into a powder that can be poured into a tube for DNA extraction.

So far, Dr. Rascovan’s biggest breakthrough didn’t come from the teeth he cut up himself, though. It came from analyzing publicly available DNA data from studies of ancient human genomes. When such genomes are sequenced from fossil teeth or bones, scientists pick out the material they need for study of our ancestors’ evolutionary history. However, among the double helixes coding hominid genetic instructions often hide scraps of microbial DNA, which in the past were frequently simply discarded.

Dr. Rascovan downloaded data from published articles on ancient human DNA that had been found in teeth and reanalyzed them, searching for bacteria. One night, when he was alone in his office going through lines and lines of data, he spotted it: DNA of the plague-causing bacteria, Y. pestis. When Dr. Rascovan cross-checked to determine in which samples the bacteria’s DNA was found, his heart raced. “It was not supposed to be there,” he says. He had just discovered the most ancient case of plague in humans – which occurred 4,900 years ago in Sweden.

Scientists used to believe that plague pandemics came to Europe from the Eurasian Steppe. Yet here was the DNA of Y. pestis lodged in the teeth of two farmers, a woman and a man, who died in Scandinavia before the plague’s supposed arrival from the East. Their bodies were buried in an unusually large common grave – of itself a possible indication of an epidemic.

When Dr. Rascovan and his colleagues applied molecular-clock analyses of the phylogenetic tree of the plague bacteria and compared various strains to see which one was the most ancestral, they confirmed that the Swedish strain of Y. pestis, named Gok2, was indeed the oldest – the origin of the Steppe strains rather than its distant cousin. Plague, it seemed, wasn’t brought to Europe during mass migrations from the East. Instead, it might have originated there.

Such work is not simply about rewriting history. By updating our knowledge of ancient pandemics, we can learn how different factors influence each other in fostering outbreaks. For Dr. Rascovan, the Swedish plague story underscores the importance of our lifestyle and environment for the emergence and spread of dangerous pathogens. The Gok2 strain didn’t contain a gene that makes plague particularly virulent, called ymt, yet it might have played an important role in Bronze Age Europe. At that time, mega-settlements of 10,000 to 20,000 people existed in what is now Ukraine, Romania, and Moldova, yet those settlements were frequently burned to the ground and abandoned. According to Dr. Rascovan and his colleagues, that could fit with the plague pandemic story (although this remains very much a hypothesis).

In Mexico, environmental factors might have played an important role in the severity of the 16th century “cocoliztli” epidemic (the word means “pestilence” in a local language), considered one of the most devastating epidemics in New World history. The disease, which caused vomiting, red spots on the skin, and bleeding from various body orifices, didn’t have a known cause. Some hypothesized the bug might have been smallpox, judging by the severity of the outbreak. A 2018 study of a victim’s DNA showed it contained the genome of Salmonella enterica, a bacterium that causes enteric fever – a microbe generally milder than smallpox. The study’s authors argued that specific conditions may have been necessary at the onset of the epidemic for the S. enterica microbe to cause such devastating outcomes. A mix of severe draught, forced relocations of the local population by their Spanish rulers, and new subsistence farming practices all negatively affected hygienic conditions in the local settlements. According to Dr. Rascovan, such research can “place pandemics into their broader context” – with potential lessons for the future.

One of the microbes Dr. Rascovan and his team are hoping to find in the ancient teeth stocked in their lab’s closet is tuberculosis – a pathogen that kills 1.5 million people a year, yet whose evolutionary history remains largely a mystery. The focus of Dr. Rascovan and his colleagues remains on fossils shipped from South America, since we still know very little about microbes that were associated with pre-Columbian populations. South Americans have been isolated from the rest of the world for 20,000 years, making them particularly interesting candidates for the study of emergence, evolution, and spread of pathogens.

Dr. Rascovan believes that ancient microbial genomic data can help scientists better understand antibiotic resistance through comparisons of bacterial evolution before and after the discovery of antibiotics. In general, he says, by studying only current pathogens and the modern outbreaks they cause, we see only a narrow sample of something that is much more diverse and much larger. “We are missing an important part of information. Ancient samples can bring us a perspective,” he says.

A version of this article first appeared on Medscape.com.

The cupboard in Dr. Nicolás Rascovan’s microbial paleogenomics lab at Institut Pasteur in Paris is filled up with cardboard boxes that look as if they were shipped from an office supply store. Yet, instead of pencils and Post-it notes, the boxes are filled with ancient human remains from South America – several-thousand-year-old vertebrae, petrus bones (which protect inner ear structures), and teeth – all neatly packed in plastic bags. From these artifacts Dr. Rascovan hopes to retrieve DNA of ancient pathogens – which could help us better understand how microbes emerge and evolve and how pandemics spread. It could even, perhaps, rewrite history. “It’s a story of a continent in a closet,” Dr. Rascovan says.

Over the past decade, technologic advances in DNA recovery and sequencing have made it possible for scientists such as Dr. Rascovan, an Argentinian molecular biologist, to analyze ancient specimens relatively quickly and affordably. They’ve been hunting for – and finding – DNA of centuries-old microbes in various archeological samples: from smallpox variola virus and Mycobacterium tuberculosis in mummified tissues, to the Black Death bacteria, Yesinia pestis, in neolithic teeth, to Plasmodium falciparum preserved in historical blood stains.

The ultramodern Parisian offices of the microbial paleogenomics group, a team of five scientists led by Dr. Rascovan, clash with the logo they half-jokingly chose for themselves and plastered all over the lab’s walls: a Jurassic Park–inspired dinosaur baring its giant, ancient teeth, made to look like an image seen under a microscope. Ancient teeth are certainly central to the group’s work, because it’s there where ancient pathogens’ DNA is most likely to be preserved – after death, teeth act like tiny, sealed-up boxes for microbes. “If you have a pathogen that is circulating in the blood, it will sometimes get into the teeth, and when you die, the DNA will stay there,” Dr. Rascovan says.

To process ancient teeth, Dr. Rascovan enters a lab clad head to toe in protective gear. That’s not so much to save himself from potentially deadly disease as to save the samples from contamination, he says. According to Sebastian Duchene Garzon, a microbiologist at the University of Melbourne, “the likelihood of ancient pathogen DNA leading to infections at present is remote, although certainly not impossible, because of how degraded the DNA usually is and because it would still need all the molecular machinery to infect a modern host.”

To process ancient teeth in his lab, Dr. Rascovan starts with a thorough cleaning that involves bleach to remove any modern DNA contamination. Next, he cuts the tooth with a Dremel rotary tool to open it up and get into its pulp – which is not only very durable but also naturally sterile – a perfect place to find ancient pathogens. He then scrapes the pulp into a powder that can be poured into a tube for DNA extraction.

So far, Dr. Rascovan’s biggest breakthrough didn’t come from the teeth he cut up himself, though. It came from analyzing publicly available DNA data from studies of ancient human genomes. When such genomes are sequenced from fossil teeth or bones, scientists pick out the material they need for study of our ancestors’ evolutionary history. However, among the double helixes coding hominid genetic instructions often hide scraps of microbial DNA, which in the past were frequently simply discarded.

Dr. Rascovan downloaded data from published articles on ancient human DNA that had been found in teeth and reanalyzed them, searching for bacteria. One night, when he was alone in his office going through lines and lines of data, he spotted it: DNA of the plague-causing bacteria, Y. pestis. When Dr. Rascovan cross-checked to determine in which samples the bacteria’s DNA was found, his heart raced. “It was not supposed to be there,” he says. He had just discovered the most ancient case of plague in humans – which occurred 4,900 years ago in Sweden.

Scientists used to believe that plague pandemics came to Europe from the Eurasian Steppe. Yet here was the DNA of Y. pestis lodged in the teeth of two farmers, a woman and a man, who died in Scandinavia before the plague’s supposed arrival from the East. Their bodies were buried in an unusually large common grave – of itself a possible indication of an epidemic.

When Dr. Rascovan and his colleagues applied molecular-clock analyses of the phylogenetic tree of the plague bacteria and compared various strains to see which one was the most ancestral, they confirmed that the Swedish strain of Y. pestis, named Gok2, was indeed the oldest – the origin of the Steppe strains rather than its distant cousin. Plague, it seemed, wasn’t brought to Europe during mass migrations from the East. Instead, it might have originated there.

Such work is not simply about rewriting history. By updating our knowledge of ancient pandemics, we can learn how different factors influence each other in fostering outbreaks. For Dr. Rascovan, the Swedish plague story underscores the importance of our lifestyle and environment for the emergence and spread of dangerous pathogens. The Gok2 strain didn’t contain a gene that makes plague particularly virulent, called ymt, yet it might have played an important role in Bronze Age Europe. At that time, mega-settlements of 10,000 to 20,000 people existed in what is now Ukraine, Romania, and Moldova, yet those settlements were frequently burned to the ground and abandoned. According to Dr. Rascovan and his colleagues, that could fit with the plague pandemic story (although this remains very much a hypothesis).

In Mexico, environmental factors might have played an important role in the severity of the 16th century “cocoliztli” epidemic (the word means “pestilence” in a local language), considered one of the most devastating epidemics in New World history. The disease, which caused vomiting, red spots on the skin, and bleeding from various body orifices, didn’t have a known cause. Some hypothesized the bug might have been smallpox, judging by the severity of the outbreak. A 2018 study of a victim’s DNA showed it contained the genome of Salmonella enterica, a bacterium that causes enteric fever – a microbe generally milder than smallpox. The study’s authors argued that specific conditions may have been necessary at the onset of the epidemic for the S. enterica microbe to cause such devastating outcomes. A mix of severe draught, forced relocations of the local population by their Spanish rulers, and new subsistence farming practices all negatively affected hygienic conditions in the local settlements. According to Dr. Rascovan, such research can “place pandemics into their broader context” – with potential lessons for the future.

One of the microbes Dr. Rascovan and his team are hoping to find in the ancient teeth stocked in their lab’s closet is tuberculosis – a pathogen that kills 1.5 million people a year, yet whose evolutionary history remains largely a mystery. The focus of Dr. Rascovan and his colleagues remains on fossils shipped from South America, since we still know very little about microbes that were associated with pre-Columbian populations. South Americans have been isolated from the rest of the world for 20,000 years, making them particularly interesting candidates for the study of emergence, evolution, and spread of pathogens.

Dr. Rascovan believes that ancient microbial genomic data can help scientists better understand antibiotic resistance through comparisons of bacterial evolution before and after the discovery of antibiotics. In general, he says, by studying only current pathogens and the modern outbreaks they cause, we see only a narrow sample of something that is much more diverse and much larger. “We are missing an important part of information. Ancient samples can bring us a perspective,” he says.

A version of this article first appeared on Medscape.com.

Not long ago, a pediatrician working in a local urgent care clinic called me about a teenage girl with a pruritic rash. She described vesicles and pustules located primarily on the face and arms with no surrounding cellulitis or other exam findings.

“She probably has impetigo,” my colleague said. “But I took a travel and exposure history and learned that her grandma had recently returned home from visiting family in the Congo. Do you think I need to worry about monkeypox?”

While most pediatricians in the United States have never seen a case of monkeypox, the virus is not new. An orthopox, it belongs to the same genus that includes smallpox and cowpox viruses. It was discovered in 1958 when two colonies of monkeys kept for research developed pox-like rashes. The earliest human case was reported in 1970 in the Democratic Republic of Congo and now the virus is endemic in some counties in Central and West Africa.

Monkeypox virus is a zoonotic disease – it can spread from animals to people. Rodents and other small mammals – not monkeys – are thought to be the most likely reservoir. The virus typically spreads from person to person through close contact with skin or respiratory secretions or contact with contaminated fomites. Typical infection begins with fever, lymphadenopathy, and flulike symptoms that include headache and malaise. One to four days after the onset of fever, the characteristic rash begins as macular lesions that evolve into papules, then vesicles, and finally pustules. Pustular lesions are deep-seated, well circumscribed, and are usually the same size and in the same stage of development on a given body site. The rash often starts on the face or the mouth, and then moves to the extremities, including the palms and soles. Over time, the lesions umbilicate and ultimately crust over.

On May 20, the Centers for Disease Control and Prevention issued a Health Advisory describing a case of monkeypox in a patient in Massachusetts. A single case normally wouldn’t cause too much alarm. In fact, there were two cases reported in the United States in 2021, both in travelers returning to the United States from Nigeria, a country in which the virus is endemic. No transmissions from these individuals to close contacts were identified.

The Massachusetts case was remarkable for two reasons. It occurred in an individual who had recently returned from a trip to Canada, which is not a country in which the virus is endemic. Additionally, it occurred in the context of a global outbreak of monkey pox that has, to date, disproportionately affected individuals who identify as men who have sex with men. Patients have often lacked the characteristic prodrome and many have had rash localized to the perianal and genital area, with or without symptoms of proctitis (anorectal pain, tenesmus, and bleeding). Clinically, some lesions mimicked sexually transmitted infections that the occur in the anogenital area, including herpes, syphilis, and lymphogranuloma venereum.

As of May 31, 2022, 17 persons in nine states had been diagnosed with presumed monkeypox virus infection. They ranged in age from 28 to 61 years and 16/17 identified as MSM. Fourteen reported international travel in the 3 weeks before developing symptoms. As of June 12, that number had grown to 53, while worldwide the number of confirmed and suspected cases reached 1,584. Up-to-date case counts are available at https://ourworldindata.org/monkeypox.

Back on the phone, my colleague laughed a little nervously. “I guess I’m not really worried about monkeypox in my patient.” She paused and then asked, “This isn’t going to be the next pandemic, is it?”

Public health experts at the Centers for Disease Control and Prevention and the World Health Organization have been reassuring in that regard. Two vaccines are available for the prevention of monkeypox. JYNNEOS is a nonreplicating live viral vaccine licensed as a two-dose series to prevent both monkeypox and smallpox. ACAM 2000 is a live Vaccinia virus preparation licensed to prevent smallpox. These vaccines are effective when given before exposure but are thought to also beneficial when given as postexposure prophylaxis. According to the CDC, vaccination within 4 days of exposure can prevent the development of disease. Vaccination within 14 days of exposure may not prevent the development of disease but may lessen symptoms. Treatment is generally supportive but antiviral therapy could be considered for individuals with severe disease. Tecovirmat is Food and Drug Administration approved for the treatment of smallpox but is available under nonresearch Expanded Access Investigational New Drug (EA-IND) protocol for the treatment of children and adults with severe orthopox infections, including monkeypox.

So, what’s a pediatrician to do? Take a good travel history, as my colleague did, because that is good medicine. At this point in an outbreak though, a lack of travel does not exclude the diagnosis. Perform a thorough exam of skin and mucosal areas. When there are rashes in the genital or perianal area, consider the possibility of monkeypox in addition to typical sexually transmitted infections. Ask about exposure to other persons with similar rashes, as well as close or intimate contact with a persons in a social network experiencing monkeypox infections. This includes MSM who meet partners through an online website, app, or at social events. Monkeypox can also be spread through contact with an animal (dead or alive) that is an African endemic species or use of a product derived from such animals. Public health experts encourage clinicians to be alert for rash illnesses consistent with monkeypox, regardless of a patient’s gender or sexual orientation, history of international travel, or specific risk factors.

Pediatricians see many kids with rashes, and while cases of monkeypox climb daily, the disease is still very rare. Given the media coverage of the outbreak, pediatricians should be prepared for questions from patients and their parents. Clinicians who suspect a case of monkeypox should contact their local or state health department for guidance and the need for testing. Tips for recognizing monkeypox and distinguishing it from more common viral illnesses such as chicken pox are available at www.cdc.gov/poxvirus/monkeypox/clinicians/clinical-recognition.html.

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville (Ky.) and Norton Children’s Hospital, also in Louisville. She said she had no relevant financial disclosures. Email her at [email protected].

Not long ago, a pediatrician working in a local urgent care clinic called me about a teenage girl with a pruritic rash. She described vesicles and pustules located primarily on the face and arms with no surrounding cellulitis or other exam findings.

“She probably has impetigo,” my colleague said. “But I took a travel and exposure history and learned that her grandma had recently returned home from visiting family in the Congo. Do you think I need to worry about monkeypox?”

While most pediatricians in the United States have never seen a case of monkeypox, the virus is not new. An orthopox, it belongs to the same genus that includes smallpox and cowpox viruses. It was discovered in 1958 when two colonies of monkeys kept for research developed pox-like rashes. The earliest human case was reported in 1970 in the Democratic Republic of Congo and now the virus is endemic in some counties in Central and West Africa.

Monkeypox virus is a zoonotic disease – it can spread from animals to people. Rodents and other small mammals – not monkeys – are thought to be the most likely reservoir. The virus typically spreads from person to person through close contact with skin or respiratory secretions or contact with contaminated fomites. Typical infection begins with fever, lymphadenopathy, and flulike symptoms that include headache and malaise. One to four days after the onset of fever, the characteristic rash begins as macular lesions that evolve into papules, then vesicles, and finally pustules. Pustular lesions are deep-seated, well circumscribed, and are usually the same size and in the same stage of development on a given body site. The rash often starts on the face or the mouth, and then moves to the extremities, including the palms and soles. Over time, the lesions umbilicate and ultimately crust over.

On May 20, the Centers for Disease Control and Prevention issued a Health Advisory describing a case of monkeypox in a patient in Massachusetts. A single case normally wouldn’t cause too much alarm. In fact, there were two cases reported in the United States in 2021, both in travelers returning to the United States from Nigeria, a country in which the virus is endemic. No transmissions from these individuals to close contacts were identified.

The Massachusetts case was remarkable for two reasons. It occurred in an individual who had recently returned from a trip to Canada, which is not a country in which the virus is endemic. Additionally, it occurred in the context of a global outbreak of monkey pox that has, to date, disproportionately affected individuals who identify as men who have sex with men. Patients have often lacked the characteristic prodrome and many have had rash localized to the perianal and genital area, with or without symptoms of proctitis (anorectal pain, tenesmus, and bleeding). Clinically, some lesions mimicked sexually transmitted infections that the occur in the anogenital area, including herpes, syphilis, and lymphogranuloma venereum.

As of May 31, 2022, 17 persons in nine states had been diagnosed with presumed monkeypox virus infection. They ranged in age from 28 to 61 years and 16/17 identified as MSM. Fourteen reported international travel in the 3 weeks before developing symptoms. As of June 12, that number had grown to 53, while worldwide the number of confirmed and suspected cases reached 1,584. Up-to-date case counts are available at https://ourworldindata.org/monkeypox.

Back on the phone, my colleague laughed a little nervously. “I guess I’m not really worried about monkeypox in my patient.” She paused and then asked, “This isn’t going to be the next pandemic, is it?”

Public health experts at the Centers for Disease Control and Prevention and the World Health Organization have been reassuring in that regard. Two vaccines are available for the prevention of monkeypox. JYNNEOS is a nonreplicating live viral vaccine licensed as a two-dose series to prevent both monkeypox and smallpox. ACAM 2000 is a live Vaccinia virus preparation licensed to prevent smallpox. These vaccines are effective when given before exposure but are thought to also beneficial when given as postexposure prophylaxis. According to the CDC, vaccination within 4 days of exposure can prevent the development of disease. Vaccination within 14 days of exposure may not prevent the development of disease but may lessen symptoms. Treatment is generally supportive but antiviral therapy could be considered for individuals with severe disease. Tecovirmat is Food and Drug Administration approved for the treatment of smallpox but is available under nonresearch Expanded Access Investigational New Drug (EA-IND) protocol for the treatment of children and adults with severe orthopox infections, including monkeypox.

So, what’s a pediatrician to do? Take a good travel history, as my colleague did, because that is good medicine. At this point in an outbreak though, a lack of travel does not exclude the diagnosis. Perform a thorough exam of skin and mucosal areas. When there are rashes in the genital or perianal area, consider the possibility of monkeypox in addition to typical sexually transmitted infections. Ask about exposure to other persons with similar rashes, as well as close or intimate contact with a persons in a social network experiencing monkeypox infections. This includes MSM who meet partners through an online website, app, or at social events. Monkeypox can also be spread through contact with an animal (dead or alive) that is an African endemic species or use of a product derived from such animals. Public health experts encourage clinicians to be alert for rash illnesses consistent with monkeypox, regardless of a patient’s gender or sexual orientation, history of international travel, or specific risk factors.

Pediatricians see many kids with rashes, and while cases of monkeypox climb daily, the disease is still very rare. Given the media coverage of the outbreak, pediatricians should be prepared for questions from patients and their parents. Clinicians who suspect a case of monkeypox should contact their local or state health department for guidance and the need for testing. Tips for recognizing monkeypox and distinguishing it from more common viral illnesses such as chicken pox are available at www.cdc.gov/poxvirus/monkeypox/clinicians/clinical-recognition.html.

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville (Ky.) and Norton Children’s Hospital, also in Louisville. She said she had no relevant financial disclosures. Email her at [email protected].

Not long ago, a pediatrician working in a local urgent care clinic called me about a teenage girl with a pruritic rash. She described vesicles and pustules located primarily on the face and arms with no surrounding cellulitis or other exam findings.

“She probably has impetigo,” my colleague said. “But I took a travel and exposure history and learned that her grandma had recently returned home from visiting family in the Congo. Do you think I need to worry about monkeypox?”

While most pediatricians in the United States have never seen a case of monkeypox, the virus is not new. An orthopox, it belongs to the same genus that includes smallpox and cowpox viruses. It was discovered in 1958 when two colonies of monkeys kept for research developed pox-like rashes. The earliest human case was reported in 1970 in the Democratic Republic of Congo and now the virus is endemic in some counties in Central and West Africa.

Monkeypox virus is a zoonotic disease – it can spread from animals to people. Rodents and other small mammals – not monkeys – are thought to be the most likely reservoir. The virus typically spreads from person to person through close contact with skin or respiratory secretions or contact with contaminated fomites. Typical infection begins with fever, lymphadenopathy, and flulike symptoms that include headache and malaise. One to four days after the onset of fever, the characteristic rash begins as macular lesions that evolve into papules, then vesicles, and finally pustules. Pustular lesions are deep-seated, well circumscribed, and are usually the same size and in the same stage of development on a given body site. The rash often starts on the face or the mouth, and then moves to the extremities, including the palms and soles. Over time, the lesions umbilicate and ultimately crust over.

On May 20, the Centers for Disease Control and Prevention issued a Health Advisory describing a case of monkeypox in a patient in Massachusetts. A single case normally wouldn’t cause too much alarm. In fact, there were two cases reported in the United States in 2021, both in travelers returning to the United States from Nigeria, a country in which the virus is endemic. No transmissions from these individuals to close contacts were identified.

The Massachusetts case was remarkable for two reasons. It occurred in an individual who had recently returned from a trip to Canada, which is not a country in which the virus is endemic. Additionally, it occurred in the context of a global outbreak of monkey pox that has, to date, disproportionately affected individuals who identify as men who have sex with men. Patients have often lacked the characteristic prodrome and many have had rash localized to the perianal and genital area, with or without symptoms of proctitis (anorectal pain, tenesmus, and bleeding). Clinically, some lesions mimicked sexually transmitted infections that the occur in the anogenital area, including herpes, syphilis, and lymphogranuloma venereum.

As of May 31, 2022, 17 persons in nine states had been diagnosed with presumed monkeypox virus infection. They ranged in age from 28 to 61 years and 16/17 identified as MSM. Fourteen reported international travel in the 3 weeks before developing symptoms. As of June 12, that number had grown to 53, while worldwide the number of confirmed and suspected cases reached 1,584. Up-to-date case counts are available at https://ourworldindata.org/monkeypox.

Back on the phone, my colleague laughed a little nervously. “I guess I’m not really worried about monkeypox in my patient.” She paused and then asked, “This isn’t going to be the next pandemic, is it?”

Public health experts at the Centers for Disease Control and Prevention and the World Health Organization have been reassuring in that regard. Two vaccines are available for the prevention of monkeypox. JYNNEOS is a nonreplicating live viral vaccine licensed as a two-dose series to prevent both monkeypox and smallpox. ACAM 2000 is a live Vaccinia virus preparation licensed to prevent smallpox. These vaccines are effective when given before exposure but are thought to also beneficial when given as postexposure prophylaxis. According to the CDC, vaccination within 4 days of exposure can prevent the development of disease. Vaccination within 14 days of exposure may not prevent the development of disease but may lessen symptoms. Treatment is generally supportive but antiviral therapy could be considered for individuals with severe disease. Tecovirmat is Food and Drug Administration approved for the treatment of smallpox but is available under nonresearch Expanded Access Investigational New Drug (EA-IND) protocol for the treatment of children and adults with severe orthopox infections, including monkeypox.

So, what’s a pediatrician to do? Take a good travel history, as my colleague did, because that is good medicine. At this point in an outbreak though, a lack of travel does not exclude the diagnosis. Perform a thorough exam of skin and mucosal areas. When there are rashes in the genital or perianal area, consider the possibility of monkeypox in addition to typical sexually transmitted infections. Ask about exposure to other persons with similar rashes, as well as close or intimate contact with a persons in a social network experiencing monkeypox infections. This includes MSM who meet partners through an online website, app, or at social events. Monkeypox can also be spread through contact with an animal (dead or alive) that is an African endemic species or use of a product derived from such animals. Public health experts encourage clinicians to be alert for rash illnesses consistent with monkeypox, regardless of a patient’s gender or sexual orientation, history of international travel, or specific risk factors.

Pediatricians see many kids with rashes, and while cases of monkeypox climb daily, the disease is still very rare. Given the media coverage of the outbreak, pediatricians should be prepared for questions from patients and their parents. Clinicians who suspect a case of monkeypox should contact their local or state health department for guidance and the need for testing. Tips for recognizing monkeypox and distinguishing it from more common viral illnesses such as chicken pox are available at www.cdc.gov/poxvirus/monkeypox/clinicians/clinical-recognition.html.

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville (Ky.) and Norton Children’s Hospital, also in Louisville. She said she had no relevant financial disclosures. Email her at [email protected].

The number of pediatric hepatitis cases has remained steady since 2017, new research from the Centers for Disease Control and Prevention suggests, despite the recent investigation into children with hepatitis of unknown cause. The study also found that there was no indication of elevated rates of adenovirus type 40/41 infection in children.

But Rohit Kohli, MBBS, MS, chief of the Division of Gastroenterology, Hepatology, and Nutrition at the Children’s Hospital Los Angeles, California, says that although the study is “well-designed and robust,” that does not mean that these hepatitis cases of unknown origin are no longer a concern. He was not involved with the CDC research. “As a clinician, I’m still worried,” he said. “Why I feel like this is not conclusive is that there are other data from entities like the United Kingdom Health Security Agency that are incongruent with [these findings],” he said.

The research was published in the CDC’s Morbidity and Mortality Weekly Report.

In November 2021, the Alabama Department of Public Health began an investigation with the CDC after a cluster of children were admitted to a children’s hospital in the state with severe hepatitis, who all tested positive for adenovirus. When the United Kingdom’s Health Security Agency announced an investigation into similar cases in early April 2022, the CDC decided to expand their search nationally.

Now, as of June 15, the agency is investigating 290 cases in 41 states and U.S. territories. Worldwide, 650 cases in 33 countries have been reported, according to the most recent update by the World Health Organization on May 27, 2022. At least 38 patients have needed liver transplants, and nine deaths have been reported to WHO.

In its most recent press call on the topic, the CDC announced that it’s aware of six deaths in the United States through May 20, 2022. The COVID-19 vaccine has been ruled out as a potential cause because the majority of affected children are unvaccinated or are too young to receive the vaccine. Adenovirus infection remains a leading suspect in these sick children because the virus has been detected in 60.8% of tested cases, WHO reports.

Investigators have detected an increase in reported pediatric hepatitis cases, compared with prior years in the United Kingdom, but it was not clear whether that same pattern would be found in the United States. Neither pediatric hepatitis nor adenovirus type 40/41 are reportable conditions in the United States. In the May 20 CDC press call, Umesh Parashar, MD, chief of the CDC’s Viral Gastroenteritis Branch, said that an estimated 1,500-2,000 children aged younger than 10 are hospitalized in the United States for hepatitis every year. “That’s a fairly large number,” he said, and it might make it difficult to detect a small increase in cases.

To better estimate trends in pediatric hepatitis and adenovirus infection in the United States, investigators collected available data on emergency department (ED) visits, hospitalizations, and liver transplants associated with hepatitis in children as well as adenovirus stool testing results. Researchers used four large databases: the National Syndromic Surveillance Program; the Premier Healthcare Database Special Release; the Organ Procurement and Transplant Network; and Labcorp, which is a large commercial lab network.

To account for changes in health care utilization in the first year of the COVID-19 pandemic, the team compared hepatitis-associated ED visits, hospitalizations, and liver transplants from October 2021 to March 2022 versus the same months (January to March and October to December) in 2017, 2018, and 2019. For adenovirus stool testing, results from October 2021 to March 2022 were compared with the same calendar months (October to March) from 2017-2018, 2018-2019, and 2019-2020, to help control for seasonality.

• Weekly ED visits with hepatitis-associated discharge codes
• Hepatitis-associated monthly hospitalizations in children aged 0-4 years (22 vs. 19.5; P = .26)
• Hepatitis-associated monthly hospitalization in children aged 5-11 years (12 vs. 10.5; P = .42)
• Monthly liver transplants (5 vs. 4; P = .19)
• Percentage of stool specimens positive for adenovirus types 40/41, though the number of specimens tested was highest in March 2022

The authors acknowledged that pediatric hepatitis is rare, so it may be difficult tease out small changes in the number of cases. Also, data on hospitalizations and liver transplants have a 2- to 3-month reporting delay, so the case counts for March 2022 “might be underreported,” they wrote. Mr. Kohli noted that because hepatitis and adenovirus are not reportable conditions, the analysis relied on retrospective data from insurance companies and electronic medical records. Retrospective data are inherently limited, compared with prospective analyses, he said, and it’s possible that certain cases could be included in more than one database and thus be double-counted, whereas other cases could be missed entirely.

These findings also conflict with data from the United Kingdom, which in May reported that the average number of hepatitis cases had increased, compared with previous years, he said. More data are needed, he said, and he is involved with a study with the North American Society for Pediatric Gastroenterology and the American Association for the Study of Liver Diseases that is also collecting data to try to understand whether there has been an uptick in pediatric hepatitis cases. The study will collect patient data directly from hospitals as well as include additional pathology data, such as biopsy results.

“We should not be inhibited to look further academically – and public health–wise – while we take into cognizance this very good, robust attempt from the CDC,” he said.

A version of this article first appeared on Medscape.com.

The number of pediatric hepatitis cases has remained steady since 2017, new research from the Centers for Disease Control and Prevention suggests, despite the recent investigation into children with hepatitis of unknown cause. The study also found that there was no indication of elevated rates of adenovirus type 40/41 infection in children.

But Rohit Kohli, MBBS, MS, chief of the Division of Gastroenterology, Hepatology, and Nutrition at the Children’s Hospital Los Angeles, California, says that although the study is “well-designed and robust,” that does not mean that these hepatitis cases of unknown origin are no longer a concern. He was not involved with the CDC research. “As a clinician, I’m still worried,” he said. “Why I feel like this is not conclusive is that there are other data from entities like the United Kingdom Health Security Agency that are incongruent with [these findings],” he said.

The research was published in the CDC’s Morbidity and Mortality Weekly Report.

In November 2021, the Alabama Department of Public Health began an investigation with the CDC after a cluster of children were admitted to a children’s hospital in the state with severe hepatitis, who all tested positive for adenovirus. When the United Kingdom’s Health Security Agency announced an investigation into similar cases in early April 2022, the CDC decided to expand their search nationally.

Now, as of June 15, the agency is investigating 290 cases in 41 states and U.S. territories. Worldwide, 650 cases in 33 countries have been reported, according to the most recent update by the World Health Organization on May 27, 2022. At least 38 patients have needed liver transplants, and nine deaths have been reported to WHO.

In its most recent press call on the topic, the CDC announced that it’s aware of six deaths in the United States through May 20, 2022. The COVID-19 vaccine has been ruled out as a potential cause because the majority of affected children are unvaccinated or are too young to receive the vaccine. Adenovirus infection remains a leading suspect in these sick children because the virus has been detected in 60.8% of tested cases, WHO reports.

Investigators have detected an increase in reported pediatric hepatitis cases, compared with prior years in the United Kingdom, but it was not clear whether that same pattern would be found in the United States. Neither pediatric hepatitis nor adenovirus type 40/41 are reportable conditions in the United States. In the May 20 CDC press call, Umesh Parashar, MD, chief of the CDC’s Viral Gastroenteritis Branch, said that an estimated 1,500-2,000 children aged younger than 10 are hospitalized in the United States for hepatitis every year. “That’s a fairly large number,” he said, and it might make it difficult to detect a small increase in cases.

To better estimate trends in pediatric hepatitis and adenovirus infection in the United States, investigators collected available data on emergency department (ED) visits, hospitalizations, and liver transplants associated with hepatitis in children as well as adenovirus stool testing results. Researchers used four large databases: the National Syndromic Surveillance Program; the Premier Healthcare Database Special Release; the Organ Procurement and Transplant Network; and Labcorp, which is a large commercial lab network.

To account for changes in health care utilization in the first year of the COVID-19 pandemic, the team compared hepatitis-associated ED visits, hospitalizations, and liver transplants from October 2021 to March 2022 versus the same months (January to March and October to December) in 2017, 2018, and 2019. For adenovirus stool testing, results from October 2021 to March 2022 were compared with the same calendar months (October to March) from 2017-2018, 2018-2019, and 2019-2020, to help control for seasonality.

• Weekly ED visits with hepatitis-associated discharge codes
• Hepatitis-associated monthly hospitalizations in children aged 0-4 years (22 vs. 19.5; P = .26)
• Hepatitis-associated monthly hospitalization in children aged 5-11 years (12 vs. 10.5; P = .42)
• Monthly liver transplants (5 vs. 4; P = .19)
• Percentage of stool specimens positive for adenovirus types 40/41, though the number of specimens tested was highest in March 2022

The authors acknowledged that pediatric hepatitis is rare, so it may be difficult tease out small changes in the number of cases. Also, data on hospitalizations and liver transplants have a 2- to 3-month reporting delay, so the case counts for March 2022 “might be underreported,” they wrote. Mr. Kohli noted that because hepatitis and adenovirus are not reportable conditions, the analysis relied on retrospective data from insurance companies and electronic medical records. Retrospective data are inherently limited, compared with prospective analyses, he said, and it’s possible that certain cases could be included in more than one database and thus be double-counted, whereas other cases could be missed entirely.

These findings also conflict with data from the United Kingdom, which in May reported that the average number of hepatitis cases had increased, compared with previous years, he said. More data are needed, he said, and he is involved with a study with the North American Society for Pediatric Gastroenterology and the American Association for the Study of Liver Diseases that is also collecting data to try to understand whether there has been an uptick in pediatric hepatitis cases. The study will collect patient data directly from hospitals as well as include additional pathology data, such as biopsy results.

“We should not be inhibited to look further academically – and public health–wise – while we take into cognizance this very good, robust attempt from the CDC,” he said.

A version of this article first appeared on Medscape.com.

The number of pediatric hepatitis cases has remained steady since 2017, new research from the Centers for Disease Control and Prevention suggests, despite the recent investigation into children with hepatitis of unknown cause. The study also found that there was no indication of elevated rates of adenovirus type 40/41 infection in children.

But Rohit Kohli, MBBS, MS, chief of the Division of Gastroenterology, Hepatology, and Nutrition at the Children’s Hospital Los Angeles, California, says that although the study is “well-designed and robust,” that does not mean that these hepatitis cases of unknown origin are no longer a concern. He was not involved with the CDC research. “As a clinician, I’m still worried,” he said. “Why I feel like this is not conclusive is that there are other data from entities like the United Kingdom Health Security Agency that are incongruent with [these findings],” he said.

The research was published in the CDC’s Morbidity and Mortality Weekly Report.

In November 2021, the Alabama Department of Public Health began an investigation with the CDC after a cluster of children were admitted to a children’s hospital in the state with severe hepatitis, who all tested positive for adenovirus. When the United Kingdom’s Health Security Agency announced an investigation into similar cases in early April 2022, the CDC decided to expand their search nationally.

Now, as of June 15, the agency is investigating 290 cases in 41 states and U.S. territories. Worldwide, 650 cases in 33 countries have been reported, according to the most recent update by the World Health Organization on May 27, 2022. At least 38 patients have needed liver transplants, and nine deaths have been reported to WHO.

In its most recent press call on the topic, the CDC announced that it’s aware of six deaths in the United States through May 20, 2022. The COVID-19 vaccine has been ruled out as a potential cause because the majority of affected children are unvaccinated or are too young to receive the vaccine. Adenovirus infection remains a leading suspect in these sick children because the virus has been detected in 60.8% of tested cases, WHO reports.

Investigators have detected an increase in reported pediatric hepatitis cases, compared with prior years in the United Kingdom, but it was not clear whether that same pattern would be found in the United States. Neither pediatric hepatitis nor adenovirus type 40/41 are reportable conditions in the United States. In the May 20 CDC press call, Umesh Parashar, MD, chief of the CDC’s Viral Gastroenteritis Branch, said that an estimated 1,500-2,000 children aged younger than 10 are hospitalized in the United States for hepatitis every year. “That’s a fairly large number,” he said, and it might make it difficult to detect a small increase in cases.

To better estimate trends in pediatric hepatitis and adenovirus infection in the United States, investigators collected available data on emergency department (ED) visits, hospitalizations, and liver transplants associated with hepatitis in children as well as adenovirus stool testing results. Researchers used four large databases: the National Syndromic Surveillance Program; the Premier Healthcare Database Special Release; the Organ Procurement and Transplant Network; and Labcorp, which is a large commercial lab network.

To account for changes in health care utilization in the first year of the COVID-19 pandemic, the team compared hepatitis-associated ED visits, hospitalizations, and liver transplants from October 2021 to March 2022 versus the same months (January to March and October to December) in 2017, 2018, and 2019. For adenovirus stool testing, results from October 2021 to March 2022 were compared with the same calendar months (October to March) from 2017-2018, 2018-2019, and 2019-2020, to help control for seasonality.

• Weekly ED visits with hepatitis-associated discharge codes
• Hepatitis-associated monthly hospitalizations in children aged 0-4 years (22 vs. 19.5; P = .26)
• Hepatitis-associated monthly hospitalization in children aged 5-11 years (12 vs. 10.5; P = .42)
• Monthly liver transplants (5 vs. 4; P = .19)
• Percentage of stool specimens positive for adenovirus types 40/41, though the number of specimens tested was highest in March 2022

The authors acknowledged that pediatric hepatitis is rare, so it may be difficult tease out small changes in the number of cases. Also, data on hospitalizations and liver transplants have a 2- to 3-month reporting delay, so the case counts for March 2022 “might be underreported,” they wrote. Mr. Kohli noted that because hepatitis and adenovirus are not reportable conditions, the analysis relied on retrospective data from insurance companies and electronic medical records. Retrospective data are inherently limited, compared with prospective analyses, he said, and it’s possible that certain cases could be included in more than one database and thus be double-counted, whereas other cases could be missed entirely.

These findings also conflict with data from the United Kingdom, which in May reported that the average number of hepatitis cases had increased, compared with previous years, he said. More data are needed, he said, and he is involved with a study with the North American Society for Pediatric Gastroenterology and the American Association for the Study of Liver Diseases that is also collecting data to try to understand whether there has been an uptick in pediatric hepatitis cases. The study will collect patient data directly from hospitals as well as include additional pathology data, such as biopsy results.

“We should not be inhibited to look further academically – and public health–wise – while we take into cognizance this very good, robust attempt from the CDC,” he said.

A version of this article first appeared on Medscape.com.

The World Health Organization has announced that it will rename the monkeypox virus after a group of scientists voiced concerns that the name is “discriminatory and stigmatizing.”

The virus has infected more than 1,600 people in 39 countries so far this year, the WHO said, including 32 countries where the virus isn’t typically detected.

“WHO is working with partners and experts from around the world on changing the name of monkeypox virus, its clades, and the disease it causes,” Tedros Adhanom Ghebreyesus, PhD, the WHO’s director-general, said during a press briefing.

“We will make announcements about the new names as soon as possible,” he said.

Last week, more than 30 international scientists urged the public health community to change the name of the virus. The scientists posted a letter on June 10, which included support from the Africa Centres for Disease Control and Prevention, noting that the name should change with the ongoing transmission among humans this year.

“The prevailing perception in the international media and scientific literature is that MPXV is endemic in people in some African countries. However, it is well established that nearly all MPXV outbreaks in Africa prior to the 2022 outbreak have been the result of spillover from animals and humans and only rarely have there been reports of sustained human-to-human transmissions,” they wrote.

“In the context of the current global outbreak, continued reference to, and nomenclature of this virus being African is not only inaccurate but is also discriminatory and stigmatizing,” they added.

As one example, they noted, news outlets have used images of African patients to depict the pox lesions, although most stories about the current outbreak have focused on the global north. The Foreign Press Association of Africa has urged the global media to stop using images of Black people to highlight the outbreak in Europe.

“Although the origin of the new global MPXV outbreak is still unknown, there is growing evidence that the most likely scenario is that cross-continent, cryptic human transmission has been ongoing for longer than previously thought,” they wrote.

The WHO has listed two known clades of the monkeypox virus in recent updates – “one identified in West Africa and one in the Congo Basin region.” The group of scientists wrote that this approach is “counter to the best practice of avoiding geographic locations in the nomenclature of diseases and disease groups.”

The scientists proposed a new classification that would name three clades in order of detection – 1, 2, and 3 – for the viral genomes detected in Central Africa, Western Africa, and the localized spillover events detected this year in global north countries. More genome sequencing could uncover additional clades, they noted.

Even within the most recent clade, there is already notable diversity among the genomes, the scientists said. Like the new naming convention adopted for the coronavirus pandemic, the nomenclature for human monkeypox could be donated as “A.1, A.2, A.1.1,” they wrote.

The largest current outbreak is in the United Kingdom, where health officials have detected 524 cases, according to the latest update from the U.K. Health Security Agency.

As of June 15, 72 cases have been reported in the United States, including 15 in California and 15 in New York, according to the latest Centers for Disease Control and Prevention data.

Also on June 15, the WHO published interim guidance on the use of smallpox vaccines for monkeypox. The WHO doesn’t recommend mass vaccination against monkeypox and said vaccines should be used on a case-by-case basis.

The WHO will convene an emergency meeting next week to determine whether the spread of the virus should be considered a global public health emergency.

“The global outbreak of monkeypox is clearly unusual and concerning,” Dr. Tedros said June 15. “It’s for that reason that I have decided to convene the emergency committee under the International Health Regulations next week to assess whether this outbreak represents a public health emergency of international concern.”

A version of this article first appeared on WebMD.com.

The World Health Organization has announced that it will rename the monkeypox virus after a group of scientists voiced concerns that the name is “discriminatory and stigmatizing.”

The virus has infected more than 1,600 people in 39 countries so far this year, the WHO said, including 32 countries where the virus isn’t typically detected.

“WHO is working with partners and experts from around the world on changing the name of monkeypox virus, its clades, and the disease it causes,” Tedros Adhanom Ghebreyesus, PhD, the WHO’s director-general, said during a press briefing.

“We will make announcements about the new names as soon as possible,” he said.

Last week, more than 30 international scientists urged the public health community to change the name of the virus. The scientists posted a letter on June 10, which included support from the Africa Centres for Disease Control and Prevention, noting that the name should change with the ongoing transmission among humans this year.

“The prevailing perception in the international media and scientific literature is that MPXV is endemic in people in some African countries. However, it is well established that nearly all MPXV outbreaks in Africa prior to the 2022 outbreak have been the result of spillover from animals and humans and only rarely have there been reports of sustained human-to-human transmissions,” they wrote.

“In the context of the current global outbreak, continued reference to, and nomenclature of this virus being African is not only inaccurate but is also discriminatory and stigmatizing,” they added.

As one example, they noted, news outlets have used images of African patients to depict the pox lesions, although most stories about the current outbreak have focused on the global north. The Foreign Press Association of Africa has urged the global media to stop using images of Black people to highlight the outbreak in Europe.

“Although the origin of the new global MPXV outbreak is still unknown, there is growing evidence that the most likely scenario is that cross-continent, cryptic human transmission has been ongoing for longer than previously thought,” they wrote.

The WHO has listed two known clades of the monkeypox virus in recent updates – “one identified in West Africa and one in the Congo Basin region.” The group of scientists wrote that this approach is “counter to the best practice of avoiding geographic locations in the nomenclature of diseases and disease groups.”

The scientists proposed a new classification that would name three clades in order of detection – 1, 2, and 3 – for the viral genomes detected in Central Africa, Western Africa, and the localized spillover events detected this year in global north countries. More genome sequencing could uncover additional clades, they noted.

Even within the most recent clade, there is already notable diversity among the genomes, the scientists said. Like the new naming convention adopted for the coronavirus pandemic, the nomenclature for human monkeypox could be donated as “A.1, A.2, A.1.1,” they wrote.

The largest current outbreak is in the United Kingdom, where health officials have detected 524 cases, according to the latest update from the U.K. Health Security Agency.

As of June 15, 72 cases have been reported in the United States, including 15 in California and 15 in New York, according to the latest Centers for Disease Control and Prevention data.

Also on June 15, the WHO published interim guidance on the use of smallpox vaccines for monkeypox. The WHO doesn’t recommend mass vaccination against monkeypox and said vaccines should be used on a case-by-case basis.

The WHO will convene an emergency meeting next week to determine whether the spread of the virus should be considered a global public health emergency.

“The global outbreak of monkeypox is clearly unusual and concerning,” Dr. Tedros said June 15. “It’s for that reason that I have decided to convene the emergency committee under the International Health Regulations next week to assess whether this outbreak represents a public health emergency of international concern.”

A version of this article first appeared on WebMD.com.

The World Health Organization has announced that it will rename the monkeypox virus after a group of scientists voiced concerns that the name is “discriminatory and stigmatizing.”

The virus has infected more than 1,600 people in 39 countries so far this year, the WHO said, including 32 countries where the virus isn’t typically detected.

“WHO is working with partners and experts from around the world on changing the name of monkeypox virus, its clades, and the disease it causes,” Tedros Adhanom Ghebreyesus, PhD, the WHO’s director-general, said during a press briefing.

“We will make announcements about the new names as soon as possible,” he said.

Last week, more than 30 international scientists urged the public health community to change the name of the virus. The scientists posted a letter on June 10, which included support from the Africa Centres for Disease Control and Prevention, noting that the name should change with the ongoing transmission among humans this year.

“The prevailing perception in the international media and scientific literature is that MPXV is endemic in people in some African countries. However, it is well established that nearly all MPXV outbreaks in Africa prior to the 2022 outbreak have been the result of spillover from animals and humans and only rarely have there been reports of sustained human-to-human transmissions,” they wrote.

“In the context of the current global outbreak, continued reference to, and nomenclature of this virus being African is not only inaccurate but is also discriminatory and stigmatizing,” they added.

As one example, they noted, news outlets have used images of African patients to depict the pox lesions, although most stories about the current outbreak have focused on the global north. The Foreign Press Association of Africa has urged the global media to stop using images of Black people to highlight the outbreak in Europe.

“Although the origin of the new global MPXV outbreak is still unknown, there is growing evidence that the most likely scenario is that cross-continent, cryptic human transmission has been ongoing for longer than previously thought,” they wrote.

The WHO has listed two known clades of the monkeypox virus in recent updates – “one identified in West Africa and one in the Congo Basin region.” The group of scientists wrote that this approach is “counter to the best practice of avoiding geographic locations in the nomenclature of diseases and disease groups.”

The scientists proposed a new classification that would name three clades in order of detection – 1, 2, and 3 – for the viral genomes detected in Central Africa, Western Africa, and the localized spillover events detected this year in global north countries. More genome sequencing could uncover additional clades, they noted.

Even within the most recent clade, there is already notable diversity among the genomes, the scientists said. Like the new naming convention adopted for the coronavirus pandemic, the nomenclature for human monkeypox could be donated as “A.1, A.2, A.1.1,” they wrote.

The largest current outbreak is in the United Kingdom, where health officials have detected 524 cases, according to the latest update from the U.K. Health Security Agency.

As of June 15, 72 cases have been reported in the United States, including 15 in California and 15 in New York, according to the latest Centers for Disease Control and Prevention data.

Also on June 15, the WHO published interim guidance on the use of smallpox vaccines for monkeypox. The WHO doesn’t recommend mass vaccination against monkeypox and said vaccines should be used on a case-by-case basis.

The WHO will convene an emergency meeting next week to determine whether the spread of the virus should be considered a global public health emergency.

“The global outbreak of monkeypox is clearly unusual and concerning,” Dr. Tedros said June 15. “It’s for that reason that I have decided to convene the emergency committee under the International Health Regulations next week to assess whether this outbreak represents a public health emergency of international concern.”

A version of this article first appeared on WebMD.com.

A small blood sample and 24 hours might be all that’s needed to find out how strong the immune system is against a first or repeat coronavirus infections.

Scientists created a test that indirectly measures T-cell response – an important, long-term component of immunity that can last long after antibody levels fall off – to a challenge by the virus in whole blood.

The test mimics what can be done in a formal laboratory now but avoids some complicated steps and specialized training for lab personnel. This test, researchers said, is faster, can scale up to test many more people, and can be adapted to detect viral mutations as they emerge in the future.

The study explaining how all this works was published online in Nature Biotechnology.

The test, called dqTACT, could help predict the likelihood of “breakthrough” infections in people who are fully vaccinated and could help determine how frequently people who are immunocompromised might need to be revaccinated, the authors noted.

Infection with the coronavirus and other viruses can trigger a one-two punch from the immunity system – a fast antibody response followed by longer-lasting cellular immunity, including T cells, which “remember” the virus. Cellular immunity can trigger a quick response if the same virus ever shows up again.

The new test adds synthetic viral peptides – strings of amino acids that make up proteins – from the coronavirus to a blood sample. If there is no T-cell reaction within 24 hours, the test is negative. If the peptides trigger T cells, the test can measure the strength of the immune response.

The researchers validated the new test against traditional laboratory testing in 91 people, about half of whom never had COVID-19 and another half who were infected and recovered. The results matched well.

They also found the test predicted immune strength up to 8 months following a second dose of COVID-19 vaccine. Furthermore, T-cell response was greater among people who received two doses of a vaccine versus others who received only one immunization.

Studies are ongoing and designed to meet authorization requirements as part of future licensing from the Food and Drug Administration.

A version of this article first appeared on WebMD.com.

A small blood sample and 24 hours might be all that’s needed to find out how strong the immune system is against a first or repeat coronavirus infections.

Scientists created a test that indirectly measures T-cell response – an important, long-term component of immunity that can last long after antibody levels fall off – to a challenge by the virus in whole blood.

The test mimics what can be done in a formal laboratory now but avoids some complicated steps and specialized training for lab personnel. This test, researchers said, is faster, can scale up to test many more people, and can be adapted to detect viral mutations as they emerge in the future.

The study explaining how all this works was published online in Nature Biotechnology.

The test, called dqTACT, could help predict the likelihood of “breakthrough” infections in people who are fully vaccinated and could help determine how frequently people who are immunocompromised might need to be revaccinated, the authors noted.

Infection with the coronavirus and other viruses can trigger a one-two punch from the immunity system – a fast antibody response followed by longer-lasting cellular immunity, including T cells, which “remember” the virus. Cellular immunity can trigger a quick response if the same virus ever shows up again.

The new test adds synthetic viral peptides – strings of amino acids that make up proteins – from the coronavirus to a blood sample. If there is no T-cell reaction within 24 hours, the test is negative. If the peptides trigger T cells, the test can measure the strength of the immune response.

The researchers validated the new test against traditional laboratory testing in 91 people, about half of whom never had COVID-19 and another half who were infected and recovered. The results matched well.

They also found the test predicted immune strength up to 8 months following a second dose of COVID-19 vaccine. Furthermore, T-cell response was greater among people who received two doses of a vaccine versus others who received only one immunization.

Studies are ongoing and designed to meet authorization requirements as part of future licensing from the Food and Drug Administration.

A version of this article first appeared on WebMD.com.

A small blood sample and 24 hours might be all that’s needed to find out how strong the immune system is against a first or repeat coronavirus infections.

Scientists created a test that indirectly measures T-cell response – an important, long-term component of immunity that can last long after antibody levels fall off – to a challenge by the virus in whole blood.

The test mimics what can be done in a formal laboratory now but avoids some complicated steps and specialized training for lab personnel. This test, researchers said, is faster, can scale up to test many more people, and can be adapted to detect viral mutations as they emerge in the future.

The study explaining how all this works was published online in Nature Biotechnology.

The test, called dqTACT, could help predict the likelihood of “breakthrough” infections in people who are fully vaccinated and could help determine how frequently people who are immunocompromised might need to be revaccinated, the authors noted.

Infection with the coronavirus and other viruses can trigger a one-two punch from the immunity system – a fast antibody response followed by longer-lasting cellular immunity, including T cells, which “remember” the virus. Cellular immunity can trigger a quick response if the same virus ever shows up again.

The new test adds synthetic viral peptides – strings of amino acids that make up proteins – from the coronavirus to a blood sample. If there is no T-cell reaction within 24 hours, the test is negative. If the peptides trigger T cells, the test can measure the strength of the immune response.

The researchers validated the new test against traditional laboratory testing in 91 people, about half of whom never had COVID-19 and another half who were infected and recovered. The results matched well.

They also found the test predicted immune strength up to 8 months following a second dose of COVID-19 vaccine. Furthermore, T-cell response was greater among people who received two doses of a vaccine versus others who received only one immunization.

Studies are ongoing and designed to meet authorization requirements as part of future licensing from the Food and Drug Administration.

A version of this article first appeared on WebMD.com.

Your gut microbiome will thank you later

A healthy gut seems like the new catch-all to better overall health these days. Nutrition and diet culture has us drinking kombucha and ginger tea and coffee, but what if we told you that going to happy hour might also help?

In a recent double-blind study published in the Journal of Agricultural and Food Chemistry, 19 men were divided into two groups and asked to drink 11 ounces of alcoholic lager (5.2% by volume) or nonalcoholic lager with dinner for 4 weeks.

Beer? Yes. Beer.

Engin Akyurt/Pixabay

We humans have trillions of microorganisms running rampant through our digestive tracts. When they’re happy, we have a lower chance of developing heart disease and diabetes. You know what else has millions of happy microorganisms from fermentation? Beer. It also has polyphenols that can help the body’s tissues fight cancers, as well as heart disease and inflammation. So beer is looking a little more healthy now, isn’t it?

In the study, the researchers found that both the alcoholic- and nonalcoholic-lager groups had a boost in bacterial diversity in the gut and higher fecal alkaline phosphatase levels, which showed improved intestinal health. They acknowledged, however, that the nonalcoholic route would be safer and healthier for overall health.

So add a lager to the list of gut-healthy foods that you should be consuming. It may give the phrase “beer gut” a whole new meaning.
 

We’ve lost our minds, but at least we know how fast they’re going

The phrase “quantum consciousness” sounds like something out of a particularly cheesy episode of Star Trek: “Oh no, Captain, the quantum consciousness has invaded our computer, and the only way to drive it out is to reverse the polarity of a focused tachyon beam.”

Massimiliano De Deo, LNGS-INFN

When it comes to understanding such basic existential issues as the origin of consciousness, however, quantum mechanics wasn’t off the table. The theory of the quantum origin of consciousness dates back to the 1990s (thanks in part to noted physician Roger Penrose), and goes something like this: There are microtubules within neurons in the brain that are small enough and isolated enough from the warm, wet, and chaotic brain environment where quantum effects can briefly come into play. We’re talking miniscule fractions of a second here, but still, long enough for quantum calculations to take place in the form of system wavefunction collapse, courtesy of gravity.

To plunge even deeper into the rabbit hole of quantum mechanics, the reason Schrödinger’s cat doesn’t occur in real life is wavefunction collapse; the more massive a quantum system is, the more likely it is to collapse into one state or another (alive or dead, in the cat’s case). The quantum origin of consciousness, or Orch OR theory, holds that human consciousness arises from electrical oscillations within the neuronal microtubules caused by the computations stemming from the collapse of small quantum systems.

That is an awful lot of overly simplified explanation, especially considering the study that just came out essentially disproved it. Oops. The research, published in Physics of Life Reviews, is pretty simple. The researchers went to a lab deep underground to avoid interference from cosmic rays, and sat around for months, observing a chunk of germanium for signs of spontaneous radiation, attributable to the same sort of wavefunction collapse that is supposedly occurring in our brains. They found nothing out of the ordinary, pretty definitively disproving most of Orch OR theory.

The researchers were unwilling to completely dismiss the idea (this is quantum mechanics, after all, uncertainty kind of goes with the territory), but it does seem like we’ll have to search elsewhere for sources of human consciousness. Personally, we’re big fans of the cymbal-playing monkey.
 

Missing links: A real fish story

Dear LOTME:

Ear’s a question that’s been keeping me up at night. Is the human middle ear the result of top-secret government experiments involving alien technology, Abraham Lincoln, and the Illuminati?

Restless in Roswell

Dear Restless:

The paleoanthropologic community has been sorting through this mystery for decades, and fossils discovered in China over the past 20 years finally provide a much less conspiratorially satisfying answer.

IVPP

For some time now, experts in the field have believed that the bones of the human middle ear evolved from the spiracular gill of a fish. The spiracle is a small hole behind each eye that opens to the mouth in some fishes and was used to breathe air in the earliest, most primitive species. But how did we get from spiracle to ear?

The missing links come in the form of the cranial anatomy of Shuyu, a 438-million-year-old, fingernail-sized skull of a jawless fish, and the 419-million-year-old fossil of a completely preserved fish with gill filaments in the first branchial chamber.

“These fossils provided the first anatomical and fossil evidence for a vertebrate spiracle originating from fish gills,” senior author Gai Zhikun, PhD, of the Institute of Vertebrate Paleontology and Paleoanthropology, Beijing, said in a written statement.

In many ways, it seems, we are fish: “Many important structures of human beings can be traced back to our fish ancestors, such as our teeth, jaws, middle ears, etc,” added Zhu Min, PhD, also of the institute.

So, Restless, the next time you hear the soothing sounds of an angry mob storming the Capitol or you chew on a slab, slice, or chunk of mutant, laboratory-produced chicken in your favorite fast-food restaurant, be sure to thank Shuyu.
 

Can you lend me an ear?

If you thought locusts were only a nuisance, think again. They have their uses. If you take a locust’s ear and put it inside a robot, the robot will be able to hear and receive signals. Who knew?

850977/Pixabay

Researchers from Tel Aviv University in Israel showed the robot’s hearing abilities by giving clap signals that told the robot what to do: One clap means go forward, two claps mean move back. What do you think the robot would do if it heard the clap break from Cha Cha Slide?

“Our task was to replace the robot’s electronic microphone with a dead insect’s ear, use the ear’s ability to detect the electrical signals from the environment, in this case vibrations in the air, and, using a special chip, convert the insect input to that of the robot,” Ben M. Maoz, PhD, said in a statement from the university.

And how does a dead locust ear work in a robot? Well, Dr. Maoz explained: “My laboratory has developed a special device – Ear-on-a-Chip – that allows the ear to be kept alive throughout the experiment by supplying oxygen and food to the organ while allowing the electrical signals to be taken out of the locust’s ear and amplified and transmitted to the robot.”

The research won’t stop at hearing, he said, as the other four senses also will be taken into consideration. This could help us sense dangers in the future, such as earthquakes or diseases. We said it before and we’ll say it again: We’re rooting for you, science!

Your gut microbiome will thank you later

A healthy gut seems like the new catch-all to better overall health these days. Nutrition and diet culture has us drinking kombucha and ginger tea and coffee, but what if we told you that going to happy hour might also help?

In a recent double-blind study published in the Journal of Agricultural and Food Chemistry, 19 men were divided into two groups and asked to drink 11 ounces of alcoholic lager (5.2% by volume) or nonalcoholic lager with dinner for 4 weeks.

Beer? Yes. Beer.

Engin Akyurt/Pixabay

We humans have trillions of microorganisms running rampant through our digestive tracts. When they’re happy, we have a lower chance of developing heart disease and diabetes. You know what else has millions of happy microorganisms from fermentation? Beer. It also has polyphenols that can help the body’s tissues fight cancers, as well as heart disease and inflammation. So beer is looking a little more healthy now, isn’t it?

In the study, the researchers found that both the alcoholic- and nonalcoholic-lager groups had a boost in bacterial diversity in the gut and higher fecal alkaline phosphatase levels, which showed improved intestinal health. They acknowledged, however, that the nonalcoholic route would be safer and healthier for overall health.

So add a lager to the list of gut-healthy foods that you should be consuming. It may give the phrase “beer gut” a whole new meaning.
 

We’ve lost our minds, but at least we know how fast they’re going

The phrase “quantum consciousness” sounds like something out of a particularly cheesy episode of Star Trek: “Oh no, Captain, the quantum consciousness has invaded our computer, and the only way to drive it out is to reverse the polarity of a focused tachyon beam.”

Massimiliano De Deo, LNGS-INFN

When it comes to understanding such basic existential issues as the origin of consciousness, however, quantum mechanics wasn’t off the table. The theory of the quantum origin of consciousness dates back to the 1990s (thanks in part to noted physician Roger Penrose), and goes something like this: There are microtubules within neurons in the brain that are small enough and isolated enough from the warm, wet, and chaotic brain environment where quantum effects can briefly come into play. We’re talking miniscule fractions of a second here, but still, long enough for quantum calculations to take place in the form of system wavefunction collapse, courtesy of gravity.

To plunge even deeper into the rabbit hole of quantum mechanics, the reason Schrödinger’s cat doesn’t occur in real life is wavefunction collapse; the more massive a quantum system is, the more likely it is to collapse into one state or another (alive or dead, in the cat’s case). The quantum origin of consciousness, or Orch OR theory, holds that human consciousness arises from electrical oscillations within the neuronal microtubules caused by the computations stemming from the collapse of small quantum systems.

That is an awful lot of overly simplified explanation, especially considering the study that just came out essentially disproved it. Oops. The research, published in Physics of Life Reviews, is pretty simple. The researchers went to a lab deep underground to avoid interference from cosmic rays, and sat around for months, observing a chunk of germanium for signs of spontaneous radiation, attributable to the same sort of wavefunction collapse that is supposedly occurring in our brains. They found nothing out of the ordinary, pretty definitively disproving most of Orch OR theory.

The researchers were unwilling to completely dismiss the idea (this is quantum mechanics, after all, uncertainty kind of goes with the territory), but it does seem like we’ll have to search elsewhere for sources of human consciousness. Personally, we’re big fans of the cymbal-playing monkey.
 

Missing links: A real fish story

Dear LOTME:

Ear’s a question that’s been keeping me up at night. Is the human middle ear the result of top-secret government experiments involving alien technology, Abraham Lincoln, and the Illuminati?

Restless in Roswell

Dear Restless:

The paleoanthropologic community has been sorting through this mystery for decades, and fossils discovered in China over the past 20 years finally provide a much less conspiratorially satisfying answer.

IVPP

For some time now, experts in the field have believed that the bones of the human middle ear evolved from the spiracular gill of a fish. The spiracle is a small hole behind each eye that opens to the mouth in some fishes and was used to breathe air in the earliest, most primitive species. But how did we get from spiracle to ear?

The missing links come in the form of the cranial anatomy of Shuyu, a 438-million-year-old, fingernail-sized skull of a jawless fish, and the 419-million-year-old fossil of a completely preserved fish with gill filaments in the first branchial chamber.

“These fossils provided the first anatomical and fossil evidence for a vertebrate spiracle originating from fish gills,” senior author Gai Zhikun, PhD, of the Institute of Vertebrate Paleontology and Paleoanthropology, Beijing, said in a written statement.

In many ways, it seems, we are fish: “Many important structures of human beings can be traced back to our fish ancestors, such as our teeth, jaws, middle ears, etc,” added Zhu Min, PhD, also of the institute.

So, Restless, the next time you hear the soothing sounds of an angry mob storming the Capitol or you chew on a slab, slice, or chunk of mutant, laboratory-produced chicken in your favorite fast-food restaurant, be sure to thank Shuyu.
 

Can you lend me an ear?

If you thought locusts were only a nuisance, think again. They have their uses. If you take a locust’s ear and put it inside a robot, the robot will be able to hear and receive signals. Who knew?

850977/Pixabay

Researchers from Tel Aviv University in Israel showed the robot’s hearing abilities by giving clap signals that told the robot what to do: One clap means go forward, two claps mean move back. What do you think the robot would do if it heard the clap break from Cha Cha Slide?

“Our task was to replace the robot’s electronic microphone with a dead insect’s ear, use the ear’s ability to detect the electrical signals from the environment, in this case vibrations in the air, and, using a special chip, convert the insect input to that of the robot,” Ben M. Maoz, PhD, said in a statement from the university.

And how does a dead locust ear work in a robot? Well, Dr. Maoz explained: “My laboratory has developed a special device – Ear-on-a-Chip – that allows the ear to be kept alive throughout the experiment by supplying oxygen and food to the organ while allowing the electrical signals to be taken out of the locust’s ear and amplified and transmitted to the robot.”

The research won’t stop at hearing, he said, as the other four senses also will be taken into consideration. This could help us sense dangers in the future, such as earthquakes or diseases. We said it before and we’ll say it again: We’re rooting for you, science!

Your gut microbiome will thank you later

A healthy gut seems like the new catch-all to better overall health these days. Nutrition and diet culture has us drinking kombucha and ginger tea and coffee, but what if we told you that going to happy hour might also help?

In a recent double-blind study published in the Journal of Agricultural and Food Chemistry, 19 men were divided into two groups and asked to drink 11 ounces of alcoholic lager (5.2% by volume) or nonalcoholic lager with dinner for 4 weeks.

Beer? Yes. Beer.

Engin Akyurt/Pixabay

We humans have trillions of microorganisms running rampant through our digestive tracts. When they’re happy, we have a lower chance of developing heart disease and diabetes. You know what else has millions of happy microorganisms from fermentation? Beer. It also has polyphenols that can help the body’s tissues fight cancers, as well as heart disease and inflammation. So beer is looking a little more healthy now, isn’t it?

In the study, the researchers found that both the alcoholic- and nonalcoholic-lager groups had a boost in bacterial diversity in the gut and higher fecal alkaline phosphatase levels, which showed improved intestinal health. They acknowledged, however, that the nonalcoholic route would be safer and healthier for overall health.

So add a lager to the list of gut-healthy foods that you should be consuming. It may give the phrase “beer gut” a whole new meaning.
 

We’ve lost our minds, but at least we know how fast they’re going

The phrase “quantum consciousness” sounds like something out of a particularly cheesy episode of Star Trek: “Oh no, Captain, the quantum consciousness has invaded our computer, and the only way to drive it out is to reverse the polarity of a focused tachyon beam.”

Massimiliano De Deo, LNGS-INFN

When it comes to understanding such basic existential issues as the origin of consciousness, however, quantum mechanics wasn’t off the table. The theory of the quantum origin of consciousness dates back to the 1990s (thanks in part to noted physician Roger Penrose), and goes something like this: There are microtubules within neurons in the brain that are small enough and isolated enough from the warm, wet, and chaotic brain environment where quantum effects can briefly come into play. We’re talking miniscule fractions of a second here, but still, long enough for quantum calculations to take place in the form of system wavefunction collapse, courtesy of gravity.

To plunge even deeper into the rabbit hole of quantum mechanics, the reason Schrödinger’s cat doesn’t occur in real life is wavefunction collapse; the more massive a quantum system is, the more likely it is to collapse into one state or another (alive or dead, in the cat’s case). The quantum origin of consciousness, or Orch OR theory, holds that human consciousness arises from electrical oscillations within the neuronal microtubules caused by the computations stemming from the collapse of small quantum systems.

That is an awful lot of overly simplified explanation, especially considering the study that just came out essentially disproved it. Oops. The research, published in Physics of Life Reviews, is pretty simple. The researchers went to a lab deep underground to avoid interference from cosmic rays, and sat around for months, observing a chunk of germanium for signs of spontaneous radiation, attributable to the same sort of wavefunction collapse that is supposedly occurring in our brains. They found nothing out of the ordinary, pretty definitively disproving most of Orch OR theory.

The researchers were unwilling to completely dismiss the idea (this is quantum mechanics, after all, uncertainty kind of goes with the territory), but it does seem like we’ll have to search elsewhere for sources of human consciousness. Personally, we’re big fans of the cymbal-playing monkey.
 

Missing links: A real fish story

Dear LOTME:

Ear’s a question that’s been keeping me up at night. Is the human middle ear the result of top-secret government experiments involving alien technology, Abraham Lincoln, and the Illuminati?

Restless in Roswell

Dear Restless:

The paleoanthropologic community has been sorting through this mystery for decades, and fossils discovered in China over the past 20 years finally provide a much less conspiratorially satisfying answer.

IVPP

For some time now, experts in the field have believed that the bones of the human middle ear evolved from the spiracular gill of a fish. The spiracle is a small hole behind each eye that opens to the mouth in some fishes and was used to breathe air in the earliest, most primitive species. But how did we get from spiracle to ear?

The missing links come in the form of the cranial anatomy of Shuyu, a 438-million-year-old, fingernail-sized skull of a jawless fish, and the 419-million-year-old fossil of a completely preserved fish with gill filaments in the first branchial chamber.

“These fossils provided the first anatomical and fossil evidence for a vertebrate spiracle originating from fish gills,” senior author Gai Zhikun, PhD, of the Institute of Vertebrate Paleontology and Paleoanthropology, Beijing, said in a written statement.

In many ways, it seems, we are fish: “Many important structures of human beings can be traced back to our fish ancestors, such as our teeth, jaws, middle ears, etc,” added Zhu Min, PhD, also of the institute.

So, Restless, the next time you hear the soothing sounds of an angry mob storming the Capitol or you chew on a slab, slice, or chunk of mutant, laboratory-produced chicken in your favorite fast-food restaurant, be sure to thank Shuyu.
 

Can you lend me an ear?

If you thought locusts were only a nuisance, think again. They have their uses. If you take a locust’s ear and put it inside a robot, the robot will be able to hear and receive signals. Who knew?

850977/Pixabay

Researchers from Tel Aviv University in Israel showed the robot’s hearing abilities by giving clap signals that told the robot what to do: One clap means go forward, two claps mean move back. What do you think the robot would do if it heard the clap break from Cha Cha Slide?

“Our task was to replace the robot’s electronic microphone with a dead insect’s ear, use the ear’s ability to detect the electrical signals from the environment, in this case vibrations in the air, and, using a special chip, convert the insect input to that of the robot,” Ben M. Maoz, PhD, said in a statement from the university.

And how does a dead locust ear work in a robot? Well, Dr. Maoz explained: “My laboratory has developed a special device – Ear-on-a-Chip – that allows the ear to be kept alive throughout the experiment by supplying oxygen and food to the organ while allowing the electrical signals to be taken out of the locust’s ear and amplified and transmitted to the robot.”

The research won’t stop at hearing, he said, as the other four senses also will be taken into consideration. This could help us sense dangers in the future, such as earthquakes or diseases. We said it before and we’ll say it again: We’re rooting for you, science!

Federal advisers to the U.S. Food and Drug Administration voted unanimously June 15 to recommend the use of the Moderna and Pfizer-BioNTech COVID-19 vaccines in infants and young children.

The Vaccines and Related Biological Products Advisory Committee (VRBPAC) of the FDA voted 21-0 to say that benefits of a two-dose series of Moderna’s mRNA vaccine outweigh risk for use in infants and children 6 months through 5 years of age.

The panel then voted 21-0 to say that benefits of a three-dose series of the Pfizer-BioNTech mRNA vaccine outweigh risk for use in infants and children 6 months through 4 years of age.

The FDA is not bound to follow the suggestions of its advisory committees, but it often does. Moderna and Pfizer are seeking to expand emergency use authorization (EUA) for their vaccines. EUAs are special clearances used to allow use of products in connection with public health crises such as the pandemic.

The Pfizer vaccine has standard, nonemergency FDA approval for use in people 16 years of age and older. The FDA also has granted EUA clearance for use of the shot in people ages 5 to 15.

The VRBPAC on June 15 recommended granting EUA clearance for Moderna’s COVID-19 vaccine for people ages 6 to 17. The Moderna vaccine already has full approval for use in people 18 years of age and older.

Many parents have been waiting for a clearance of COVID vaccines for their infants and young children, seeking protection for them at a time of continued spread of the virus.

The White House on June 9 outlined plans for making 10 million doses of COVID vaccines available for children under the age of 5 in the coming weeks.

The Centers for Disease Control and Prevention (CDC) has scheduled a June 18 meeting of its Advisory Committee on Immunization Practices, where members of that panel will vote on recommendations about use of the Moderna and Pfizer-BioNTech vaccines in infants and young children. The last step in the approval process to get shots into arms will be endorsement by the CDC director if the committee votes in favor of the vaccines.

For and against

During the public session during the June 15 FDA meeting, speakers offered varied opinions.

Some urged the panel to vote against the EUA expansion, citing concerns about risks of COVID vaccines in general.

But at the close of the meeting, top FDA vaccine official Peter Marks, MD, PhD, urged the public to be cautious about drawing conclusions from reading incident reports of side effects.

He said he has seen a “Twitter storm” during the day about claims of side effects. but stressed that the FDA has reported to the public on the rare side effects linked to the COVID vaccines, such as myocarditis, with advisories based on a review of reports of side effects. But many of these reports, gathered from the Vaccine Adverse Event Reporting System (VAERS) system, will turn out on further inspection not to be related to vaccination.

Many other speakers urged members of the panel to support expanded use of the vaccines for infants and young children. These speakers emphasized how lack of a vaccine to date has isolated young children who remain unprotected, even with about 83% of those age 5 and older in the United States having received at least one COVID shot.

Dr. Marks noted that there have been 442 deaths from COVID among children under 4 years of age during the pandemic, a number that he compared with the 78 deaths reported in the H1N1 flu. He urged the panel “to be careful that we don’t become numb to the number of pediatric deaths because of the overwhelming number of older deaths here.”

Panelist H. Cody Meissner, MD, a pediatric infectious disease specialist from Tufts University, said the vaccine should be made available -- particularly for children considered to be at high risk for complications from COVID --but health officials need to present a clear picture of the relatively low risks to children of harm from the vaccines-- and from COVID.

“That has to be communicated clearly to parents so that they can participate in the decision about vaccinating a child in this age group,” Dr. Meissner said.

The results presented June 15 from studies of the shots in younger children were less impressive than those from the initial COVID vaccine trials done in adults. This was not a surprise to panelists given the rise of the omicron variant and the evolution of the pandemic, but it still led to comments about the need for further continued study of the vaccines in young children even if they are authorized.

Consider that in 2020, Pfizer won the first EUA for a COVID vaccine of any kind with data that pegged the shot’s efficacy rate at 95%. Statisticians estimated a likely possible range, or 95% confidence interval, for the vaccine efficacy rate at 90.3% to 97.6%.

Those estimates were based on finding eight cases of COVID reported among 18,198 study participants who got the Pfizer-BioNTech shot, compared with 162 cases among the 18,325 people in the placebo group, according to the FDA review of Pifzer’s initial application.

Study data

But on June 15, FDA advisers had to consider an EUA application for which the data did not make as strong a case for the vaccine’s benefit among younger patients.

Pfizer presented what the FDA called a “preliminary descriptive analysis” of vaccine efficacy among participants in Study C4591007 who received three study vaccinations, following accrual of 10 total confirmed COVID-19 cases occurring at least 7 days after the third dose.

Looking at results for study participants ages 6 to 23 months of age, there was one case in the group that got the Pfizer-BioNTech shot and two in the placebo group, pegged as a 75.6% vaccine efficacy rate -- but one with caveats to the small numbers of cases. The 95% confidence interval for this vaccine efficacy rate was reported as-369.1% to 99.6% according to the FDA staff review.

For participants 2-4 years of age with and without evidence of prior SARS-CoV-

2 infection, there were two cases in the group that got the shot and five in the placebo group showing a vaccine efficacy rate of 82.4%, with a 95% confidence interval estimated ranging between -7.6% and 98.3%. For the combined analysis of both age groups, the efficacy rate was estimated at 80.4%, with a 95% confidence interval of 14.1% and 96.7%.

Doran Fink, MD, PhD, a top official in the FDA’s vaccines division, noted that the current EUA application for expanded pediatric use involved “some very preliminary” results that involved “a small number of cases and limited follow up time.”

But he stressed that the evidence gathered to date for the Pifzer application for use of its COVID shot in infants and young children met the threshold for conditional clearance during a crisis.

“We do feel very confident that the evidentiary standard for benefit for an EUA has been met here,” but added that more data would be needed to address questions about the efficacy of the vaccine beyond a third dose and whether an additional dose may be needed.

Pfizer also used a comparison known as “immunobridging” in support of the application. This looked at SARS- CoV-2 50% neutralizing antibody titers for the children in the age group covered by the EUA application and compared them to a randomly selected subset of 16-25-year-old participants in another study,

Key data for the pending Moderna EUA for use of its shot in infants and young children came from study P204. In it, Moderna found 51 cases of COVID among 1,511 children ages 6 months to 23 months who got the vaccines, versus 34 cases among 513 children who received a placebo, according to an FDA staff review.

That resulted in a vaccine efficacy rate pegged at 50.6%, with a 95% confidence interval of 21.4% to 68.6%.

Looking at the children ages 2 to 5 years in the P204 study, there were 119 cases out of 2,594 participants who got the shot, versus 61 cases of 858 in the placebo arm, or 7.1%. That translated to a 36.8% vaccine efficacy rate, with a confidence interval 12.5% to 54.0%.

Panelist Jay Portnoy, MD, of Children’s Mercy Hospital in Kansas City said all of the pediatricians he knows are waiting for the FDA to authorize the new uses of these vaccines in infants and young children.

“The death rate from COVID in young children may not be extremely high, but it’s absolutely terrifying to parents to have their child be sick, have to go to the hospital or even go to the emergency room or their primary care doctor because they’re sick and having trouble breathing,” said Dr. Portnoy, who served as the panel’s consumer representative.

A version of this article first appeared on WebMD.com.

This article was updated on 6/16/22.

Federal advisers to the U.S. Food and Drug Administration voted unanimously June 15 to recommend the use of the Moderna and Pfizer-BioNTech COVID-19 vaccines in infants and young children.

The Vaccines and Related Biological Products Advisory Committee (VRBPAC) of the FDA voted 21-0 to say that benefits of a two-dose series of Moderna’s mRNA vaccine outweigh risk for use in infants and children 6 months through 5 years of age.

The panel then voted 21-0 to say that benefits of a three-dose series of the Pfizer-BioNTech mRNA vaccine outweigh risk for use in infants and children 6 months through 4 years of age.

The FDA is not bound to follow the suggestions of its advisory committees, but it often does. Moderna and Pfizer are seeking to expand emergency use authorization (EUA) for their vaccines. EUAs are special clearances used to allow use of products in connection with public health crises such as the pandemic.

The Pfizer vaccine has standard, nonemergency FDA approval for use in people 16 years of age and older. The FDA also has granted EUA clearance for use of the shot in people ages 5 to 15.

The VRBPAC on June 15 recommended granting EUA clearance for Moderna’s COVID-19 vaccine for people ages 6 to 17. The Moderna vaccine already has full approval for use in people 18 years of age and older.

Many parents have been waiting for a clearance of COVID vaccines for their infants and young children, seeking protection for them at a time of continued spread of the virus.

The White House on June 9 outlined plans for making 10 million doses of COVID vaccines available for children under the age of 5 in the coming weeks.

The Centers for Disease Control and Prevention (CDC) has scheduled a June 18 meeting of its Advisory Committee on Immunization Practices, where members of that panel will vote on recommendations about use of the Moderna and Pfizer-BioNTech vaccines in infants and young children. The last step in the approval process to get shots into arms will be endorsement by the CDC director if the committee votes in favor of the vaccines.

For and against

During the public session during the June 15 FDA meeting, speakers offered varied opinions.

Some urged the panel to vote against the EUA expansion, citing concerns about risks of COVID vaccines in general.

But at the close of the meeting, top FDA vaccine official Peter Marks, MD, PhD, urged the public to be cautious about drawing conclusions from reading incident reports of side effects.

He said he has seen a “Twitter storm” during the day about claims of side effects. but stressed that the FDA has reported to the public on the rare side effects linked to the COVID vaccines, such as myocarditis, with advisories based on a review of reports of side effects. But many of these reports, gathered from the Vaccine Adverse Event Reporting System (VAERS) system, will turn out on further inspection not to be related to vaccination.

Many other speakers urged members of the panel to support expanded use of the vaccines for infants and young children. These speakers emphasized how lack of a vaccine to date has isolated young children who remain unprotected, even with about 83% of those age 5 and older in the United States having received at least one COVID shot.

Dr. Marks noted that there have been 442 deaths from COVID among children under 4 years of age during the pandemic, a number that he compared with the 78 deaths reported in the H1N1 flu. He urged the panel “to be careful that we don’t become numb to the number of pediatric deaths because of the overwhelming number of older deaths here.”

Panelist H. Cody Meissner, MD, a pediatric infectious disease specialist from Tufts University, said the vaccine should be made available -- particularly for children considered to be at high risk for complications from COVID --but health officials need to present a clear picture of the relatively low risks to children of harm from the vaccines-- and from COVID.

“That has to be communicated clearly to parents so that they can participate in the decision about vaccinating a child in this age group,” Dr. Meissner said.

The results presented June 15 from studies of the shots in younger children were less impressive than those from the initial COVID vaccine trials done in adults. This was not a surprise to panelists given the rise of the omicron variant and the evolution of the pandemic, but it still led to comments about the need for further continued study of the vaccines in young children even if they are authorized.

Consider that in 2020, Pfizer won the first EUA for a COVID vaccine of any kind with data that pegged the shot’s efficacy rate at 95%. Statisticians estimated a likely possible range, or 95% confidence interval, for the vaccine efficacy rate at 90.3% to 97.6%.

Those estimates were based on finding eight cases of COVID reported among 18,198 study participants who got the Pfizer-BioNTech shot, compared with 162 cases among the 18,325 people in the placebo group, according to the FDA review of Pifzer’s initial application.

Study data

But on June 15, FDA advisers had to consider an EUA application for which the data did not make as strong a case for the vaccine’s benefit among younger patients.

Pfizer presented what the FDA called a “preliminary descriptive analysis” of vaccine efficacy among participants in Study C4591007 who received three study vaccinations, following accrual of 10 total confirmed COVID-19 cases occurring at least 7 days after the third dose.

Looking at results for study participants ages 6 to 23 months of age, there was one case in the group that got the Pfizer-BioNTech shot and two in the placebo group, pegged as a 75.6% vaccine efficacy rate -- but one with caveats to the small numbers of cases. The 95% confidence interval for this vaccine efficacy rate was reported as-369.1% to 99.6% according to the FDA staff review.

For participants 2-4 years of age with and without evidence of prior SARS-CoV-

2 infection, there were two cases in the group that got the shot and five in the placebo group showing a vaccine efficacy rate of 82.4%, with a 95% confidence interval estimated ranging between -7.6% and 98.3%. For the combined analysis of both age groups, the efficacy rate was estimated at 80.4%, with a 95% confidence interval of 14.1% and 96.7%.

Doran Fink, MD, PhD, a top official in the FDA’s vaccines division, noted that the current EUA application for expanded pediatric use involved “some very preliminary” results that involved “a small number of cases and limited follow up time.”

But he stressed that the evidence gathered to date for the Pifzer application for use of its COVID shot in infants and young children met the threshold for conditional clearance during a crisis.

“We do feel very confident that the evidentiary standard for benefit for an EUA has been met here,” but added that more data would be needed to address questions about the efficacy of the vaccine beyond a third dose and whether an additional dose may be needed.

Pfizer also used a comparison known as “immunobridging” in support of the application. This looked at SARS- CoV-2 50% neutralizing antibody titers for the children in the age group covered by the EUA application and compared them to a randomly selected subset of 16-25-year-old participants in another study,

Key data for the pending Moderna EUA for use of its shot in infants and young children came from study P204. In it, Moderna found 51 cases of COVID among 1,511 children ages 6 months to 23 months who got the vaccines, versus 34 cases among 513 children who received a placebo, according to an FDA staff review.

That resulted in a vaccine efficacy rate pegged at 50.6%, with a 95% confidence interval of 21.4% to 68.6%.

Looking at the children ages 2 to 5 years in the P204 study, there were 119 cases out of 2,594 participants who got the shot, versus 61 cases of 858 in the placebo arm, or 7.1%. That translated to a 36.8% vaccine efficacy rate, with a confidence interval 12.5% to 54.0%.

Panelist Jay Portnoy, MD, of Children’s Mercy Hospital in Kansas City said all of the pediatricians he knows are waiting for the FDA to authorize the new uses of these vaccines in infants and young children.

“The death rate from COVID in young children may not be extremely high, but it’s absolutely terrifying to parents to have their child be sick, have to go to the hospital or even go to the emergency room or their primary care doctor because they’re sick and having trouble breathing,” said Dr. Portnoy, who served as the panel’s consumer representative.

A version of this article first appeared on WebMD.com.

This article was updated on 6/16/22.

Federal advisers to the U.S. Food and Drug Administration voted unanimously June 15 to recommend the use of the Moderna and Pfizer-BioNTech COVID-19 vaccines in infants and young children.

The Vaccines and Related Biological Products Advisory Committee (VRBPAC) of the FDA voted 21-0 to say that benefits of a two-dose series of Moderna’s mRNA vaccine outweigh risk for use in infants and children 6 months through 5 years of age.

The panel then voted 21-0 to say that benefits of a three-dose series of the Pfizer-BioNTech mRNA vaccine outweigh risk for use in infants and children 6 months through 4 years of age.

The FDA is not bound to follow the suggestions of its advisory committees, but it often does. Moderna and Pfizer are seeking to expand emergency use authorization (EUA) for their vaccines. EUAs are special clearances used to allow use of products in connection with public health crises such as the pandemic.

The Pfizer vaccine has standard, nonemergency FDA approval for use in people 16 years of age and older. The FDA also has granted EUA clearance for use of the shot in people ages 5 to 15.

The VRBPAC on June 15 recommended granting EUA clearance for Moderna’s COVID-19 vaccine for people ages 6 to 17. The Moderna vaccine already has full approval for use in people 18 years of age and older.

Many parents have been waiting for a clearance of COVID vaccines for their infants and young children, seeking protection for them at a time of continued spread of the virus.

The White House on June 9 outlined plans for making 10 million doses of COVID vaccines available for children under the age of 5 in the coming weeks.

The Centers for Disease Control and Prevention (CDC) has scheduled a June 18 meeting of its Advisory Committee on Immunization Practices, where members of that panel will vote on recommendations about use of the Moderna and Pfizer-BioNTech vaccines in infants and young children. The last step in the approval process to get shots into arms will be endorsement by the CDC director if the committee votes in favor of the vaccines.

For and against

During the public session during the June 15 FDA meeting, speakers offered varied opinions.

Some urged the panel to vote against the EUA expansion, citing concerns about risks of COVID vaccines in general.

But at the close of the meeting, top FDA vaccine official Peter Marks, MD, PhD, urged the public to be cautious about drawing conclusions from reading incident reports of side effects.

He said he has seen a “Twitter storm” during the day about claims of side effects. but stressed that the FDA has reported to the public on the rare side effects linked to the COVID vaccines, such as myocarditis, with advisories based on a review of reports of side effects. But many of these reports, gathered from the Vaccine Adverse Event Reporting System (VAERS) system, will turn out on further inspection not to be related to vaccination.

Many other speakers urged members of the panel to support expanded use of the vaccines for infants and young children. These speakers emphasized how lack of a vaccine to date has isolated young children who remain unprotected, even with about 83% of those age 5 and older in the United States having received at least one COVID shot.

Dr. Marks noted that there have been 442 deaths from COVID among children under 4 years of age during the pandemic, a number that he compared with the 78 deaths reported in the H1N1 flu. He urged the panel “to be careful that we don’t become numb to the number of pediatric deaths because of the overwhelming number of older deaths here.”

Panelist H. Cody Meissner, MD, a pediatric infectious disease specialist from Tufts University, said the vaccine should be made available -- particularly for children considered to be at high risk for complications from COVID --but health officials need to present a clear picture of the relatively low risks to children of harm from the vaccines-- and from COVID.

“That has to be communicated clearly to parents so that they can participate in the decision about vaccinating a child in this age group,” Dr. Meissner said.

The results presented June 15 from studies of the shots in younger children were less impressive than those from the initial COVID vaccine trials done in adults. This was not a surprise to panelists given the rise of the omicron variant and the evolution of the pandemic, but it still led to comments about the need for further continued study of the vaccines in young children even if they are authorized.

Consider that in 2020, Pfizer won the first EUA for a COVID vaccine of any kind with data that pegged the shot’s efficacy rate at 95%. Statisticians estimated a likely possible range, or 95% confidence interval, for the vaccine efficacy rate at 90.3% to 97.6%.

Those estimates were based on finding eight cases of COVID reported among 18,198 study participants who got the Pfizer-BioNTech shot, compared with 162 cases among the 18,325 people in the placebo group, according to the FDA review of Pifzer’s initial application.

Study data

But on June 15, FDA advisers had to consider an EUA application for which the data did not make as strong a case for the vaccine’s benefit among younger patients.

Pfizer presented what the FDA called a “preliminary descriptive analysis” of vaccine efficacy among participants in Study C4591007 who received three study vaccinations, following accrual of 10 total confirmed COVID-19 cases occurring at least 7 days after the third dose.

Looking at results for study participants ages 6 to 23 months of age, there was one case in the group that got the Pfizer-BioNTech shot and two in the placebo group, pegged as a 75.6% vaccine efficacy rate -- but one with caveats to the small numbers of cases. The 95% confidence interval for this vaccine efficacy rate was reported as-369.1% to 99.6% according to the FDA staff review.

For participants 2-4 years of age with and without evidence of prior SARS-CoV-

2 infection, there were two cases in the group that got the shot and five in the placebo group showing a vaccine efficacy rate of 82.4%, with a 95% confidence interval estimated ranging between -7.6% and 98.3%. For the combined analysis of both age groups, the efficacy rate was estimated at 80.4%, with a 95% confidence interval of 14.1% and 96.7%.

Doran Fink, MD, PhD, a top official in the FDA’s vaccines division, noted that the current EUA application for expanded pediatric use involved “some very preliminary” results that involved “a small number of cases and limited follow up time.”

But he stressed that the evidence gathered to date for the Pifzer application for use of its COVID shot in infants and young children met the threshold for conditional clearance during a crisis.

“We do feel very confident that the evidentiary standard for benefit for an EUA has been met here,” but added that more data would be needed to address questions about the efficacy of the vaccine beyond a third dose and whether an additional dose may be needed.

Pfizer also used a comparison known as “immunobridging” in support of the application. This looked at SARS- CoV-2 50% neutralizing antibody titers for the children in the age group covered by the EUA application and compared them to a randomly selected subset of 16-25-year-old participants in another study,

Key data for the pending Moderna EUA for use of its shot in infants and young children came from study P204. In it, Moderna found 51 cases of COVID among 1,511 children ages 6 months to 23 months who got the vaccines, versus 34 cases among 513 children who received a placebo, according to an FDA staff review.

That resulted in a vaccine efficacy rate pegged at 50.6%, with a 95% confidence interval of 21.4% to 68.6%.

Looking at the children ages 2 to 5 years in the P204 study, there were 119 cases out of 2,594 participants who got the shot, versus 61 cases of 858 in the placebo arm, or 7.1%. That translated to a 36.8% vaccine efficacy rate, with a confidence interval 12.5% to 54.0%.

Panelist Jay Portnoy, MD, of Children’s Mercy Hospital in Kansas City said all of the pediatricians he knows are waiting for the FDA to authorize the new uses of these vaccines in infants and young children.

“The death rate from COVID in young children may not be extremely high, but it’s absolutely terrifying to parents to have their child be sick, have to go to the hospital or even go to the emergency room or their primary care doctor because they’re sick and having trouble breathing,” said Dr. Portnoy, who served as the panel’s consumer representative.

A version of this article first appeared on WebMD.com.

This article was updated on 6/16/22.

A 32-year-old woman had sex with a man she met while on vacation 6 weeks ago. She was intoxicated at the time and does not know much about the person. She recalls having engaged in vaginal intercourse without a condom. She does not have any symptoms.

She previously received baseline lab testing per Centers for Disease Control and Prevention guidelines 2 years ago with a negative HIV test and negative hepatitis C test. She asks for testing for STIs. What would you recommend?

A. HIV, hepatitis C, gonorrhea, chlamydia, and human papillomavirus

B. HIV, hepatitis C, gonorrhea, chlamydia, and herpes simplex virus

C. HIV, hepatitis C, gonorrhea, and chlamydia

D. HIV, gonorrhea, and chlamydia

E. Gonorrhea and chlamydia

HIV risk estimate

The most practical answer is E, check for gonorrhea and chlamydia. Many protocols in place for evaluating people for STIs will test for hepatitis C as well as HIV with single exposures. In this column, we will look at the lack of evidence of heterosexual sexual transmission of hepatitis C.

In regards to HIV risk, the estimated risk of transmission male to female from an HIV-infected individual is 0.08% per sexual encounter.¹ The prevalence in the United States – where HIV occurs in about 0.5% of the adult population – was used to estimate the risk of a person with unknown HIV status acquiring HIV. The calculated risk from one sexual encounter would be 0.0004 (1 in 250,000).
 

Studies of hepatitis C transmission

Tahan and colleagues did a prospective study of 600 heterosexual couples where one partner had hepatitis C and the other didn’t. Over a mean of 3 years of follow-up, none of the seronegative spouses developed hepatitis C.²

Terrault and colleagues completed a cross-sectional study of hepatitis C virus (HCV)–positive individuals and their monogamous heterosexual partners to evaluate risk of sexual transmission of HCV.³ Based on 8,377 person-years of follow-up, the estimated maximum transmission rate was 0.07%/year, which was about 1/190,000 sexual contacts. No specific sexual practices were associated with transmission. The authors of this study concurred with CDC recommendations that persons with HCV infection in long-term monogamous relationships need not change their sexual practices.⁴

Vandelli and colleagues followed 776 heterosexual partners of HCV-infected individuals over 10 years.⁵ None of the couples reported condom use. Over the follow up period, three HCV infections occurred, but based on discordance of the typing of viral isolates, sexual transmission was excluded.

Jin and colleagues completed a systematic review of studies looking at possible sexual transmission of HCV in gay and bisexual men.⁶ HIV-positive men had a HCV incidence of 6.4 per 1,000 person-years, compared with 0.4 per 1000 person-years in HIV-negative men. The authors discussed several possible causes for increased transmission risk in HIV-infected individuals including coexisting STIs and higher HCV viral load in semen of HIV-infected individuals, as well as lower immunity.
 

Summary

In hepatitis C–discordant heterosexual couples, hepatitis C does not appear to be sexually transmitted.

The risk of sexual transmission of hepatitis C to non–HIV-infected individuals appears to be exceedingly low.

Many thanks to Hunter Handsfield, MD, for suggesting this topic and sharing supporting articles.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

1. Boily MC et al. Lancet Infect Dis. 2009 Feb;9(2):118-29.

2. Tahan V et al. Am J Gastroenterol. 2005;100:821-4.

3. Terrault NA et al. Hepatology. 2013;57:881-9

4. Centers for Disease Control and Prevention. MMWR Recomm Rep. 1998;47:1-38.

5. Vandelli C et al. Am J Gastroenterol. 2004;99:855-9.

6. Jin F et al. Sexual Health.2017;14:28-41.

A 32-year-old woman had sex with a man she met while on vacation 6 weeks ago. She was intoxicated at the time and does not know much about the person. She recalls having engaged in vaginal intercourse without a condom. She does not have any symptoms.

She previously received baseline lab testing per Centers for Disease Control and Prevention guidelines 2 years ago with a negative HIV test and negative hepatitis C test. She asks for testing for STIs. What would you recommend?

A. HIV, hepatitis C, gonorrhea, chlamydia, and human papillomavirus

B. HIV, hepatitis C, gonorrhea, chlamydia, and herpes simplex virus

C. HIV, hepatitis C, gonorrhea, and chlamydia

D. HIV, gonorrhea, and chlamydia

E. Gonorrhea and chlamydia

HIV risk estimate

The most practical answer is E, check for gonorrhea and chlamydia. Many protocols in place for evaluating people for STIs will test for hepatitis C as well as HIV with single exposures. In this column, we will look at the lack of evidence of heterosexual sexual transmission of hepatitis C.

In regards to HIV risk, the estimated risk of transmission male to female from an HIV-infected individual is 0.08% per sexual encounter.¹ The prevalence in the United States – where HIV occurs in about 0.5% of the adult population – was used to estimate the risk of a person with unknown HIV status acquiring HIV. The calculated risk from one sexual encounter would be 0.0004 (1 in 250,000).
 

Studies of hepatitis C transmission

Tahan and colleagues did a prospective study of 600 heterosexual couples where one partner had hepatitis C and the other didn’t. Over a mean of 3 years of follow-up, none of the seronegative spouses developed hepatitis C.²

Terrault and colleagues completed a cross-sectional study of hepatitis C virus (HCV)–positive individuals and their monogamous heterosexual partners to evaluate risk of sexual transmission of HCV.³ Based on 8,377 person-years of follow-up, the estimated maximum transmission rate was 0.07%/year, which was about 1/190,000 sexual contacts. No specific sexual practices were associated with transmission. The authors of this study concurred with CDC recommendations that persons with HCV infection in long-term monogamous relationships need not change their sexual practices.⁴

Vandelli and colleagues followed 776 heterosexual partners of HCV-infected individuals over 10 years.⁵ None of the couples reported condom use. Over the follow up period, three HCV infections occurred, but based on discordance of the typing of viral isolates, sexual transmission was excluded.

Jin and colleagues completed a systematic review of studies looking at possible sexual transmission of HCV in gay and bisexual men.⁶ HIV-positive men had a HCV incidence of 6.4 per 1,000 person-years, compared with 0.4 per 1000 person-years in HIV-negative men. The authors discussed several possible causes for increased transmission risk in HIV-infected individuals including coexisting STIs and higher HCV viral load in semen of HIV-infected individuals, as well as lower immunity.
 

Summary

In hepatitis C–discordant heterosexual couples, hepatitis C does not appear to be sexually transmitted.

The risk of sexual transmission of hepatitis C to non–HIV-infected individuals appears to be exceedingly low.

Many thanks to Hunter Handsfield, MD, for suggesting this topic and sharing supporting articles.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

1. Boily MC et al. Lancet Infect Dis. 2009 Feb;9(2):118-29.

2. Tahan V et al. Am J Gastroenterol. 2005;100:821-4.

3. Terrault NA et al. Hepatology. 2013;57:881-9

4. Centers for Disease Control and Prevention. MMWR Recomm Rep. 1998;47:1-38.

5. Vandelli C et al. Am J Gastroenterol. 2004;99:855-9.

6. Jin F et al. Sexual Health.2017;14:28-41.

A 32-year-old woman had sex with a man she met while on vacation 6 weeks ago. She was intoxicated at the time and does not know much about the person. She recalls having engaged in vaginal intercourse without a condom. She does not have any symptoms.

She previously received baseline lab testing per Centers for Disease Control and Prevention guidelines 2 years ago with a negative HIV test and negative hepatitis C test. She asks for testing for STIs. What would you recommend?

A. HIV, hepatitis C, gonorrhea, chlamydia, and human papillomavirus

B. HIV, hepatitis C, gonorrhea, chlamydia, and herpes simplex virus

C. HIV, hepatitis C, gonorrhea, and chlamydia

D. HIV, gonorrhea, and chlamydia

E. Gonorrhea and chlamydia

HIV risk estimate

The most practical answer is E, check for gonorrhea and chlamydia. Many protocols in place for evaluating people for STIs will test for hepatitis C as well as HIV with single exposures. In this column, we will look at the lack of evidence of heterosexual sexual transmission of hepatitis C.

In regards to HIV risk, the estimated risk of transmission male to female from an HIV-infected individual is 0.08% per sexual encounter.¹ The prevalence in the United States – where HIV occurs in about 0.5% of the adult population – was used to estimate the risk of a person with unknown HIV status acquiring HIV. The calculated risk from one sexual encounter would be 0.0004 (1 in 250,000).
 

Studies of hepatitis C transmission

Tahan and colleagues did a prospective study of 600 heterosexual couples where one partner had hepatitis C and the other didn’t. Over a mean of 3 years of follow-up, none of the seronegative spouses developed hepatitis C.²

Terrault and colleagues completed a cross-sectional study of hepatitis C virus (HCV)–positive individuals and their monogamous heterosexual partners to evaluate risk of sexual transmission of HCV.³ Based on 8,377 person-years of follow-up, the estimated maximum transmission rate was 0.07%/year, which was about 1/190,000 sexual contacts. No specific sexual practices were associated with transmission. The authors of this study concurred with CDC recommendations that persons with HCV infection in long-term monogamous relationships need not change their sexual practices.⁴

Vandelli and colleagues followed 776 heterosexual partners of HCV-infected individuals over 10 years.⁵ None of the couples reported condom use. Over the follow up period, three HCV infections occurred, but based on discordance of the typing of viral isolates, sexual transmission was excluded.

Jin and colleagues completed a systematic review of studies looking at possible sexual transmission of HCV in gay and bisexual men.⁶ HIV-positive men had a HCV incidence of 6.4 per 1,000 person-years, compared with 0.4 per 1000 person-years in HIV-negative men. The authors discussed several possible causes for increased transmission risk in HIV-infected individuals including coexisting STIs and higher HCV viral load in semen of HIV-infected individuals, as well as lower immunity.
 

Summary

In hepatitis C–discordant heterosexual couples, hepatitis C does not appear to be sexually transmitted.

The risk of sexual transmission of hepatitis C to non–HIV-infected individuals appears to be exceedingly low.

Many thanks to Hunter Handsfield, MD, for suggesting this topic and sharing supporting articles.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

1. Boily MC et al. Lancet Infect Dis. 2009 Feb;9(2):118-29.

2. Tahan V et al. Am J Gastroenterol. 2005;100:821-4.

3. Terrault NA et al. Hepatology. 2013;57:881-9

4. Centers for Disease Control and Prevention. MMWR Recomm Rep. 1998;47:1-38.

5. Vandelli C et al. Am J Gastroenterol. 2004;99:855-9.

6. Jin F et al. Sexual Health.2017;14:28-41.