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COVID-19 cases dropping in U.S., but variants threaten progress
COVID-19 cases are continuing to fall in the United States, according to the New York Times tracker, though the number of deaths from the disease again neared 4,000 on Feb. 3.
The United States has averaged 141,146 cases a day in the past week, down 30% from the average 2 weeks ago. For the first time since November 2020, the country is averaging fewer than 150,000 cases a day, according to the tracker.
“Although we have seen declines in cases and admissions and a recent slowing of deaths, cases remain extraordinarily high, still twice as high as the peak number of cases over the summer. And the continued proliferation of variants, variants that likely have increased transmissibility, that spread more easily, threatens to reverse these recent trends.
“Based on contact tracing of recent variant cases, not wearing masks and participating in in-person social gatherings have contributed to the variants’ spread,” she said at a White House COVID-19 briefing on Feb. 3, 2021.
The number of cases worldwide neared 104 million on Feb. 3 and the U.S. numbers made up 26.4 million of that total.
As of Feb. 4, COVID-19 had killed at least 454,000 people and infected about 26.6 million in the United States since January 2020, according to the Johns Hopkins University tracker.
The Johns Hopkins tracker found that, per capita, North Dakota, South Dakota, and Rhode Island have reported the most cases while New Jersey and New York have recorded the most deaths.
According to the COVID tracking project, hospitalizations for COVID-19 nationwide were down to 91,440 on Feb. 3.
The tracking report noted, “compared to last week, the number of people currently hospitalized with COVID-19 is down by 10% or more in 38 states.”
Even in hard-hit Los Angeles County, infections and case numbers are on the decline, according to the Los Angeles Times. However, officials, warn the numbers remain well above presurge levels. Over the past week, 201 city residents have died every day.
Reuters also reports that Anthony S. Fauci, MD, the government’s top infectious disease expert, said despite some good news in the numbers, Americans should continue to follow social distancing guidelines. He added that double-masking may add protection.
A version of this article first appeared on Medscape.com.
COVID-19 cases are continuing to fall in the United States, according to the New York Times tracker, though the number of deaths from the disease again neared 4,000 on Feb. 3.
The United States has averaged 141,146 cases a day in the past week, down 30% from the average 2 weeks ago. For the first time since November 2020, the country is averaging fewer than 150,000 cases a day, according to the tracker.
“Although we have seen declines in cases and admissions and a recent slowing of deaths, cases remain extraordinarily high, still twice as high as the peak number of cases over the summer. And the continued proliferation of variants, variants that likely have increased transmissibility, that spread more easily, threatens to reverse these recent trends.
“Based on contact tracing of recent variant cases, not wearing masks and participating in in-person social gatherings have contributed to the variants’ spread,” she said at a White House COVID-19 briefing on Feb. 3, 2021.
The number of cases worldwide neared 104 million on Feb. 3 and the U.S. numbers made up 26.4 million of that total.
As of Feb. 4, COVID-19 had killed at least 454,000 people and infected about 26.6 million in the United States since January 2020, according to the Johns Hopkins University tracker.
The Johns Hopkins tracker found that, per capita, North Dakota, South Dakota, and Rhode Island have reported the most cases while New Jersey and New York have recorded the most deaths.
According to the COVID tracking project, hospitalizations for COVID-19 nationwide were down to 91,440 on Feb. 3.
The tracking report noted, “compared to last week, the number of people currently hospitalized with COVID-19 is down by 10% or more in 38 states.”
Even in hard-hit Los Angeles County, infections and case numbers are on the decline, according to the Los Angeles Times. However, officials, warn the numbers remain well above presurge levels. Over the past week, 201 city residents have died every day.
Reuters also reports that Anthony S. Fauci, MD, the government’s top infectious disease expert, said despite some good news in the numbers, Americans should continue to follow social distancing guidelines. He added that double-masking may add protection.
A version of this article first appeared on Medscape.com.
COVID-19 cases are continuing to fall in the United States, according to the New York Times tracker, though the number of deaths from the disease again neared 4,000 on Feb. 3.
The United States has averaged 141,146 cases a day in the past week, down 30% from the average 2 weeks ago. For the first time since November 2020, the country is averaging fewer than 150,000 cases a day, according to the tracker.
“Although we have seen declines in cases and admissions and a recent slowing of deaths, cases remain extraordinarily high, still twice as high as the peak number of cases over the summer. And the continued proliferation of variants, variants that likely have increased transmissibility, that spread more easily, threatens to reverse these recent trends.
“Based on contact tracing of recent variant cases, not wearing masks and participating in in-person social gatherings have contributed to the variants’ spread,” she said at a White House COVID-19 briefing on Feb. 3, 2021.
The number of cases worldwide neared 104 million on Feb. 3 and the U.S. numbers made up 26.4 million of that total.
As of Feb. 4, COVID-19 had killed at least 454,000 people and infected about 26.6 million in the United States since January 2020, according to the Johns Hopkins University tracker.
The Johns Hopkins tracker found that, per capita, North Dakota, South Dakota, and Rhode Island have reported the most cases while New Jersey and New York have recorded the most deaths.
According to the COVID tracking project, hospitalizations for COVID-19 nationwide were down to 91,440 on Feb. 3.
The tracking report noted, “compared to last week, the number of people currently hospitalized with COVID-19 is down by 10% or more in 38 states.”
Even in hard-hit Los Angeles County, infections and case numbers are on the decline, according to the Los Angeles Times. However, officials, warn the numbers remain well above presurge levels. Over the past week, 201 city residents have died every day.
Reuters also reports that Anthony S. Fauci, MD, the government’s top infectious disease expert, said despite some good news in the numbers, Americans should continue to follow social distancing guidelines. He added that double-masking may add protection.
A version of this article first appeared on Medscape.com.
Investigating the Increase in Group A Streptococcus Among Indigenous Peoples
Invasive group A Streptococcus (iGAS) disease has been on the rise among indigenous populations around the world. Researchers from University of Alberta, Alberta Ministry of Health, both in Edmonton, and Alberta First Nations Information Governance Center in Alberta conducted a study to find out more. Between 2003 and 2017, they investigated iGAS cases among First Nations, Inuit, and Métis members in Alberta.
During that time, 669 cases of iGAS were reported. The incidence increased from 10 cases per 100,000 in 2003 to 52 cases per 100,000 in 2017—an incidence rate > 6 times that of non–First Nations populations. The researchers say the disproportionately high rates are seen in other Native American groups compared with the rates in the general population: One study, for instance, found the incidence rate for Alaska Natives was 13.7 cases per 100,000 compared with 3.9 cases per 100,000 for non–Alaska Natives.
What’s driving the higher rates isn’t completely clear, the researchers say. They note that risk factor data in their study “frequently” indicated nonsurgical wounds, addiction abuse, and homelessness. They also cite research that has found skin infections and skin breakdown are common among iGAS patients who were injection drug users or homeless. Diabetes mellitus—rampant among Native Americans—was another risk factor.
The researchers found a “striking difference” in that the First Nations members had more skin and soft tissue infections and, unexpectedly, fewer streptococcal toxic shock syndrome cases than did the non–First Nations groups.
Moreover, skin-to-skin transmission may be more common than respiratory transmission: When they grouped emm types (the bacteria are typed according to a protein encoded by the emm gene) by cluster, they found the bulk of disease among the First Nations population was associated with skin-related infections, not throat-related clusters. This may be a consequence of overcrowded households or inadequate housing, both issues for Native American communities. The researchers say emm59, the most prevalent emm type in the First Nations population in the study, displays a tropism for skin infections. Since 2006, they add, when a large outbreak of emm59 was reported, it has become common throughout western Canada and the US, where it had previously been relatively rare.
Of note, the researchers conclude, substantial emm differences could have potential implications for future vaccine.
Source: Tyrrell GJ, Bell B, Bill L, Fathima S. Increasing incidence of invasive group A Streptococcus Disease in First Nations population, Alberta, Canada, 2003-2017. Emerg Infect Dis. 2021;27(2):443-451. doi:doi:10.3201/eid2702.20194
Invasive group A Streptococcus (iGAS) disease has been on the rise among indigenous populations around the world. Researchers from University of Alberta, Alberta Ministry of Health, both in Edmonton, and Alberta First Nations Information Governance Center in Alberta conducted a study to find out more. Between 2003 and 2017, they investigated iGAS cases among First Nations, Inuit, and Métis members in Alberta.
During that time, 669 cases of iGAS were reported. The incidence increased from 10 cases per 100,000 in 2003 to 52 cases per 100,000 in 2017—an incidence rate > 6 times that of non–First Nations populations. The researchers say the disproportionately high rates are seen in other Native American groups compared with the rates in the general population: One study, for instance, found the incidence rate for Alaska Natives was 13.7 cases per 100,000 compared with 3.9 cases per 100,000 for non–Alaska Natives.
What’s driving the higher rates isn’t completely clear, the researchers say. They note that risk factor data in their study “frequently” indicated nonsurgical wounds, addiction abuse, and homelessness. They also cite research that has found skin infections and skin breakdown are common among iGAS patients who were injection drug users or homeless. Diabetes mellitus—rampant among Native Americans—was another risk factor.
The researchers found a “striking difference” in that the First Nations members had more skin and soft tissue infections and, unexpectedly, fewer streptococcal toxic shock syndrome cases than did the non–First Nations groups.
Moreover, skin-to-skin transmission may be more common than respiratory transmission: When they grouped emm types (the bacteria are typed according to a protein encoded by the emm gene) by cluster, they found the bulk of disease among the First Nations population was associated with skin-related infections, not throat-related clusters. This may be a consequence of overcrowded households or inadequate housing, both issues for Native American communities. The researchers say emm59, the most prevalent emm type in the First Nations population in the study, displays a tropism for skin infections. Since 2006, they add, when a large outbreak of emm59 was reported, it has become common throughout western Canada and the US, where it had previously been relatively rare.
Of note, the researchers conclude, substantial emm differences could have potential implications for future vaccine.
Source: Tyrrell GJ, Bell B, Bill L, Fathima S. Increasing incidence of invasive group A Streptococcus Disease in First Nations population, Alberta, Canada, 2003-2017. Emerg Infect Dis. 2021;27(2):443-451. doi:doi:10.3201/eid2702.20194
Invasive group A Streptococcus (iGAS) disease has been on the rise among indigenous populations around the world. Researchers from University of Alberta, Alberta Ministry of Health, both in Edmonton, and Alberta First Nations Information Governance Center in Alberta conducted a study to find out more. Between 2003 and 2017, they investigated iGAS cases among First Nations, Inuit, and Métis members in Alberta.
During that time, 669 cases of iGAS were reported. The incidence increased from 10 cases per 100,000 in 2003 to 52 cases per 100,000 in 2017—an incidence rate > 6 times that of non–First Nations populations. The researchers say the disproportionately high rates are seen in other Native American groups compared with the rates in the general population: One study, for instance, found the incidence rate for Alaska Natives was 13.7 cases per 100,000 compared with 3.9 cases per 100,000 for non–Alaska Natives.
What’s driving the higher rates isn’t completely clear, the researchers say. They note that risk factor data in their study “frequently” indicated nonsurgical wounds, addiction abuse, and homelessness. They also cite research that has found skin infections and skin breakdown are common among iGAS patients who were injection drug users or homeless. Diabetes mellitus—rampant among Native Americans—was another risk factor.
The researchers found a “striking difference” in that the First Nations members had more skin and soft tissue infections and, unexpectedly, fewer streptococcal toxic shock syndrome cases than did the non–First Nations groups.
Moreover, skin-to-skin transmission may be more common than respiratory transmission: When they grouped emm types (the bacteria are typed according to a protein encoded by the emm gene) by cluster, they found the bulk of disease among the First Nations population was associated with skin-related infections, not throat-related clusters. This may be a consequence of overcrowded households or inadequate housing, both issues for Native American communities. The researchers say emm59, the most prevalent emm type in the First Nations population in the study, displays a tropism for skin infections. Since 2006, they add, when a large outbreak of emm59 was reported, it has become common throughout western Canada and the US, where it had previously been relatively rare.
Of note, the researchers conclude, substantial emm differences could have potential implications for future vaccine.
Source: Tyrrell GJ, Bell B, Bill L, Fathima S. Increasing incidence of invasive group A Streptococcus Disease in First Nations population, Alberta, Canada, 2003-2017. Emerg Infect Dis. 2021;27(2):443-451. doi:doi:10.3201/eid2702.20194
COVID-19: Another study links colchicine to better results
The gout drug colchicine appears to lower the severity of COVID-19, a small new Brazilian study finds, adding to evidence that the familiar medication holds promise as a treatment for hospitalized patients.
Patients who received colchicine in this randomized, double-blinded, placebo-controlled clinical trial presented better evolution in terms of the need for supplemental oxygen and the length of hospitalisation. ... Colchicine was safe and well tolerated,” the study authors wrote in RMD Open. However, deaths were rare in the trial, they added, and it is impossible to “evaluate the capacity of colchicine to avoid admission to ICU and reduce mortality.”
The oral anti-inflammatory colchicine, widely used as treatment in rheumatic disease, was first approved in the United States 60 years ago. Researchers began to explore its potential as a COVID-19 treatment in the early months of the pandemic.
On Jan. 25, an international team of researchers reported in a press release – but not yet a published paper – that the drug seemed to reduce hospitalizations, mechanical ventilation, and deaths in the ColCORONA trial. Earlier, a much-smaller, randomized, open-label, Greek trial linked the drug to reduced time to clinical deterioration and hospital stay.
The Brazilian authors of the new study, led by Maria Isabel Lopes of the University of São Paulo’s Ribeirão Preto Medical School, randomly assigned 75 hospitalized patients with moderate to severe COVID-19 to colchicine or placebo. A total of 72 subjects completed the April-August 2020 trial: 36 received colchicine (typically 0.5 mg three times for 5 days, then 0.5 mg twice daily for 5 days; doses were adjusted in low-weight patients and those with chronic kidney disease). The other 36 received the placebo.
(In the United States, 0.6-mg tablets of generic colchicine cost as little as $1.90 each with free coupons, according to goodrx.com.)
The median age in the groups was similar (55 years); and the placebo group had more women (61% vs. 47% in the colchicine group, P = .34). All 72 patients received the same COVID-19 treatment at the time of the trial: azithromycin, hydroxychloroquine, and unfractionated heparin. Most patients, about two-thirds in both groups, also received methylprednisolone because they needed higher amounts of supplemental oxygen.
Patients in the colchicine group needed supplemental oxygen for less time: Their median time of need was 4.0 days (interquartile range [IQR], 2.0-6.0) vs. 6.5 days (IQR, 4.0-9.0) for the placebo group (P < .001). The median time for hospitalization was also lower at 7.0 days (IQR, 5.0–9.0) for the colchicine group vs. 9.0 (IQR, 7.0–12.0) for the placebo group (log rank test, 10.6; P = .001).
The researchers also reported the percentage of patients who needed supplemental oxygen at day 2 as 67% with colchicine vs. 86% with placebo, and at day 7 as 9% vs. 42% (log rank test, 10.6; P = .001). Two patients in the placebo group died, both from ventilator-associated pneumonia.
As for side effects, new or worsened diarrhea was reported more often in the colchicine group (17% vs. 6% with placebo), but the difference was not statistically significant (P = .26), and diarrhea was controlled via medication.
The researchers reported that limitations include the exclusion criteria and their inability to link colchicine to rates of ICU admissions and death.
The drug appears to help patients with COVID-19, the study authors wrote, by “inhibiting inflammasome, reducing neutrophil migration and activation, or preventing endothelial damage.”
A “well-conceived and well-designed” study
In an interview, NYU Langone Health rheumatologist Michael H. Pillinger, MD – an investigator with the ColCORONA trial – praised the Brazilian study. It “appears well-conceived and well-designed, and was enrolled at a rate that was greater than the sample size that was estimated to be needed based on power analysis,” he said.
The Brazilian study is small, he noted. (In contrast, the ColCORONA trial had 4,488 outpatient participants.) “This study differs from ColCORONA in several ways – the most important being that it is a study of inpatients with moderate to severe COVID (really mostly moderate),” he added. “ColCORONA is looking at a target audience that is much larger – outpatients with mild to moderate COVID with risk factors for hospitalization. Both questions are really important and certainly not mutually exclusive, since our care remains inadequate in both venues. This study also adds value in that several other studies have been conducted in hospital patients with enrollment criteria relatively similar to this one, and all showed benefit, but those were open-label or retrospective, and this is blinded and placebo-controlled.”
Using colchicine in patients with COVID-19
Should physicians turn to colchicine in patients with COVID-19? “I would rather that it still be used in the context of research until formal recommendations can be made by bodies like the NIH and CDC,” Dr. Pillinger said. “But certainly, there may be times when physicians feel compelled to treat patients off label.”
He cautioned, however, that colchicine should never be used with some other drugs. Its interaction with the antibiotic clarithromycin can be fatal, he noted. And, he said, the drug must be monitored in general since it can cause rare, severe problems.
“Overall, colchicine probably works on the overabundant inflammatory response to COVID, and it may be that it can be combined with other drugs that affect viral replication or promote immunity – e.g. vaccines,” Dr. Pillinger said. “So far, it seems as if there is no safety problem with combining colchicine with other approaches, but this has not been studied in a rigorous manner.”
Moving forward, he said, the drug’s very low price outside of the United States “could provide resource-poor countries with a way to help keep patients out of precious hospital beds – or help them go home sooner once admitted.” For now, however, “we need a large-scale inpatient study, and one is currently going on in Great Britain. We also need validation of the outpatient ColCORONA study, and studies to look at whether colchicine can work in conjunction with other strategies.”
The study was funded by grants from the São Paulo Research Foundation, Brazilian National Council for Scientific and Technological Development, and CAPES Foundation. No disclosures are reported. Dr. Pillinger reports serving as an investigator for the ColCORONA trial and receiving a unrelated investigator-initiated grant from Hikma, a colchicine manufacturer.
The gout drug colchicine appears to lower the severity of COVID-19, a small new Brazilian study finds, adding to evidence that the familiar medication holds promise as a treatment for hospitalized patients.
Patients who received colchicine in this randomized, double-blinded, placebo-controlled clinical trial presented better evolution in terms of the need for supplemental oxygen and the length of hospitalisation. ... Colchicine was safe and well tolerated,” the study authors wrote in RMD Open. However, deaths were rare in the trial, they added, and it is impossible to “evaluate the capacity of colchicine to avoid admission to ICU and reduce mortality.”
The oral anti-inflammatory colchicine, widely used as treatment in rheumatic disease, was first approved in the United States 60 years ago. Researchers began to explore its potential as a COVID-19 treatment in the early months of the pandemic.
On Jan. 25, an international team of researchers reported in a press release – but not yet a published paper – that the drug seemed to reduce hospitalizations, mechanical ventilation, and deaths in the ColCORONA trial. Earlier, a much-smaller, randomized, open-label, Greek trial linked the drug to reduced time to clinical deterioration and hospital stay.
The Brazilian authors of the new study, led by Maria Isabel Lopes of the University of São Paulo’s Ribeirão Preto Medical School, randomly assigned 75 hospitalized patients with moderate to severe COVID-19 to colchicine or placebo. A total of 72 subjects completed the April-August 2020 trial: 36 received colchicine (typically 0.5 mg three times for 5 days, then 0.5 mg twice daily for 5 days; doses were adjusted in low-weight patients and those with chronic kidney disease). The other 36 received the placebo.
(In the United States, 0.6-mg tablets of generic colchicine cost as little as $1.90 each with free coupons, according to goodrx.com.)
The median age in the groups was similar (55 years); and the placebo group had more women (61% vs. 47% in the colchicine group, P = .34). All 72 patients received the same COVID-19 treatment at the time of the trial: azithromycin, hydroxychloroquine, and unfractionated heparin. Most patients, about two-thirds in both groups, also received methylprednisolone because they needed higher amounts of supplemental oxygen.
Patients in the colchicine group needed supplemental oxygen for less time: Their median time of need was 4.0 days (interquartile range [IQR], 2.0-6.0) vs. 6.5 days (IQR, 4.0-9.0) for the placebo group (P < .001). The median time for hospitalization was also lower at 7.0 days (IQR, 5.0–9.0) for the colchicine group vs. 9.0 (IQR, 7.0–12.0) for the placebo group (log rank test, 10.6; P = .001).
The researchers also reported the percentage of patients who needed supplemental oxygen at day 2 as 67% with colchicine vs. 86% with placebo, and at day 7 as 9% vs. 42% (log rank test, 10.6; P = .001). Two patients in the placebo group died, both from ventilator-associated pneumonia.
As for side effects, new or worsened diarrhea was reported more often in the colchicine group (17% vs. 6% with placebo), but the difference was not statistically significant (P = .26), and diarrhea was controlled via medication.
The researchers reported that limitations include the exclusion criteria and their inability to link colchicine to rates of ICU admissions and death.
The drug appears to help patients with COVID-19, the study authors wrote, by “inhibiting inflammasome, reducing neutrophil migration and activation, or preventing endothelial damage.”
A “well-conceived and well-designed” study
In an interview, NYU Langone Health rheumatologist Michael H. Pillinger, MD – an investigator with the ColCORONA trial – praised the Brazilian study. It “appears well-conceived and well-designed, and was enrolled at a rate that was greater than the sample size that was estimated to be needed based on power analysis,” he said.
The Brazilian study is small, he noted. (In contrast, the ColCORONA trial had 4,488 outpatient participants.) “This study differs from ColCORONA in several ways – the most important being that it is a study of inpatients with moderate to severe COVID (really mostly moderate),” he added. “ColCORONA is looking at a target audience that is much larger – outpatients with mild to moderate COVID with risk factors for hospitalization. Both questions are really important and certainly not mutually exclusive, since our care remains inadequate in both venues. This study also adds value in that several other studies have been conducted in hospital patients with enrollment criteria relatively similar to this one, and all showed benefit, but those were open-label or retrospective, and this is blinded and placebo-controlled.”
Using colchicine in patients with COVID-19
Should physicians turn to colchicine in patients with COVID-19? “I would rather that it still be used in the context of research until formal recommendations can be made by bodies like the NIH and CDC,” Dr. Pillinger said. “But certainly, there may be times when physicians feel compelled to treat patients off label.”
He cautioned, however, that colchicine should never be used with some other drugs. Its interaction with the antibiotic clarithromycin can be fatal, he noted. And, he said, the drug must be monitored in general since it can cause rare, severe problems.
“Overall, colchicine probably works on the overabundant inflammatory response to COVID, and it may be that it can be combined with other drugs that affect viral replication or promote immunity – e.g. vaccines,” Dr. Pillinger said. “So far, it seems as if there is no safety problem with combining colchicine with other approaches, but this has not been studied in a rigorous manner.”
Moving forward, he said, the drug’s very low price outside of the United States “could provide resource-poor countries with a way to help keep patients out of precious hospital beds – or help them go home sooner once admitted.” For now, however, “we need a large-scale inpatient study, and one is currently going on in Great Britain. We also need validation of the outpatient ColCORONA study, and studies to look at whether colchicine can work in conjunction with other strategies.”
The study was funded by grants from the São Paulo Research Foundation, Brazilian National Council for Scientific and Technological Development, and CAPES Foundation. No disclosures are reported. Dr. Pillinger reports serving as an investigator for the ColCORONA trial and receiving a unrelated investigator-initiated grant from Hikma, a colchicine manufacturer.
The gout drug colchicine appears to lower the severity of COVID-19, a small new Brazilian study finds, adding to evidence that the familiar medication holds promise as a treatment for hospitalized patients.
Patients who received colchicine in this randomized, double-blinded, placebo-controlled clinical trial presented better evolution in terms of the need for supplemental oxygen and the length of hospitalisation. ... Colchicine was safe and well tolerated,” the study authors wrote in RMD Open. However, deaths were rare in the trial, they added, and it is impossible to “evaluate the capacity of colchicine to avoid admission to ICU and reduce mortality.”
The oral anti-inflammatory colchicine, widely used as treatment in rheumatic disease, was first approved in the United States 60 years ago. Researchers began to explore its potential as a COVID-19 treatment in the early months of the pandemic.
On Jan. 25, an international team of researchers reported in a press release – but not yet a published paper – that the drug seemed to reduce hospitalizations, mechanical ventilation, and deaths in the ColCORONA trial. Earlier, a much-smaller, randomized, open-label, Greek trial linked the drug to reduced time to clinical deterioration and hospital stay.
The Brazilian authors of the new study, led by Maria Isabel Lopes of the University of São Paulo’s Ribeirão Preto Medical School, randomly assigned 75 hospitalized patients with moderate to severe COVID-19 to colchicine or placebo. A total of 72 subjects completed the April-August 2020 trial: 36 received colchicine (typically 0.5 mg three times for 5 days, then 0.5 mg twice daily for 5 days; doses were adjusted in low-weight patients and those with chronic kidney disease). The other 36 received the placebo.
(In the United States, 0.6-mg tablets of generic colchicine cost as little as $1.90 each with free coupons, according to goodrx.com.)
The median age in the groups was similar (55 years); and the placebo group had more women (61% vs. 47% in the colchicine group, P = .34). All 72 patients received the same COVID-19 treatment at the time of the trial: azithromycin, hydroxychloroquine, and unfractionated heparin. Most patients, about two-thirds in both groups, also received methylprednisolone because they needed higher amounts of supplemental oxygen.
Patients in the colchicine group needed supplemental oxygen for less time: Their median time of need was 4.0 days (interquartile range [IQR], 2.0-6.0) vs. 6.5 days (IQR, 4.0-9.0) for the placebo group (P < .001). The median time for hospitalization was also lower at 7.0 days (IQR, 5.0–9.0) for the colchicine group vs. 9.0 (IQR, 7.0–12.0) for the placebo group (log rank test, 10.6; P = .001).
The researchers also reported the percentage of patients who needed supplemental oxygen at day 2 as 67% with colchicine vs. 86% with placebo, and at day 7 as 9% vs. 42% (log rank test, 10.6; P = .001). Two patients in the placebo group died, both from ventilator-associated pneumonia.
As for side effects, new or worsened diarrhea was reported more often in the colchicine group (17% vs. 6% with placebo), but the difference was not statistically significant (P = .26), and diarrhea was controlled via medication.
The researchers reported that limitations include the exclusion criteria and their inability to link colchicine to rates of ICU admissions and death.
The drug appears to help patients with COVID-19, the study authors wrote, by “inhibiting inflammasome, reducing neutrophil migration and activation, or preventing endothelial damage.”
A “well-conceived and well-designed” study
In an interview, NYU Langone Health rheumatologist Michael H. Pillinger, MD – an investigator with the ColCORONA trial – praised the Brazilian study. It “appears well-conceived and well-designed, and was enrolled at a rate that was greater than the sample size that was estimated to be needed based on power analysis,” he said.
The Brazilian study is small, he noted. (In contrast, the ColCORONA trial had 4,488 outpatient participants.) “This study differs from ColCORONA in several ways – the most important being that it is a study of inpatients with moderate to severe COVID (really mostly moderate),” he added. “ColCORONA is looking at a target audience that is much larger – outpatients with mild to moderate COVID with risk factors for hospitalization. Both questions are really important and certainly not mutually exclusive, since our care remains inadequate in both venues. This study also adds value in that several other studies have been conducted in hospital patients with enrollment criteria relatively similar to this one, and all showed benefit, but those were open-label or retrospective, and this is blinded and placebo-controlled.”
Using colchicine in patients with COVID-19
Should physicians turn to colchicine in patients with COVID-19? “I would rather that it still be used in the context of research until formal recommendations can be made by bodies like the NIH and CDC,” Dr. Pillinger said. “But certainly, there may be times when physicians feel compelled to treat patients off label.”
He cautioned, however, that colchicine should never be used with some other drugs. Its interaction with the antibiotic clarithromycin can be fatal, he noted. And, he said, the drug must be monitored in general since it can cause rare, severe problems.
“Overall, colchicine probably works on the overabundant inflammatory response to COVID, and it may be that it can be combined with other drugs that affect viral replication or promote immunity – e.g. vaccines,” Dr. Pillinger said. “So far, it seems as if there is no safety problem with combining colchicine with other approaches, but this has not been studied in a rigorous manner.”
Moving forward, he said, the drug’s very low price outside of the United States “could provide resource-poor countries with a way to help keep patients out of precious hospital beds – or help them go home sooner once admitted.” For now, however, “we need a large-scale inpatient study, and one is currently going on in Great Britain. We also need validation of the outpatient ColCORONA study, and studies to look at whether colchicine can work in conjunction with other strategies.”
The study was funded by grants from the São Paulo Research Foundation, Brazilian National Council for Scientific and Technological Development, and CAPES Foundation. No disclosures are reported. Dr. Pillinger reports serving as an investigator for the ColCORONA trial and receiving a unrelated investigator-initiated grant from Hikma, a colchicine manufacturer.
FROM RMD OPEN
Weekly COVID-19 cases in children continue to drop
Despite a drop in the number of weekly COVID-19 cases, children made up a larger share of cases for the fourth consecutive week, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.
Just over 140,000 new cases of COVID-19 in children were reported for the week of Jan. 22-28, down from 165,000 the week before and down from the record high of 211,000 2 weeks earlier, the AAP and the CHA said in their weekly COVID-19 report.
Since the beginning of January, however, the proportion of weekly cases occurring in children has risen from 12.9% to 15.1%, based on data collected by the AAP/CHA from the health department websites of 49 states (excluding New York), the District of Columbia, New York City, Puerto Rico, and Guam.
Since the beginning of the pandemic, 2.81 million children have been infected by the coronavirus, representing 12.8% of the total for all ages, which is almost 22 million. The cumulative rate since the start of the pandemic passed 3,700 cases per 100,000 children after increasing by 5.2% over the previous week, the AAP and CHA said in their report.
Cumulative hospitalizations in children just passed 11,000 in the 24 states (and New York City) that are reporting data for children, which represents 1.8% of COVID-19–related admissions for all ages, a proportion that has not changed since mid-November. Ten more deaths in children were reported during Jan. 22-28, bringing the total to 215 in the 43 states, along with New York City and Guam, that are tracking mortality.
In the 10 states that are reporting data on testing, rates of positive results in children range from 7.1% in Indiana, in which children make up the largest proportion of total tests performed (18.1%) to 28.4% in Iowa, where children make up the smallest proportion of tests (6.0%), the AAP and CHA said.
Despite a drop in the number of weekly COVID-19 cases, children made up a larger share of cases for the fourth consecutive week, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.
Just over 140,000 new cases of COVID-19 in children were reported for the week of Jan. 22-28, down from 165,000 the week before and down from the record high of 211,000 2 weeks earlier, the AAP and the CHA said in their weekly COVID-19 report.
Since the beginning of January, however, the proportion of weekly cases occurring in children has risen from 12.9% to 15.1%, based on data collected by the AAP/CHA from the health department websites of 49 states (excluding New York), the District of Columbia, New York City, Puerto Rico, and Guam.
Since the beginning of the pandemic, 2.81 million children have been infected by the coronavirus, representing 12.8% of the total for all ages, which is almost 22 million. The cumulative rate since the start of the pandemic passed 3,700 cases per 100,000 children after increasing by 5.2% over the previous week, the AAP and CHA said in their report.
Cumulative hospitalizations in children just passed 11,000 in the 24 states (and New York City) that are reporting data for children, which represents 1.8% of COVID-19–related admissions for all ages, a proportion that has not changed since mid-November. Ten more deaths in children were reported during Jan. 22-28, bringing the total to 215 in the 43 states, along with New York City and Guam, that are tracking mortality.
In the 10 states that are reporting data on testing, rates of positive results in children range from 7.1% in Indiana, in which children make up the largest proportion of total tests performed (18.1%) to 28.4% in Iowa, where children make up the smallest proportion of tests (6.0%), the AAP and CHA said.
Despite a drop in the number of weekly COVID-19 cases, children made up a larger share of cases for the fourth consecutive week, according to a report from the American Academy of Pediatrics and the Children’s Hospital Association.
Just over 140,000 new cases of COVID-19 in children were reported for the week of Jan. 22-28, down from 165,000 the week before and down from the record high of 211,000 2 weeks earlier, the AAP and the CHA said in their weekly COVID-19 report.
Since the beginning of January, however, the proportion of weekly cases occurring in children has risen from 12.9% to 15.1%, based on data collected by the AAP/CHA from the health department websites of 49 states (excluding New York), the District of Columbia, New York City, Puerto Rico, and Guam.
Since the beginning of the pandemic, 2.81 million children have been infected by the coronavirus, representing 12.8% of the total for all ages, which is almost 22 million. The cumulative rate since the start of the pandemic passed 3,700 cases per 100,000 children after increasing by 5.2% over the previous week, the AAP and CHA said in their report.
Cumulative hospitalizations in children just passed 11,000 in the 24 states (and New York City) that are reporting data for children, which represents 1.8% of COVID-19–related admissions for all ages, a proportion that has not changed since mid-November. Ten more deaths in children were reported during Jan. 22-28, bringing the total to 215 in the 43 states, along with New York City and Guam, that are tracking mortality.
In the 10 states that are reporting data on testing, rates of positive results in children range from 7.1% in Indiana, in which children make up the largest proportion of total tests performed (18.1%) to 28.4% in Iowa, where children make up the smallest proportion of tests (6.0%), the AAP and CHA said.
FDA approves intramuscular administration for peginterferon beta-1a in MS
“The new IM administration offers people living with relapsing MS the well-characterized efficacy and safety of Plegridy with the potential for significantly reduced injection site reactions,” Biogen said in a news release announcing the FDA action.
Plegridy is a pegylated version of interferon beta-1a, which prolongs the circulation time of the molecule in the body by increasing its size. The process extends the drug’s half-life, allowing for a less-frequent dosing schedule.
Peginterferon beta-1a administered subcutaneously was first approved by the FDA in 2014 based on data showing it significantly reduces MS relapses, disability progression, and brain lesions.
The FDA approved IM administration for peginterferon beta-1a based on data evaluating bioequivalence and adverse reactions associated with IM administration compared with subcutaneous (SC) administration in healthy volunteers.
Bioequivalence of the IM and SC dosing regimens was confirmed and volunteers receiving the drug through IM administration experienced fewer injection site reactions relative to those receiving SC administration (14.4% vs. 32.1%), the company said.
The overall safety profiles of IM and SC administration were generally similar, with no new safety signals.
The European Commission allowed marketing authorization for IM administration of peginterferon beta-1a in December 2020.
A version of this article first appeared on Medscape.com.
“The new IM administration offers people living with relapsing MS the well-characterized efficacy and safety of Plegridy with the potential for significantly reduced injection site reactions,” Biogen said in a news release announcing the FDA action.
Plegridy is a pegylated version of interferon beta-1a, which prolongs the circulation time of the molecule in the body by increasing its size. The process extends the drug’s half-life, allowing for a less-frequent dosing schedule.
Peginterferon beta-1a administered subcutaneously was first approved by the FDA in 2014 based on data showing it significantly reduces MS relapses, disability progression, and brain lesions.
The FDA approved IM administration for peginterferon beta-1a based on data evaluating bioequivalence and adverse reactions associated with IM administration compared with subcutaneous (SC) administration in healthy volunteers.
Bioequivalence of the IM and SC dosing regimens was confirmed and volunteers receiving the drug through IM administration experienced fewer injection site reactions relative to those receiving SC administration (14.4% vs. 32.1%), the company said.
The overall safety profiles of IM and SC administration were generally similar, with no new safety signals.
The European Commission allowed marketing authorization for IM administration of peginterferon beta-1a in December 2020.
A version of this article first appeared on Medscape.com.
“The new IM administration offers people living with relapsing MS the well-characterized efficacy and safety of Plegridy with the potential for significantly reduced injection site reactions,” Biogen said in a news release announcing the FDA action.
Plegridy is a pegylated version of interferon beta-1a, which prolongs the circulation time of the molecule in the body by increasing its size. The process extends the drug’s half-life, allowing for a less-frequent dosing schedule.
Peginterferon beta-1a administered subcutaneously was first approved by the FDA in 2014 based on data showing it significantly reduces MS relapses, disability progression, and brain lesions.
The FDA approved IM administration for peginterferon beta-1a based on data evaluating bioequivalence and adverse reactions associated with IM administration compared with subcutaneous (SC) administration in healthy volunteers.
Bioequivalence of the IM and SC dosing regimens was confirmed and volunteers receiving the drug through IM administration experienced fewer injection site reactions relative to those receiving SC administration (14.4% vs. 32.1%), the company said.
The overall safety profiles of IM and SC administration were generally similar, with no new safety signals.
The European Commission allowed marketing authorization for IM administration of peginterferon beta-1a in December 2020.
A version of this article first appeared on Medscape.com.
Microthrombi, necrosis seen in COVID-19 hearts on autopsy
Autopsies on patients who died from COVID-19 are providing important clues on how to treat the disease. In an analysis of 40 hearts from COVID-19 patients who died early in the pandemic, myocyte necrosis was seen in 14 hearts, or 35%.
In the majority of these hearts, pathologists found both small areas of focal necrosis and cardiac thrombi, most of which were microthrombi in myocardial capillaries, arterioles, and small muscular cells.
In an interview, senior author Aloke V. Finn, MD, CVPath Institute, Gaithersburg, Md., stressed the importance of understanding what they saw, but also what they didn’t see.
“What we saw in the majority of patients with myocardial injury were these small areas of infarct and microthrombi in small vessels. What we didn’t see was any evidence of myocarditis and or huge infarcts in, like, the LAD artery,” he said.
“What we’re seeing here is not clinically detectable. ... There is no test that will tell you there are microthrombi and no imaging tests that will show these focal areas of necrosis, but that doesn’t mean it’s not there,” he added.
The finding of myocyte necrosis in about one-third of samples is consistent with another study that showed that 30%-40% of patients hospitalized with COVID-19 have elevated troponins, noted Dr. Finn. The investigators were unable to obtain troponin levels on their patients, which could limit the clinical translation of myocardial necrosis detected at autopsy.
Dr. Finn and colleagues, including first author Dario Pellegrini, MD, from Ospedale Papa Giovanni XXIII in Bergamo, Italy, published their findings online in Circulation on Jan. 22, 2020.
The report is a follow-up to another just published by Dr. Finn’s group in the Journal of the American College of Cardiology, which showed that myocarditis is a very rare finding in COVID-19 autopsies.
Only three of 14 individuals (21.4%) with evidence of myocyte necrosis showed evidence of acute MI, which Dr. Finn and colleagues define as an area of necrosis at least 1 cm2 in size. The remaining 11 (78.6%) had only discrete areas of myocyte necrosis (>20 necrotic myocytes with an area of ≥0.05 mm2, but <1 cm2).
“This makes sense when we saw what type of thrombus there was in these cases; it wasn’t thrombus in major epicardial vessels but microthombi in small vessels,” said Dr. Finn.
In those with necrosis, cardiac thrombi were present in 11 of 14 (78.6%) cases, with 2 of 14 (14.2%) having epicardial coronary artery thrombi and 0 of 14 (64.3%) having microthrombi in myocardial capillaries, arterioles, and small muscular arteries.
Further supporting the role of COVID-19–related hypercoagulability as the cause of myocardial injury in many patients, the investigators noted that the incidence of severe coronary artery disease (defined as >75% cross sectional narrowing) did not differ significantly between those with and without necrosis.
COVID-19 vs. non–COVID-19 thrombi
Going one step further, Dr. Finn’s team compared cardiac microthrombi from their COVID-19–positive autopsy cases with intramyocardial thromboemboli from COVID-19 cases. They also compared the samples with aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19–infected patients presenting with ST-segment elevation MI (STEMI).
The autopsy-obtained microthrombi had significantly more fibrin and terminal complement C5b-9 immunostaining than intramyocardial thromboemboli from COVID-19–negative subjects and than aspirated thrombi from either COVID-positive or COVID-negative STEMI patients.
“Basically, what we’re seeing in these thrombi is evidence of an immune-mediated reaction,” said Dr. Finn, explaining that complement C5b-9 is an innate immune system protein that circulates in the blood in response to any kind of activation of the immune system. “It is nonspecific but can also lead to coagulation problems,” he said.
Anticoagulation, yes, but dose unclear
These findings clearly support the use of anticoagulation in hospitalized COVID patients, said Jeffrey Weitz, MD, director of the Thrombosis & Atherosclerosis Research Institute, McMaster University, Hamilton, Ont. But the details of how much anticoagulation, what kind, and for whom are still a moving target.
“I think what we can say at this point is that these autopsy findings fit with previous studies that have shown microthrombi in the lungs and thrombi in the legs and gut, and support the notion that these patients should receive prophylactic doses of anticoagulants if they’re sick enough to be hospitalized,” said Dr. Weitz.
“But it’s not as simple as to say that this study shows clots form in the heart of COVID patients and therefore more anticoagulation is going to be better than less anticoagulation,” he said in an interview.
Recent top-line findings from three linked clinical trials – REMAP-CAP, ACTIV-4, and ATTACC – show that full-dose anticoagulation was beneficial in moderately ill patients hospitalized for COVID-19 and reduced the need for mechanical ventilation.
Moderately ill patients are those not in intensive care and who did not require organ support, such as mechanical ventilation, at the time of enrollment.
However, the same group reported findings in December that showed that routine use of full-dose anticoagulation when started in the ICU in critically ill patients was not beneficial and possibly harmful.
Dr. Weitz was only a little bit surprised by this finding of potential harm in the sickest patients. “I figured everybody should get prophylaxis but I wasn’t sure that everybody should get intensified anticoagulant. But my assumption was that if anybody is going to benefit from it, it would be the ICU patients.”
It was notable, said Dr. Weitz, that levels of D-dimer, a fibrin degradation product, were not associated with outcomes. “So, it doesn’t seem to be that patients with evidence of more clotting are more likely to benefit, which might indicate that it’s not the anticoagulant effect of the heparin that’s helping, but maybe the anti-inflammatory effect. At this point, we just don’t know.”
All three studies have paused enrollment of the critically ill subgroup, but are continuing to enroll patients with moderate illness and expect to publish results in the coming months, according to previous coverage from this news organization.
The study was funded by CVPath, a nonprofit institute that receives funding from a number of different industry entities. Dr. Finn and Dr. Weitz reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
Autopsies on patients who died from COVID-19 are providing important clues on how to treat the disease. In an analysis of 40 hearts from COVID-19 patients who died early in the pandemic, myocyte necrosis was seen in 14 hearts, or 35%.
In the majority of these hearts, pathologists found both small areas of focal necrosis and cardiac thrombi, most of which were microthrombi in myocardial capillaries, arterioles, and small muscular cells.
In an interview, senior author Aloke V. Finn, MD, CVPath Institute, Gaithersburg, Md., stressed the importance of understanding what they saw, but also what they didn’t see.
“What we saw in the majority of patients with myocardial injury were these small areas of infarct and microthrombi in small vessels. What we didn’t see was any evidence of myocarditis and or huge infarcts in, like, the LAD artery,” he said.
“What we’re seeing here is not clinically detectable. ... There is no test that will tell you there are microthrombi and no imaging tests that will show these focal areas of necrosis, but that doesn’t mean it’s not there,” he added.
The finding of myocyte necrosis in about one-third of samples is consistent with another study that showed that 30%-40% of patients hospitalized with COVID-19 have elevated troponins, noted Dr. Finn. The investigators were unable to obtain troponin levels on their patients, which could limit the clinical translation of myocardial necrosis detected at autopsy.
Dr. Finn and colleagues, including first author Dario Pellegrini, MD, from Ospedale Papa Giovanni XXIII in Bergamo, Italy, published their findings online in Circulation on Jan. 22, 2020.
The report is a follow-up to another just published by Dr. Finn’s group in the Journal of the American College of Cardiology, which showed that myocarditis is a very rare finding in COVID-19 autopsies.
Only three of 14 individuals (21.4%) with evidence of myocyte necrosis showed evidence of acute MI, which Dr. Finn and colleagues define as an area of necrosis at least 1 cm2 in size. The remaining 11 (78.6%) had only discrete areas of myocyte necrosis (>20 necrotic myocytes with an area of ≥0.05 mm2, but <1 cm2).
“This makes sense when we saw what type of thrombus there was in these cases; it wasn’t thrombus in major epicardial vessels but microthombi in small vessels,” said Dr. Finn.
In those with necrosis, cardiac thrombi were present in 11 of 14 (78.6%) cases, with 2 of 14 (14.2%) having epicardial coronary artery thrombi and 0 of 14 (64.3%) having microthrombi in myocardial capillaries, arterioles, and small muscular arteries.
Further supporting the role of COVID-19–related hypercoagulability as the cause of myocardial injury in many patients, the investigators noted that the incidence of severe coronary artery disease (defined as >75% cross sectional narrowing) did not differ significantly between those with and without necrosis.
COVID-19 vs. non–COVID-19 thrombi
Going one step further, Dr. Finn’s team compared cardiac microthrombi from their COVID-19–positive autopsy cases with intramyocardial thromboemboli from COVID-19 cases. They also compared the samples with aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19–infected patients presenting with ST-segment elevation MI (STEMI).
The autopsy-obtained microthrombi had significantly more fibrin and terminal complement C5b-9 immunostaining than intramyocardial thromboemboli from COVID-19–negative subjects and than aspirated thrombi from either COVID-positive or COVID-negative STEMI patients.
“Basically, what we’re seeing in these thrombi is evidence of an immune-mediated reaction,” said Dr. Finn, explaining that complement C5b-9 is an innate immune system protein that circulates in the blood in response to any kind of activation of the immune system. “It is nonspecific but can also lead to coagulation problems,” he said.
Anticoagulation, yes, but dose unclear
These findings clearly support the use of anticoagulation in hospitalized COVID patients, said Jeffrey Weitz, MD, director of the Thrombosis & Atherosclerosis Research Institute, McMaster University, Hamilton, Ont. But the details of how much anticoagulation, what kind, and for whom are still a moving target.
“I think what we can say at this point is that these autopsy findings fit with previous studies that have shown microthrombi in the lungs and thrombi in the legs and gut, and support the notion that these patients should receive prophylactic doses of anticoagulants if they’re sick enough to be hospitalized,” said Dr. Weitz.
“But it’s not as simple as to say that this study shows clots form in the heart of COVID patients and therefore more anticoagulation is going to be better than less anticoagulation,” he said in an interview.
Recent top-line findings from three linked clinical trials – REMAP-CAP, ACTIV-4, and ATTACC – show that full-dose anticoagulation was beneficial in moderately ill patients hospitalized for COVID-19 and reduced the need for mechanical ventilation.
Moderately ill patients are those not in intensive care and who did not require organ support, such as mechanical ventilation, at the time of enrollment.
However, the same group reported findings in December that showed that routine use of full-dose anticoagulation when started in the ICU in critically ill patients was not beneficial and possibly harmful.
Dr. Weitz was only a little bit surprised by this finding of potential harm in the sickest patients. “I figured everybody should get prophylaxis but I wasn’t sure that everybody should get intensified anticoagulant. But my assumption was that if anybody is going to benefit from it, it would be the ICU patients.”
It was notable, said Dr. Weitz, that levels of D-dimer, a fibrin degradation product, were not associated with outcomes. “So, it doesn’t seem to be that patients with evidence of more clotting are more likely to benefit, which might indicate that it’s not the anticoagulant effect of the heparin that’s helping, but maybe the anti-inflammatory effect. At this point, we just don’t know.”
All three studies have paused enrollment of the critically ill subgroup, but are continuing to enroll patients with moderate illness and expect to publish results in the coming months, according to previous coverage from this news organization.
The study was funded by CVPath, a nonprofit institute that receives funding from a number of different industry entities. Dr. Finn and Dr. Weitz reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
Autopsies on patients who died from COVID-19 are providing important clues on how to treat the disease. In an analysis of 40 hearts from COVID-19 patients who died early in the pandemic, myocyte necrosis was seen in 14 hearts, or 35%.
In the majority of these hearts, pathologists found both small areas of focal necrosis and cardiac thrombi, most of which were microthrombi in myocardial capillaries, arterioles, and small muscular cells.
In an interview, senior author Aloke V. Finn, MD, CVPath Institute, Gaithersburg, Md., stressed the importance of understanding what they saw, but also what they didn’t see.
“What we saw in the majority of patients with myocardial injury were these small areas of infarct and microthrombi in small vessels. What we didn’t see was any evidence of myocarditis and or huge infarcts in, like, the LAD artery,” he said.
“What we’re seeing here is not clinically detectable. ... There is no test that will tell you there are microthrombi and no imaging tests that will show these focal areas of necrosis, but that doesn’t mean it’s not there,” he added.
The finding of myocyte necrosis in about one-third of samples is consistent with another study that showed that 30%-40% of patients hospitalized with COVID-19 have elevated troponins, noted Dr. Finn. The investigators were unable to obtain troponin levels on their patients, which could limit the clinical translation of myocardial necrosis detected at autopsy.
Dr. Finn and colleagues, including first author Dario Pellegrini, MD, from Ospedale Papa Giovanni XXIII in Bergamo, Italy, published their findings online in Circulation on Jan. 22, 2020.
The report is a follow-up to another just published by Dr. Finn’s group in the Journal of the American College of Cardiology, which showed that myocarditis is a very rare finding in COVID-19 autopsies.
Only three of 14 individuals (21.4%) with evidence of myocyte necrosis showed evidence of acute MI, which Dr. Finn and colleagues define as an area of necrosis at least 1 cm2 in size. The remaining 11 (78.6%) had only discrete areas of myocyte necrosis (>20 necrotic myocytes with an area of ≥0.05 mm2, but <1 cm2).
“This makes sense when we saw what type of thrombus there was in these cases; it wasn’t thrombus in major epicardial vessels but microthombi in small vessels,” said Dr. Finn.
In those with necrosis, cardiac thrombi were present in 11 of 14 (78.6%) cases, with 2 of 14 (14.2%) having epicardial coronary artery thrombi and 0 of 14 (64.3%) having microthrombi in myocardial capillaries, arterioles, and small muscular arteries.
Further supporting the role of COVID-19–related hypercoagulability as the cause of myocardial injury in many patients, the investigators noted that the incidence of severe coronary artery disease (defined as >75% cross sectional narrowing) did not differ significantly between those with and without necrosis.
COVID-19 vs. non–COVID-19 thrombi
Going one step further, Dr. Finn’s team compared cardiac microthrombi from their COVID-19–positive autopsy cases with intramyocardial thromboemboli from COVID-19 cases. They also compared the samples with aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19–infected patients presenting with ST-segment elevation MI (STEMI).
The autopsy-obtained microthrombi had significantly more fibrin and terminal complement C5b-9 immunostaining than intramyocardial thromboemboli from COVID-19–negative subjects and than aspirated thrombi from either COVID-positive or COVID-negative STEMI patients.
“Basically, what we’re seeing in these thrombi is evidence of an immune-mediated reaction,” said Dr. Finn, explaining that complement C5b-9 is an innate immune system protein that circulates in the blood in response to any kind of activation of the immune system. “It is nonspecific but can also lead to coagulation problems,” he said.
Anticoagulation, yes, but dose unclear
These findings clearly support the use of anticoagulation in hospitalized COVID patients, said Jeffrey Weitz, MD, director of the Thrombosis & Atherosclerosis Research Institute, McMaster University, Hamilton, Ont. But the details of how much anticoagulation, what kind, and for whom are still a moving target.
“I think what we can say at this point is that these autopsy findings fit with previous studies that have shown microthrombi in the lungs and thrombi in the legs and gut, and support the notion that these patients should receive prophylactic doses of anticoagulants if they’re sick enough to be hospitalized,” said Dr. Weitz.
“But it’s not as simple as to say that this study shows clots form in the heart of COVID patients and therefore more anticoagulation is going to be better than less anticoagulation,” he said in an interview.
Recent top-line findings from three linked clinical trials – REMAP-CAP, ACTIV-4, and ATTACC – show that full-dose anticoagulation was beneficial in moderately ill patients hospitalized for COVID-19 and reduced the need for mechanical ventilation.
Moderately ill patients are those not in intensive care and who did not require organ support, such as mechanical ventilation, at the time of enrollment.
However, the same group reported findings in December that showed that routine use of full-dose anticoagulation when started in the ICU in critically ill patients was not beneficial and possibly harmful.
Dr. Weitz was only a little bit surprised by this finding of potential harm in the sickest patients. “I figured everybody should get prophylaxis but I wasn’t sure that everybody should get intensified anticoagulant. But my assumption was that if anybody is going to benefit from it, it would be the ICU patients.”
It was notable, said Dr. Weitz, that levels of D-dimer, a fibrin degradation product, were not associated with outcomes. “So, it doesn’t seem to be that patients with evidence of more clotting are more likely to benefit, which might indicate that it’s not the anticoagulant effect of the heparin that’s helping, but maybe the anti-inflammatory effect. At this point, we just don’t know.”
All three studies have paused enrollment of the critically ill subgroup, but are continuing to enroll patients with moderate illness and expect to publish results in the coming months, according to previous coverage from this news organization.
The study was funded by CVPath, a nonprofit institute that receives funding from a number of different industry entities. Dr. Finn and Dr. Weitz reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
New NIH database will track neurologic effects of COVID-19
“We know COVID-19 can disrupt multiple body systems, but the effects of the virus and the body’s response to COVID-19 infection on the brain, spinal cord, nerves, and muscle can be particularly devastating and contribute to persistence of disability even after the virus is cleared,” said Barbara Karp, MD, program director at the National Institute of Neurological Disorders and Stroke.
“There is an urgent need to understand COVID-19–related neurological problems, which not uncommonly include headaches, fatigue, cognitive difficulties, stroke, pain, and sleep disorders as well as some very rare complications of serious infections,” said Dr. Karp.
The COVID-19 NeuroDatabank/BioBank (NeuroCOVID) is funded by the NINDS. It was created and will be maintained by researchers at NYU Langone Health in New York.
The project is led by Andrea Troxel, ScD, professor of population health, and Eva Petkova, PhD, professor of population health and child and adolescent psychiatry, both at New York University.
“We’ve built a pretty comprehensive database that will accept deidentified patient information about new neurological issues that coincide with their COVID disease or worsening of preexisting neurological problems,” said Dr. Troxel. “In addition, we have a bio repository that will accept almost any kind of biological sample, such as blood, plasma, cerebrospinal fluid, and tissue,” she said.
“Neuroimages are very difficult to store because the files are so enormous, but we’ve had some questions about that, and we’re looking into whether we can accommodate neuroimages,” Dr. Troxel noted.
Dr. Troxel said a “blast of information and invitations” has gone out in an effort to acquire data and biospecimens. “We’ve been really pleased with the amount of interest already, interest not only from large academic medical centers, as you might expect, but also from some smaller stand-alone clinics and even some individuals who have either experienced some of these neurological problems of COVID or know those who have and are really eager to try to provide information,” she added.
Researchers interested in using data and biosamples from the database may submit requests to the NeuroCOVID Steering Committee. More information is available online on the NeuroCOVID website.
A version of this article first appeared on Medscape.com.
“We know COVID-19 can disrupt multiple body systems, but the effects of the virus and the body’s response to COVID-19 infection on the brain, spinal cord, nerves, and muscle can be particularly devastating and contribute to persistence of disability even after the virus is cleared,” said Barbara Karp, MD, program director at the National Institute of Neurological Disorders and Stroke.
“There is an urgent need to understand COVID-19–related neurological problems, which not uncommonly include headaches, fatigue, cognitive difficulties, stroke, pain, and sleep disorders as well as some very rare complications of serious infections,” said Dr. Karp.
The COVID-19 NeuroDatabank/BioBank (NeuroCOVID) is funded by the NINDS. It was created and will be maintained by researchers at NYU Langone Health in New York.
The project is led by Andrea Troxel, ScD, professor of population health, and Eva Petkova, PhD, professor of population health and child and adolescent psychiatry, both at New York University.
“We’ve built a pretty comprehensive database that will accept deidentified patient information about new neurological issues that coincide with their COVID disease or worsening of preexisting neurological problems,” said Dr. Troxel. “In addition, we have a bio repository that will accept almost any kind of biological sample, such as blood, plasma, cerebrospinal fluid, and tissue,” she said.
“Neuroimages are very difficult to store because the files are so enormous, but we’ve had some questions about that, and we’re looking into whether we can accommodate neuroimages,” Dr. Troxel noted.
Dr. Troxel said a “blast of information and invitations” has gone out in an effort to acquire data and biospecimens. “We’ve been really pleased with the amount of interest already, interest not only from large academic medical centers, as you might expect, but also from some smaller stand-alone clinics and even some individuals who have either experienced some of these neurological problems of COVID or know those who have and are really eager to try to provide information,” she added.
Researchers interested in using data and biosamples from the database may submit requests to the NeuroCOVID Steering Committee. More information is available online on the NeuroCOVID website.
A version of this article first appeared on Medscape.com.
“We know COVID-19 can disrupt multiple body systems, but the effects of the virus and the body’s response to COVID-19 infection on the brain, spinal cord, nerves, and muscle can be particularly devastating and contribute to persistence of disability even after the virus is cleared,” said Barbara Karp, MD, program director at the National Institute of Neurological Disorders and Stroke.
“There is an urgent need to understand COVID-19–related neurological problems, which not uncommonly include headaches, fatigue, cognitive difficulties, stroke, pain, and sleep disorders as well as some very rare complications of serious infections,” said Dr. Karp.
The COVID-19 NeuroDatabank/BioBank (NeuroCOVID) is funded by the NINDS. It was created and will be maintained by researchers at NYU Langone Health in New York.
The project is led by Andrea Troxel, ScD, professor of population health, and Eva Petkova, PhD, professor of population health and child and adolescent psychiatry, both at New York University.
“We’ve built a pretty comprehensive database that will accept deidentified patient information about new neurological issues that coincide with their COVID disease or worsening of preexisting neurological problems,” said Dr. Troxel. “In addition, we have a bio repository that will accept almost any kind of biological sample, such as blood, plasma, cerebrospinal fluid, and tissue,” she said.
“Neuroimages are very difficult to store because the files are so enormous, but we’ve had some questions about that, and we’re looking into whether we can accommodate neuroimages,” Dr. Troxel noted.
Dr. Troxel said a “blast of information and invitations” has gone out in an effort to acquire data and biospecimens. “We’ve been really pleased with the amount of interest already, interest not only from large academic medical centers, as you might expect, but also from some smaller stand-alone clinics and even some individuals who have either experienced some of these neurological problems of COVID or know those who have and are really eager to try to provide information,” she added.
Researchers interested in using data and biosamples from the database may submit requests to the NeuroCOVID Steering Committee. More information is available online on the NeuroCOVID website.
A version of this article first appeared on Medscape.com.
Advanced Imaging Study Reveals How COVID-19 Attacks the Brain
Researchers from the National Institute of Neurological Disorders and Stroke studying the brains of patients who died from COVID-19, “consistently” found microvascular damage—but no signs of COVID-19 infection. Of the 19 patients in the study, 14 had chronic illnesses, including diabetes mellitus and hypertension, and 11 had ben found dead or had died unexpectedly. Of the 16 with available medical histories, one had delirium and the others had respiratory or unknown symptoms. Two had pulmonary embolism.
Patients with COVID-19 often have neurological problems, such as headaches, delirium, and dizziness. Some have strokes. Several studies have shown that COVID-19 can cause inflammation and blood vessel damage, but the precise mode of action is still unclear. In this study, the researchers used a magnetic resonance imaging (MRI) scanner 4 to 10 times more sensitive than most MRI scanners to examine samples of the olfactory bulbs and brainstems from the samples.
In 9 patients, the MRI scan showed punctate hyperintensities (bright spots representing areas of microvascular injury and fibrinogen leakage) that often indicate inflammation. In 10 brains, they found punctate hypointensities (dark spots) that corresponded to congested blood vessels, with surrounding areas of fibrinogen leakage and relatively intact vasculature. Areas of linear hypointensities (dark spots) were interpreted as microhemorrhages.
Using the scans as a guide, the researchers examined the spots more closely under a microscope. They found that the bright spots contained blood vessels that were thinner than normal and sometimes leaked blood proteins into the brain. This, the researchers say, seemed to trigger an immune reaction. The spots were surrounded by T cells from the blood and the brain’s own immune cells. In contrast, the dark spots contained clotted and leaky blood vessels but no immune response.
Moreover, although they used several methods for detecting genetic material or proteins from SAS-CoV-2, they found none. It’s possible, the researchers say, that the virus was cleared by the time of death or that viral copy numbers were undetectable by their assays.
We were completely surprised,” said Avindra Nath, MD, NINDS clinical director. “Originally, we expected to see damage that is caused by a lack of oxygen. Instead, we saw multifocal areas of damage that is usually associated with strokes and neuroinflammatory diseases.”
In future, Nath says, they plan to study how COVID-19 harms the blood vessels and whether that produces some of the short- and long-term symptoms seen. “We hope these results will help doctors understand the full spectrum of problems patients may suffer so that we can come up with better treatments.”
Researchers from the National Institute of Neurological Disorders and Stroke studying the brains of patients who died from COVID-19, “consistently” found microvascular damage—but no signs of COVID-19 infection. Of the 19 patients in the study, 14 had chronic illnesses, including diabetes mellitus and hypertension, and 11 had ben found dead or had died unexpectedly. Of the 16 with available medical histories, one had delirium and the others had respiratory or unknown symptoms. Two had pulmonary embolism.
Patients with COVID-19 often have neurological problems, such as headaches, delirium, and dizziness. Some have strokes. Several studies have shown that COVID-19 can cause inflammation and blood vessel damage, but the precise mode of action is still unclear. In this study, the researchers used a magnetic resonance imaging (MRI) scanner 4 to 10 times more sensitive than most MRI scanners to examine samples of the olfactory bulbs and brainstems from the samples.
In 9 patients, the MRI scan showed punctate hyperintensities (bright spots representing areas of microvascular injury and fibrinogen leakage) that often indicate inflammation. In 10 brains, they found punctate hypointensities (dark spots) that corresponded to congested blood vessels, with surrounding areas of fibrinogen leakage and relatively intact vasculature. Areas of linear hypointensities (dark spots) were interpreted as microhemorrhages.
Using the scans as a guide, the researchers examined the spots more closely under a microscope. They found that the bright spots contained blood vessels that were thinner than normal and sometimes leaked blood proteins into the brain. This, the researchers say, seemed to trigger an immune reaction. The spots were surrounded by T cells from the blood and the brain’s own immune cells. In contrast, the dark spots contained clotted and leaky blood vessels but no immune response.
Moreover, although they used several methods for detecting genetic material or proteins from SAS-CoV-2, they found none. It’s possible, the researchers say, that the virus was cleared by the time of death or that viral copy numbers were undetectable by their assays.
We were completely surprised,” said Avindra Nath, MD, NINDS clinical director. “Originally, we expected to see damage that is caused by a lack of oxygen. Instead, we saw multifocal areas of damage that is usually associated with strokes and neuroinflammatory diseases.”
In future, Nath says, they plan to study how COVID-19 harms the blood vessels and whether that produces some of the short- and long-term symptoms seen. “We hope these results will help doctors understand the full spectrum of problems patients may suffer so that we can come up with better treatments.”
Researchers from the National Institute of Neurological Disorders and Stroke studying the brains of patients who died from COVID-19, “consistently” found microvascular damage—but no signs of COVID-19 infection. Of the 19 patients in the study, 14 had chronic illnesses, including diabetes mellitus and hypertension, and 11 had ben found dead or had died unexpectedly. Of the 16 with available medical histories, one had delirium and the others had respiratory or unknown symptoms. Two had pulmonary embolism.
Patients with COVID-19 often have neurological problems, such as headaches, delirium, and dizziness. Some have strokes. Several studies have shown that COVID-19 can cause inflammation and blood vessel damage, but the precise mode of action is still unclear. In this study, the researchers used a magnetic resonance imaging (MRI) scanner 4 to 10 times more sensitive than most MRI scanners to examine samples of the olfactory bulbs and brainstems from the samples.
In 9 patients, the MRI scan showed punctate hyperintensities (bright spots representing areas of microvascular injury and fibrinogen leakage) that often indicate inflammation. In 10 brains, they found punctate hypointensities (dark spots) that corresponded to congested blood vessels, with surrounding areas of fibrinogen leakage and relatively intact vasculature. Areas of linear hypointensities (dark spots) were interpreted as microhemorrhages.
Using the scans as a guide, the researchers examined the spots more closely under a microscope. They found that the bright spots contained blood vessels that were thinner than normal and sometimes leaked blood proteins into the brain. This, the researchers say, seemed to trigger an immune reaction. The spots were surrounded by T cells from the blood and the brain’s own immune cells. In contrast, the dark spots contained clotted and leaky blood vessels but no immune response.
Moreover, although they used several methods for detecting genetic material or proteins from SAS-CoV-2, they found none. It’s possible, the researchers say, that the virus was cleared by the time of death or that viral copy numbers were undetectable by their assays.
We were completely surprised,” said Avindra Nath, MD, NINDS clinical director. “Originally, we expected to see damage that is caused by a lack of oxygen. Instead, we saw multifocal areas of damage that is usually associated with strokes and neuroinflammatory diseases.”
In future, Nath says, they plan to study how COVID-19 harms the blood vessels and whether that produces some of the short- and long-term symptoms seen. “We hope these results will help doctors understand the full spectrum of problems patients may suffer so that we can come up with better treatments.”
Influenza Plus COVID-19 Equals Greater Concern
Coinfection with COVID-19 and influenza was reported early in the pandemic. Although both infections on their own can cause severe complications and death, coinfection can double the odds of death when compared with COVID infection alone. Moreover, those odds can be raised by chronic medical conditions and environmental or occupational factors, such as congregate living settings, say physicians who report on the first 2 confirmed cases of COVID-19 and influenza coinfection among US Department of Defense personnel within the US Central Command area of responsibility.
In the first case, a 56-year-old contractor presented to a Role I clinic with anorexia, fever, chills, and headache, which had begun 3 days before. His initial vital signs were “unremarkable,” and he did not have symptoms of respiratory distress. An antigen test was positive for influenza type A. A COVID-19 test also was positive. He was placed on isolation and treated with oseltamivir, amlodipine, hydrochlorothiazide, and losartan. His condition did not warrant hospitalization. Of 3 close contacts, 1 tested positive and was isolated. Two remained asymptomatic during the 14-day quarantine. Ten days after onset, the patient returned to duty.
The second patient, a 34-year-old officer in the Army, was initially identified as a close contact of a confirmed COVID-19 case and placed in quarantine. He was asymptomatic but tested positive and was placed in isolation with precautions. As with the first patient, his vital signs were unremarkable. He continued to be asymptomatic, although he reported myalgias 2 days later. Since those are a classic sign of seasonal influenzas, he was tested and proved positive for type B influenza. He, too, was started on oseltamivir. By the end of the first week, he experienced loss of taste and smell, cough, and shortness of breath, but his vital signs remained normal. His symptoms improved through supportive care. All 6 of his close contacts remained asymptomatic. Ten days after his symptoms began, he also returned to duty.
Influenza-associated deaths among the US military have been relatively few, the authors say, most likely because of the good preexisting health status of the US military, prompt detection with rapid influenza diagnostic tests, several effective antiviral therapeutics, and a “robust, compulsory vaccination program.” Nonetheless, neither patient had received the 2020-2021 influenza vaccine, which underscores the importance of this intervention, the authors say.
Because both infections present with a wide variety of clinical manifestations and overlapping symptoms, providers should stay alert to the possibility of coinfection, especially among personnel who are higher risk. For instance, as a linguist who interacted daily with host nation partners, the civilian contractor had a high occupational exposure.
While the authors only discuss 2 cases, a Medical Surveillance Monthly Report editorial comment says their report “nevertheless supports the importance of implementing force health protection (FHP) measures to prevent, detect, and respond to the spread of both of these health threats.” It’s particularly important, the comment notes, in the current context of a drawdown in forces in many deployed locations, as further losses of personnel to illness may degrade the execution of critical missions.
Coinfection with COVID-19 and influenza was reported early in the pandemic. Although both infections on their own can cause severe complications and death, coinfection can double the odds of death when compared with COVID infection alone. Moreover, those odds can be raised by chronic medical conditions and environmental or occupational factors, such as congregate living settings, say physicians who report on the first 2 confirmed cases of COVID-19 and influenza coinfection among US Department of Defense personnel within the US Central Command area of responsibility.
In the first case, a 56-year-old contractor presented to a Role I clinic with anorexia, fever, chills, and headache, which had begun 3 days before. His initial vital signs were “unremarkable,” and he did not have symptoms of respiratory distress. An antigen test was positive for influenza type A. A COVID-19 test also was positive. He was placed on isolation and treated with oseltamivir, amlodipine, hydrochlorothiazide, and losartan. His condition did not warrant hospitalization. Of 3 close contacts, 1 tested positive and was isolated. Two remained asymptomatic during the 14-day quarantine. Ten days after onset, the patient returned to duty.
The second patient, a 34-year-old officer in the Army, was initially identified as a close contact of a confirmed COVID-19 case and placed in quarantine. He was asymptomatic but tested positive and was placed in isolation with precautions. As with the first patient, his vital signs were unremarkable. He continued to be asymptomatic, although he reported myalgias 2 days later. Since those are a classic sign of seasonal influenzas, he was tested and proved positive for type B influenza. He, too, was started on oseltamivir. By the end of the first week, he experienced loss of taste and smell, cough, and shortness of breath, but his vital signs remained normal. His symptoms improved through supportive care. All 6 of his close contacts remained asymptomatic. Ten days after his symptoms began, he also returned to duty.
Influenza-associated deaths among the US military have been relatively few, the authors say, most likely because of the good preexisting health status of the US military, prompt detection with rapid influenza diagnostic tests, several effective antiviral therapeutics, and a “robust, compulsory vaccination program.” Nonetheless, neither patient had received the 2020-2021 influenza vaccine, which underscores the importance of this intervention, the authors say.
Because both infections present with a wide variety of clinical manifestations and overlapping symptoms, providers should stay alert to the possibility of coinfection, especially among personnel who are higher risk. For instance, as a linguist who interacted daily with host nation partners, the civilian contractor had a high occupational exposure.
While the authors only discuss 2 cases, a Medical Surveillance Monthly Report editorial comment says their report “nevertheless supports the importance of implementing force health protection (FHP) measures to prevent, detect, and respond to the spread of both of these health threats.” It’s particularly important, the comment notes, in the current context of a drawdown in forces in many deployed locations, as further losses of personnel to illness may degrade the execution of critical missions.
Coinfection with COVID-19 and influenza was reported early in the pandemic. Although both infections on their own can cause severe complications and death, coinfection can double the odds of death when compared with COVID infection alone. Moreover, those odds can be raised by chronic medical conditions and environmental or occupational factors, such as congregate living settings, say physicians who report on the first 2 confirmed cases of COVID-19 and influenza coinfection among US Department of Defense personnel within the US Central Command area of responsibility.
In the first case, a 56-year-old contractor presented to a Role I clinic with anorexia, fever, chills, and headache, which had begun 3 days before. His initial vital signs were “unremarkable,” and he did not have symptoms of respiratory distress. An antigen test was positive for influenza type A. A COVID-19 test also was positive. He was placed on isolation and treated with oseltamivir, amlodipine, hydrochlorothiazide, and losartan. His condition did not warrant hospitalization. Of 3 close contacts, 1 tested positive and was isolated. Two remained asymptomatic during the 14-day quarantine. Ten days after onset, the patient returned to duty.
The second patient, a 34-year-old officer in the Army, was initially identified as a close contact of a confirmed COVID-19 case and placed in quarantine. He was asymptomatic but tested positive and was placed in isolation with precautions. As with the first patient, his vital signs were unremarkable. He continued to be asymptomatic, although he reported myalgias 2 days later. Since those are a classic sign of seasonal influenzas, he was tested and proved positive for type B influenza. He, too, was started on oseltamivir. By the end of the first week, he experienced loss of taste and smell, cough, and shortness of breath, but his vital signs remained normal. His symptoms improved through supportive care. All 6 of his close contacts remained asymptomatic. Ten days after his symptoms began, he also returned to duty.
Influenza-associated deaths among the US military have been relatively few, the authors say, most likely because of the good preexisting health status of the US military, prompt detection with rapid influenza diagnostic tests, several effective antiviral therapeutics, and a “robust, compulsory vaccination program.” Nonetheless, neither patient had received the 2020-2021 influenza vaccine, which underscores the importance of this intervention, the authors say.
Because both infections present with a wide variety of clinical manifestations and overlapping symptoms, providers should stay alert to the possibility of coinfection, especially among personnel who are higher risk. For instance, as a linguist who interacted daily with host nation partners, the civilian contractor had a high occupational exposure.
While the authors only discuss 2 cases, a Medical Surveillance Monthly Report editorial comment says their report “nevertheless supports the importance of implementing force health protection (FHP) measures to prevent, detect, and respond to the spread of both of these health threats.” It’s particularly important, the comment notes, in the current context of a drawdown in forces in many deployed locations, as further losses of personnel to illness may degrade the execution of critical missions.
‘Category 5’ COVID hurricane approaches, expert says
The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.
“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.
The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.
Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”
Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.
Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.
“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.
The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.
“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”
A version of this article first appeared on WebMD.com.
The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.
“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.
The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.
Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”
Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.
Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.
“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.
The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.
“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”
A version of this article first appeared on WebMD.com.
The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.
“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.
The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.
Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”
Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.
Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.
“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.
The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.
“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”
A version of this article first appeared on WebMD.com.