Emerging Infections

 

Fecal microbiota transplants (FMTs) should be considered for use in patients with recurrent Clostridium difficile infection that has not responded to antibiotic therapy, according to new guidelines.

The updated Clinical Practice Guidelines for Clostridium difficile Infection in Adults and Children, published in the Feb. 15 edition of Clinical Infectious Diseases (doi: 10.1093/cid/cix1085), address changes in management and diagnosis of the infection, and include recommendations for pediatric infection. The guidelines from the Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America were lasted published in 2010.

One of the strongest recommendations was on the use of FMTs to treat recurrent C. difficile infection after the failure of antibiotic therapy.

Courtesy CDC/Dr. Gilda Jones

L. Clifford McDonald, MD, of the Centers for Disease Control and Prevention, and his coauthors commented that approximately one-quarter of patients whose infection is treated with vancomycin will likely experience at least one additional episode of infection. Those whose recurrent infection fails to resolve despite repeat courses of antibiotics are a challenging group for clinicians, but one for whom FMT could be a viable alternative treatment approach.

“Anecdotal treatment success rates of fecal microbiota transplantation for recurrent CDI [C. difficile infection] have been high regardless of route of instillation of feces, and have ranged between 77% and 94% with administration via the proximal small bowel; the highest success rates (80%-100%) have been associated with instillation of feces via the colon,” they wrote.

The guidelines also addressed what the authors described as the “evolving controversy” over the best methods for diagnosis, pointing out that there is little consensus about the best laboratory testing method.

“Given these various conundrums and the paucity of large prospective studies, the recommendations, while strong in some instances, are based upon a very low to low quality of evidence,” the authors said.

That aside, they advised that patients with unexplained and new-onset diarrhea (three or more unformed stools in 24 hours) were the preferred target population for testing for C. difficile infection. The most sensitive method of diagnosis in patients with clinical symptoms likely to be C. difficile infection was a nucleic acid amplification test, or a multistep algorithm, rather than a toxin test alone.

The guidelines committee also strongly advised against repeat testing within 7 days during the same episode of diarrhea, and against testing stool from asymptomatic patients, except for the purpose of epidemiologic study. They also noted there was insufficient evidence for the use of biologic markers such as fecal lactoferrin as an adjunct to testing.

The guidelines’ authors found there was not enough evidence to recommend discontinuing proton pump inhibitors to reduce the incidence of C. difficile infection, despite epidemiologic evidence of an association between proton pump inhibitor use and C. difficile infection. Similarly, there was a lack of evidence for the use of probiotics for primary prevention, but the authors noted that meta-analyses suggest probiotics may help prevent C. difficile infection in patients on antibiotics without a history of C. difficile infection.

With respect to antibiotic treatment, they recommended that patients diagnosed with C. difficile infection should first discontinue the inciting antibiotic treatment and then begin therapy with either vancomycin or fidaxomicin. For recurrent infection, they advised a tapered and pulsed regimen of oral vancomycin or a 10-day course of fidaxomicin. If patients had received metronidazole for the primary episode, they should be given a standard 10-day course of vancomycin for recurrent infection, the authors said.

In terms of diagnosis and management of pediatric C. difficile, the guidelines advised against routinely testing infants under 2 years of age with diarrhea, as the rate of C. difficile colonization even among asymptomatic infants can be higher than 40%. Even in children older than age 2, there was only a “weak” recommendation for C. difficile testing in patients with prolonged or worsening diarrhea and other risk factors such as inflammatory bowel disease or recent antibiotic exposure.

Children with a first episode or first recurrence of nonsevere C. difficile should be treated with either metronidazole or vancomycin, the authors wrote, but in the case of more severe illness or second recurrence, oral vancomycin was preferred over metronidazole.

The authors also suggested clinicians consider FMTs for children with recurrent infection that had failed to respond to antibiotics, but noted the quality of evidence for this was very low.

The guidelines were funded by the Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America. Six authors declared grants, consultancies, board positions, and other payments from the pharmaceutical industry outside the submitted work. One author also held patents relating to the treatment and prevention of C. difficile infection.

 

 

SOURCE: McDonald CL et al. Clin Infect Dis. 2018 Feb 15. doi: 10.1093/cid/cix1085.
 

 

Fecal microbiota transplants (FMTs) should be considered for use in patients with recurrent Clostridium difficile infection that has not responded to antibiotic therapy, according to new guidelines.

The updated Clinical Practice Guidelines for Clostridium difficile Infection in Adults and Children, published in the Feb. 15 edition of Clinical Infectious Diseases (doi: 10.1093/cid/cix1085), address changes in management and diagnosis of the infection, and include recommendations for pediatric infection. The guidelines from the Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America were lasted published in 2010.

One of the strongest recommendations was on the use of FMTs to treat recurrent C. difficile infection after the failure of antibiotic therapy.

Courtesy CDC/Dr. Gilda Jones

L. Clifford McDonald, MD, of the Centers for Disease Control and Prevention, and his coauthors commented that approximately one-quarter of patients whose infection is treated with vancomycin will likely experience at least one additional episode of infection. Those whose recurrent infection fails to resolve despite repeat courses of antibiotics are a challenging group for clinicians, but one for whom FMT could be a viable alternative treatment approach.

“Anecdotal treatment success rates of fecal microbiota transplantation for recurrent CDI [C. difficile infection] have been high regardless of route of instillation of feces, and have ranged between 77% and 94% with administration via the proximal small bowel; the highest success rates (80%-100%) have been associated with instillation of feces via the colon,” they wrote.

The guidelines also addressed what the authors described as the “evolving controversy” over the best methods for diagnosis, pointing out that there is little consensus about the best laboratory testing method.

“Given these various conundrums and the paucity of large prospective studies, the recommendations, while strong in some instances, are based upon a very low to low quality of evidence,” the authors said.

That aside, they advised that patients with unexplained and new-onset diarrhea (three or more unformed stools in 24 hours) were the preferred target population for testing for C. difficile infection. The most sensitive method of diagnosis in patients with clinical symptoms likely to be C. difficile infection was a nucleic acid amplification test, or a multistep algorithm, rather than a toxin test alone.

The guidelines committee also strongly advised against repeat testing within 7 days during the same episode of diarrhea, and against testing stool from asymptomatic patients, except for the purpose of epidemiologic study. They also noted there was insufficient evidence for the use of biologic markers such as fecal lactoferrin as an adjunct to testing.

The guidelines’ authors found there was not enough evidence to recommend discontinuing proton pump inhibitors to reduce the incidence of C. difficile infection, despite epidemiologic evidence of an association between proton pump inhibitor use and C. difficile infection. Similarly, there was a lack of evidence for the use of probiotics for primary prevention, but the authors noted that meta-analyses suggest probiotics may help prevent C. difficile infection in patients on antibiotics without a history of C. difficile infection.

With respect to antibiotic treatment, they recommended that patients diagnosed with C. difficile infection should first discontinue the inciting antibiotic treatment and then begin therapy with either vancomycin or fidaxomicin. For recurrent infection, they advised a tapered and pulsed regimen of oral vancomycin or a 10-day course of fidaxomicin. If patients had received metronidazole for the primary episode, they should be given a standard 10-day course of vancomycin for recurrent infection, the authors said.

In terms of diagnosis and management of pediatric C. difficile, the guidelines advised against routinely testing infants under 2 years of age with diarrhea, as the rate of C. difficile colonization even among asymptomatic infants can be higher than 40%. Even in children older than age 2, there was only a “weak” recommendation for C. difficile testing in patients with prolonged or worsening diarrhea and other risk factors such as inflammatory bowel disease or recent antibiotic exposure.

Children with a first episode or first recurrence of nonsevere C. difficile should be treated with either metronidazole or vancomycin, the authors wrote, but in the case of more severe illness or second recurrence, oral vancomycin was preferred over metronidazole.

The authors also suggested clinicians consider FMTs for children with recurrent infection that had failed to respond to antibiotics, but noted the quality of evidence for this was very low.

The guidelines were funded by the Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America. Six authors declared grants, consultancies, board positions, and other payments from the pharmaceutical industry outside the submitted work. One author also held patents relating to the treatment and prevention of C. difficile infection.

 

 

SOURCE: McDonald CL et al. Clin Infect Dis. 2018 Feb 15. doi: 10.1093/cid/cix1085.
 

 

Fecal microbiota transplants (FMTs) should be considered for use in patients with recurrent Clostridium difficile infection that has not responded to antibiotic therapy, according to new guidelines.

The updated Clinical Practice Guidelines for Clostridium difficile Infection in Adults and Children, published in the Feb. 15 edition of Clinical Infectious Diseases (doi: 10.1093/cid/cix1085), address changes in management and diagnosis of the infection, and include recommendations for pediatric infection. The guidelines from the Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America were lasted published in 2010.

One of the strongest recommendations was on the use of FMTs to treat recurrent C. difficile infection after the failure of antibiotic therapy.

Courtesy CDC/Dr. Gilda Jones

L. Clifford McDonald, MD, of the Centers for Disease Control and Prevention, and his coauthors commented that approximately one-quarter of patients whose infection is treated with vancomycin will likely experience at least one additional episode of infection. Those whose recurrent infection fails to resolve despite repeat courses of antibiotics are a challenging group for clinicians, but one for whom FMT could be a viable alternative treatment approach.

“Anecdotal treatment success rates of fecal microbiota transplantation for recurrent CDI [C. difficile infection] have been high regardless of route of instillation of feces, and have ranged between 77% and 94% with administration via the proximal small bowel; the highest success rates (80%-100%) have been associated with instillation of feces via the colon,” they wrote.

The guidelines also addressed what the authors described as the “evolving controversy” over the best methods for diagnosis, pointing out that there is little consensus about the best laboratory testing method.

“Given these various conundrums and the paucity of large prospective studies, the recommendations, while strong in some instances, are based upon a very low to low quality of evidence,” the authors said.

That aside, they advised that patients with unexplained and new-onset diarrhea (three or more unformed stools in 24 hours) were the preferred target population for testing for C. difficile infection. The most sensitive method of diagnosis in patients with clinical symptoms likely to be C. difficile infection was a nucleic acid amplification test, or a multistep algorithm, rather than a toxin test alone.

The guidelines committee also strongly advised against repeat testing within 7 days during the same episode of diarrhea, and against testing stool from asymptomatic patients, except for the purpose of epidemiologic study. They also noted there was insufficient evidence for the use of biologic markers such as fecal lactoferrin as an adjunct to testing.

The guidelines’ authors found there was not enough evidence to recommend discontinuing proton pump inhibitors to reduce the incidence of C. difficile infection, despite epidemiologic evidence of an association between proton pump inhibitor use and C. difficile infection. Similarly, there was a lack of evidence for the use of probiotics for primary prevention, but the authors noted that meta-analyses suggest probiotics may help prevent C. difficile infection in patients on antibiotics without a history of C. difficile infection.

With respect to antibiotic treatment, they recommended that patients diagnosed with C. difficile infection should first discontinue the inciting antibiotic treatment and then begin therapy with either vancomycin or fidaxomicin. For recurrent infection, they advised a tapered and pulsed regimen of oral vancomycin or a 10-day course of fidaxomicin. If patients had received metronidazole for the primary episode, they should be given a standard 10-day course of vancomycin for recurrent infection, the authors said.

In terms of diagnosis and management of pediatric C. difficile, the guidelines advised against routinely testing infants under 2 years of age with diarrhea, as the rate of C. difficile colonization even among asymptomatic infants can be higher than 40%. Even in children older than age 2, there was only a “weak” recommendation for C. difficile testing in patients with prolonged or worsening diarrhea and other risk factors such as inflammatory bowel disease or recent antibiotic exposure.

Children with a first episode or first recurrence of nonsevere C. difficile should be treated with either metronidazole or vancomycin, the authors wrote, but in the case of more severe illness or second recurrence, oral vancomycin was preferred over metronidazole.

The authors also suggested clinicians consider FMTs for children with recurrent infection that had failed to respond to antibiotics, but noted the quality of evidence for this was very low.

The guidelines were funded by the Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America. Six authors declared grants, consultancies, board positions, and other payments from the pharmaceutical industry outside the submitted work. One author also held patents relating to the treatment and prevention of C. difficile infection.

 

 

SOURCE: McDonald CL et al. Clin Infect Dis. 2018 Feb 15. doi: 10.1093/cid/cix1085.
 

 

The Food and Drug Administration announced Jan. 30 that is has issued a MedWatch safety alert on the use of the over-the-counter (OTC) antidiarrhea drug, loperamide.

Currently, the FDA is working with manufacturers to use blister packs or other single-dose packaging and to limit the number of doses in a package.

The alert comes after receiving continuous reports of serious heart problems and deaths with the use of much higher than recommended doses of loperamide, mainly among people who are intentionally misusing or abusing the product, regardless of the addition of a warning to the medicine label and a previous communication. The FDA states that loperamide is a safe drug when used as directed.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Two particular methods of abuse are of concern. In some cases, abusers use other drugs together with loperamide in an effort to increase absorption and penetration across the blood-brain barrier, enhancing the euphoric effects of loperamide. Additionally, some individuals are using high doses of loperamide to mitigate against the symptoms of opioid withdrawal, according to the FDA.

Loperamide is approved to help control symptoms of diarrhea. The maximum recommended daily dose for adults is 8 mg per day for OTC use and 16 mg per day for prescription use. It acts on opioid receptors in the gut to slow the movement in the intestines and decrease the number of bowel movements.

It is noted that much higher than recommended doses of loperamide, either intentionally or unintentionally, can result in serious cardiac adverse events, including QT interval prolongation, torsade de pointes or other ventricular arrhythmias, syncope, and cardiac arrest. Health care professionals and patients can report adverse events or side effects related to the use of these products to the FDA’s MedWatch Safety Information and Adverse Event Reporting Program.

In 2016, the FDA issued a Drug Safety Communication and added warnings about serious heart problems to the drug label of prescription loperamide and to the Drug Facts label of OTC loperamide products. The FDA is working to evaluate this safety issue and will update the public when more information is available.

Read the full safety alert here.

[email protected]

 

The Food and Drug Administration announced Jan. 30 that is has issued a MedWatch safety alert on the use of the over-the-counter (OTC) antidiarrhea drug, loperamide.

Currently, the FDA is working with manufacturers to use blister packs or other single-dose packaging and to limit the number of doses in a package.

The alert comes after receiving continuous reports of serious heart problems and deaths with the use of much higher than recommended doses of loperamide, mainly among people who are intentionally misusing or abusing the product, regardless of the addition of a warning to the medicine label and a previous communication. The FDA states that loperamide is a safe drug when used as directed.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Two particular methods of abuse are of concern. In some cases, abusers use other drugs together with loperamide in an effort to increase absorption and penetration across the blood-brain barrier, enhancing the euphoric effects of loperamide. Additionally, some individuals are using high doses of loperamide to mitigate against the symptoms of opioid withdrawal, according to the FDA.

Loperamide is approved to help control symptoms of diarrhea. The maximum recommended daily dose for adults is 8 mg per day for OTC use and 16 mg per day for prescription use. It acts on opioid receptors in the gut to slow the movement in the intestines and decrease the number of bowel movements.

It is noted that much higher than recommended doses of loperamide, either intentionally or unintentionally, can result in serious cardiac adverse events, including QT interval prolongation, torsade de pointes or other ventricular arrhythmias, syncope, and cardiac arrest. Health care professionals and patients can report adverse events or side effects related to the use of these products to the FDA’s MedWatch Safety Information and Adverse Event Reporting Program.

In 2016, the FDA issued a Drug Safety Communication and added warnings about serious heart problems to the drug label of prescription loperamide and to the Drug Facts label of OTC loperamide products. The FDA is working to evaluate this safety issue and will update the public when more information is available.

Read the full safety alert here.

[email protected]

 

The Food and Drug Administration announced Jan. 30 that is has issued a MedWatch safety alert on the use of the over-the-counter (OTC) antidiarrhea drug, loperamide.

Currently, the FDA is working with manufacturers to use blister packs or other single-dose packaging and to limit the number of doses in a package.

The alert comes after receiving continuous reports of serious heart problems and deaths with the use of much higher than recommended doses of loperamide, mainly among people who are intentionally misusing or abusing the product, regardless of the addition of a warning to the medicine label and a previous communication. The FDA states that loperamide is a safe drug when used as directed.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Two particular methods of abuse are of concern. In some cases, abusers use other drugs together with loperamide in an effort to increase absorption and penetration across the blood-brain barrier, enhancing the euphoric effects of loperamide. Additionally, some individuals are using high doses of loperamide to mitigate against the symptoms of opioid withdrawal, according to the FDA.

Loperamide is approved to help control symptoms of diarrhea. The maximum recommended daily dose for adults is 8 mg per day for OTC use and 16 mg per day for prescription use. It acts on opioid receptors in the gut to slow the movement in the intestines and decrease the number of bowel movements.

It is noted that much higher than recommended doses of loperamide, either intentionally or unintentionally, can result in serious cardiac adverse events, including QT interval prolongation, torsade de pointes or other ventricular arrhythmias, syncope, and cardiac arrest. Health care professionals and patients can report adverse events or side effects related to the use of these products to the FDA’s MedWatch Safety Information and Adverse Event Reporting Program.

In 2016, the FDA issued a Drug Safety Communication and added warnings about serious heart problems to the drug label of prescription loperamide and to the Drug Facts label of OTC loperamide products. The FDA is working to evaluate this safety issue and will update the public when more information is available.

Read the full safety alert here.

[email protected]

 

The prevalence of birth defects strongly linked with congenital Zika virus infection increased 21% from the first to the second half of 2016 in areas of the United States with local, endemic transmission: Puerto Rico, south Florida, and southern Texas, according to a report in the Jan. 26 edition of Morbidity and Mortality Weekly Report.

In those areas, complications strongly associated with Zika – including microcephaly; brain and eye abnormalities; and neurogenic hip dislocation, clubfoot, hearing loss, and arthrogryposis – jumped from 2.0 to 2.4 cases per 1,000 live births, with 140 cases in the first half of the year and 169 cases in the second (P = .009). Microcephaly and brain abnormalities were the most common problems.

Sumaia Villela/Agência Brasil/CC BY 3.0 BR

Meanwhile, in areas with one or more cases of confirmed travel-associated Zika per 100,000 residents, such as New York and Georgia, the prevalence of those problems held steady throughout 2016 at 2.4 cases per 1,000 live births.

In places with less than one confirmed Zika case from travel per 100,000 residents, such as Hawaii and Utah, the prevalence of birth defects strongly linked to Zika actually dropped from 2.8 cases per 1,000 live births to 2.4 in 2016.

The 15 U.S. jurisdictions in the study included nearly 1 million live births, representing approximately one fourth of the total live births in the United States in 2016. The live birth rate was 92% among the 2,962 infants and fetuses with Zika-associated birth defects.

All the jurisdictions had existing birth defects surveillance systems that quickly adapted to monitor for potential Zika defects. However, although strongly associated with Zika, there’s no guarantee that the birth defects in the study were actually caused by the virus, the researchers noted.

“These data will help communities plan for needed resources to care for affected patients and families and can serve as a foundation for linking and evaluating health and developmental outcomes of affected children,” said the investigators, led by Augustina Delaney, PhD, of the National Center on Birth Defects and Developmental Disabilities at the Centers for Disease Control and Prevention in Atlanta.

The work was the first population-based birth defect surveillance report for Zika. The CDC follows confirmed Zika cases in pregnant women and their offspring closely, but only a small portion of women are actually tested, so there’s likely far more cases of congenital Zika infection than show up in registries. Despite its limits, birth defect surveillance likely provides a more accurate picture of the actual extent of the problem.

It’s not known why Zika-linked birth defects dropped off in areas with low or no travel-associated cases. “However ... further case ascertainment from the final quarter of 2016 is anticipated in all jurisdictions,” so the numbers could change, the authors said.

They had no conflicts of interest.

[email protected]

SOURCE: Delaney A, et. al. MMWR Morb Mortal Wkly Rep. 2018 Jan 26;67(3):91-6

 

The prevalence of birth defects strongly linked with congenital Zika virus infection increased 21% from the first to the second half of 2016 in areas of the United States with local, endemic transmission: Puerto Rico, south Florida, and southern Texas, according to a report in the Jan. 26 edition of Morbidity and Mortality Weekly Report.

In those areas, complications strongly associated with Zika – including microcephaly; brain and eye abnormalities; and neurogenic hip dislocation, clubfoot, hearing loss, and arthrogryposis – jumped from 2.0 to 2.4 cases per 1,000 live births, with 140 cases in the first half of the year and 169 cases in the second (P = .009). Microcephaly and brain abnormalities were the most common problems.

Sumaia Villela/Agência Brasil/CC BY 3.0 BR

Meanwhile, in areas with one or more cases of confirmed travel-associated Zika per 100,000 residents, such as New York and Georgia, the prevalence of those problems held steady throughout 2016 at 2.4 cases per 1,000 live births.

In places with less than one confirmed Zika case from travel per 100,000 residents, such as Hawaii and Utah, the prevalence of birth defects strongly linked to Zika actually dropped from 2.8 cases per 1,000 live births to 2.4 in 2016.

The 15 U.S. jurisdictions in the study included nearly 1 million live births, representing approximately one fourth of the total live births in the United States in 2016. The live birth rate was 92% among the 2,962 infants and fetuses with Zika-associated birth defects.

All the jurisdictions had existing birth defects surveillance systems that quickly adapted to monitor for potential Zika defects. However, although strongly associated with Zika, there’s no guarantee that the birth defects in the study were actually caused by the virus, the researchers noted.

“These data will help communities plan for needed resources to care for affected patients and families and can serve as a foundation for linking and evaluating health and developmental outcomes of affected children,” said the investigators, led by Augustina Delaney, PhD, of the National Center on Birth Defects and Developmental Disabilities at the Centers for Disease Control and Prevention in Atlanta.

The work was the first population-based birth defect surveillance report for Zika. The CDC follows confirmed Zika cases in pregnant women and their offspring closely, but only a small portion of women are actually tested, so there’s likely far more cases of congenital Zika infection than show up in registries. Despite its limits, birth defect surveillance likely provides a more accurate picture of the actual extent of the problem.

It’s not known why Zika-linked birth defects dropped off in areas with low or no travel-associated cases. “However ... further case ascertainment from the final quarter of 2016 is anticipated in all jurisdictions,” so the numbers could change, the authors said.

They had no conflicts of interest.

[email protected]

SOURCE: Delaney A, et. al. MMWR Morb Mortal Wkly Rep. 2018 Jan 26;67(3):91-6

 

The prevalence of birth defects strongly linked with congenital Zika virus infection increased 21% from the first to the second half of 2016 in areas of the United States with local, endemic transmission: Puerto Rico, south Florida, and southern Texas, according to a report in the Jan. 26 edition of Morbidity and Mortality Weekly Report.

In those areas, complications strongly associated with Zika – including microcephaly; brain and eye abnormalities; and neurogenic hip dislocation, clubfoot, hearing loss, and arthrogryposis – jumped from 2.0 to 2.4 cases per 1,000 live births, with 140 cases in the first half of the year and 169 cases in the second (P = .009). Microcephaly and brain abnormalities were the most common problems.

Sumaia Villela/Agência Brasil/CC BY 3.0 BR

Meanwhile, in areas with one or more cases of confirmed travel-associated Zika per 100,000 residents, such as New York and Georgia, the prevalence of those problems held steady throughout 2016 at 2.4 cases per 1,000 live births.

In places with less than one confirmed Zika case from travel per 100,000 residents, such as Hawaii and Utah, the prevalence of birth defects strongly linked to Zika actually dropped from 2.8 cases per 1,000 live births to 2.4 in 2016.

The 15 U.S. jurisdictions in the study included nearly 1 million live births, representing approximately one fourth of the total live births in the United States in 2016. The live birth rate was 92% among the 2,962 infants and fetuses with Zika-associated birth defects.

All the jurisdictions had existing birth defects surveillance systems that quickly adapted to monitor for potential Zika defects. However, although strongly associated with Zika, there’s no guarantee that the birth defects in the study were actually caused by the virus, the researchers noted.

“These data will help communities plan for needed resources to care for affected patients and families and can serve as a foundation for linking and evaluating health and developmental outcomes of affected children,” said the investigators, led by Augustina Delaney, PhD, of the National Center on Birth Defects and Developmental Disabilities at the Centers for Disease Control and Prevention in Atlanta.

The work was the first population-based birth defect surveillance report for Zika. The CDC follows confirmed Zika cases in pregnant women and their offspring closely, but only a small portion of women are actually tested, so there’s likely far more cases of congenital Zika infection than show up in registries. Despite its limits, birth defect surveillance likely provides a more accurate picture of the actual extent of the problem.

It’s not known why Zika-linked birth defects dropped off in areas with low or no travel-associated cases. “However ... further case ascertainment from the final quarter of 2016 is anticipated in all jurisdictions,” so the numbers could change, the authors said.

They had no conflicts of interest.

[email protected]

SOURCE: Delaney A, et. al. MMWR Morb Mortal Wkly Rep. 2018 Jan 26;67(3):91-6

 

Up to a quarter of patients infected with chikungunya virus who reported joint pain as one of their initial symptoms continue to have joint pain after 20 months of follow-up, and evidence suggests that the persistent joint symptoms are not related to the continued presence of the virus in synovial fluid, according to two studies of patients infected during the 2014-2015 Colombian epidemic.

In the first large-scale, cross-sectional follow-up of a prospective cohort from the Colombian epidemic, Aileen Chang, MD, of George Washington University, Washington, and her colleagues at multiple other institutions reported persistent joint pain and multiple swollen and/or tender joints after 20 months in 123 of 485 Colombian patients who initially had joint pain with their Chikungunya virus infection (CHIKV) diagnosis. In their report in Arthritis & Rheumatology, they said that increased initial viral load and severe initial joint pain were predictors of persistent arthritis, which is consistent with the work of other researchers.

CDC/Cynthia Goldsmith

In another study reported separately in Arthritis & Rheumatology from the same population of CHIKV patients with chronic arthritis, synovial fluid and blood plasma samples obtained from 38 patients at a median of 22 months of follow-up showed no signs of CHIKV RNA.

Dr. Chang worked with a variety of coinvestigators, some of whom were also involved in the larger symptom follow-up study, to conduct this Study of Chikungunya Arthritis Mechanisms in the Americas (CAMA). They collected synovial fluid and blood plasma from these 38 patients as well as 10 healthy controls who were serologically negative for CHIKV and never had arthritis, and analyzed the fluid and plasma for signs of CHIKV. They assessed viral RNA via quantitative reverse transcription polymerase chain reaction (qRT-PCR) testing, looked at viral proteins via mass spectrometry, and did viral cultures.

All samples from the 38 patients in the study were negative for CHIKV in two separate qRT-PCR assays. To determine if low-level viremia was present in synovial fluid samples, the samples were added to cell cultures to expand viral replication. No viral growth was found after three attempts and 10 days of culture. Conversely, controls with low quantities of virus (about 1 plaque-forming unit per well) yielded growth and detection of the virus.

Patients with CHIKV-associated arthritis also had no significant increase in rheumatoid arthritis markers or C-reactive protein. In fact, plasma markers for rheumatoid arthritis were found in only a fraction of patients with CHIKV arthritis: rheumatoid factor (RF) IgM antibody in 9%, RF IgG antibody in 12%, and anti–cyclic citrullinated peptide in 0%.

The more probable potential mechanisms through which CHIKV could cause persistent arthritis symptoms is through the presence of persistent CHIKV or viral antigens at low enough levels in the synovial tissue that it is undetectable in the synovial fluid, Dr. Chang and her associates suggested. There is also a possibility of epigenetic changes to the host DNA, altering host gene transcription. Other epigenetic changes, like epigenetic imprinting, could be possible in macrophages, leading to more aggressive cell behavior, they said. Unlikelier scenarios would be the presence of seronegative RA in these patients or, alternatively, the presence of seronegative RA indicating prior infection with CHIKV or other arthritogenic viruses.

Whatever mechanisms are causing CHIKV-associated arthritis, “these study findings may have important clinical relevance for CHIKV in the Americas. Since there is no current standard of care guidance for the treatment of CHIKV arthritis, some patients are currently being treated with immunosuppressant medications such as methotrexate, hydroxychloroquine, etanercept, adalimumab, sulfasalazine, fingolimod, abatacept, and tofacitinib,” Dr. Chang and her colleagues wrote. “This practice could be potentially harmful in the setting of replicating virus in the synovium as it could permit reemergence of a systemic viral infection.”

The CAMA study has several important limitations , the investigators said, the first being that during collection of synovial fluid, 0-20 mL of saline solution were used to flush the joints, which could have affected the ability to detect virus in the samples. In an attempt to mitigate this, the researchers cultured 0.5-1.5 mL of sampled synovial fluid to expand any replication-competent virus present in the sample, used two complementary PCR assays to detect nucleic acids, and a proteomic approach to look for viral proteins.

The researchers acknowledged that despite these measures, “proving the absence of a target is difficult, and we recognize that it is possible that our approach failed to detect low-level viral antigen; however, our orthogonal approach clearly demonstrates that if viral antigen exists in the synovial fluid, it is at extremely low levels.” They advised that future studies may want to use synovial biopsies rather than extracted fluid.

The investigators also did not include patients who had previously been infected by CHIKV without chronic arthritis. This issue was compounded by the lack of age- and sex-matched healthy controls.

All researchers involved in the studies reported no financial conflicts of interest. The studies were supported by various grants from the National Institutes of Health and the Rheumatology Research Foundation.

[email protected]

SOURCE: Chang A et al. Arthritis Rheumatol. 2017 Dec 20. doi: 10.1002/art.40383 and Chang A et al. Arthritis Rheumatol. 2017 Dec 20. doi: 10.1002/art.40384

 

Up to a quarter of patients infected with chikungunya virus who reported joint pain as one of their initial symptoms continue to have joint pain after 20 months of follow-up, and evidence suggests that the persistent joint symptoms are not related to the continued presence of the virus in synovial fluid, according to two studies of patients infected during the 2014-2015 Colombian epidemic.

In the first large-scale, cross-sectional follow-up of a prospective cohort from the Colombian epidemic, Aileen Chang, MD, of George Washington University, Washington, and her colleagues at multiple other institutions reported persistent joint pain and multiple swollen and/or tender joints after 20 months in 123 of 485 Colombian patients who initially had joint pain with their Chikungunya virus infection (CHIKV) diagnosis. In their report in Arthritis & Rheumatology, they said that increased initial viral load and severe initial joint pain were predictors of persistent arthritis, which is consistent with the work of other researchers.

CDC/Cynthia Goldsmith

In another study reported separately in Arthritis & Rheumatology from the same population of CHIKV patients with chronic arthritis, synovial fluid and blood plasma samples obtained from 38 patients at a median of 22 months of follow-up showed no signs of CHIKV RNA.

Dr. Chang worked with a variety of coinvestigators, some of whom were also involved in the larger symptom follow-up study, to conduct this Study of Chikungunya Arthritis Mechanisms in the Americas (CAMA). They collected synovial fluid and blood plasma from these 38 patients as well as 10 healthy controls who were serologically negative for CHIKV and never had arthritis, and analyzed the fluid and plasma for signs of CHIKV. They assessed viral RNA via quantitative reverse transcription polymerase chain reaction (qRT-PCR) testing, looked at viral proteins via mass spectrometry, and did viral cultures.

All samples from the 38 patients in the study were negative for CHIKV in two separate qRT-PCR assays. To determine if low-level viremia was present in synovial fluid samples, the samples were added to cell cultures to expand viral replication. No viral growth was found after three attempts and 10 days of culture. Conversely, controls with low quantities of virus (about 1 plaque-forming unit per well) yielded growth and detection of the virus.

Patients with CHIKV-associated arthritis also had no significant increase in rheumatoid arthritis markers or C-reactive protein. In fact, plasma markers for rheumatoid arthritis were found in only a fraction of patients with CHIKV arthritis: rheumatoid factor (RF) IgM antibody in 9%, RF IgG antibody in 12%, and anti–cyclic citrullinated peptide in 0%.

The more probable potential mechanisms through which CHIKV could cause persistent arthritis symptoms is through the presence of persistent CHIKV or viral antigens at low enough levels in the synovial tissue that it is undetectable in the synovial fluid, Dr. Chang and her associates suggested. There is also a possibility of epigenetic changes to the host DNA, altering host gene transcription. Other epigenetic changes, like epigenetic imprinting, could be possible in macrophages, leading to more aggressive cell behavior, they said. Unlikelier scenarios would be the presence of seronegative RA in these patients or, alternatively, the presence of seronegative RA indicating prior infection with CHIKV or other arthritogenic viruses.

Whatever mechanisms are causing CHIKV-associated arthritis, “these study findings may have important clinical relevance for CHIKV in the Americas. Since there is no current standard of care guidance for the treatment of CHIKV arthritis, some patients are currently being treated with immunosuppressant medications such as methotrexate, hydroxychloroquine, etanercept, adalimumab, sulfasalazine, fingolimod, abatacept, and tofacitinib,” Dr. Chang and her colleagues wrote. “This practice could be potentially harmful in the setting of replicating virus in the synovium as it could permit reemergence of a systemic viral infection.”

The CAMA study has several important limitations , the investigators said, the first being that during collection of synovial fluid, 0-20 mL of saline solution were used to flush the joints, which could have affected the ability to detect virus in the samples. In an attempt to mitigate this, the researchers cultured 0.5-1.5 mL of sampled synovial fluid to expand any replication-competent virus present in the sample, used two complementary PCR assays to detect nucleic acids, and a proteomic approach to look for viral proteins.

The researchers acknowledged that despite these measures, “proving the absence of a target is difficult, and we recognize that it is possible that our approach failed to detect low-level viral antigen; however, our orthogonal approach clearly demonstrates that if viral antigen exists in the synovial fluid, it is at extremely low levels.” They advised that future studies may want to use synovial biopsies rather than extracted fluid.

The investigators also did not include patients who had previously been infected by CHIKV without chronic arthritis. This issue was compounded by the lack of age- and sex-matched healthy controls.

All researchers involved in the studies reported no financial conflicts of interest. The studies were supported by various grants from the National Institutes of Health and the Rheumatology Research Foundation.

[email protected]

SOURCE: Chang A et al. Arthritis Rheumatol. 2017 Dec 20. doi: 10.1002/art.40383 and Chang A et al. Arthritis Rheumatol. 2017 Dec 20. doi: 10.1002/art.40384

 

Up to a quarter of patients infected with chikungunya virus who reported joint pain as one of their initial symptoms continue to have joint pain after 20 months of follow-up, and evidence suggests that the persistent joint symptoms are not related to the continued presence of the virus in synovial fluid, according to two studies of patients infected during the 2014-2015 Colombian epidemic.

In the first large-scale, cross-sectional follow-up of a prospective cohort from the Colombian epidemic, Aileen Chang, MD, of George Washington University, Washington, and her colleagues at multiple other institutions reported persistent joint pain and multiple swollen and/or tender joints after 20 months in 123 of 485 Colombian patients who initially had joint pain with their Chikungunya virus infection (CHIKV) diagnosis. In their report in Arthritis & Rheumatology, they said that increased initial viral load and severe initial joint pain were predictors of persistent arthritis, which is consistent with the work of other researchers.

CDC/Cynthia Goldsmith

In another study reported separately in Arthritis & Rheumatology from the same population of CHIKV patients with chronic arthritis, synovial fluid and blood plasma samples obtained from 38 patients at a median of 22 months of follow-up showed no signs of CHIKV RNA.

Dr. Chang worked with a variety of coinvestigators, some of whom were also involved in the larger symptom follow-up study, to conduct this Study of Chikungunya Arthritis Mechanisms in the Americas (CAMA). They collected synovial fluid and blood plasma from these 38 patients as well as 10 healthy controls who were serologically negative for CHIKV and never had arthritis, and analyzed the fluid and plasma for signs of CHIKV. They assessed viral RNA via quantitative reverse transcription polymerase chain reaction (qRT-PCR) testing, looked at viral proteins via mass spectrometry, and did viral cultures.

All samples from the 38 patients in the study were negative for CHIKV in two separate qRT-PCR assays. To determine if low-level viremia was present in synovial fluid samples, the samples were added to cell cultures to expand viral replication. No viral growth was found after three attempts and 10 days of culture. Conversely, controls with low quantities of virus (about 1 plaque-forming unit per well) yielded growth and detection of the virus.

Patients with CHIKV-associated arthritis also had no significant increase in rheumatoid arthritis markers or C-reactive protein. In fact, plasma markers for rheumatoid arthritis were found in only a fraction of patients with CHIKV arthritis: rheumatoid factor (RF) IgM antibody in 9%, RF IgG antibody in 12%, and anti–cyclic citrullinated peptide in 0%.

The more probable potential mechanisms through which CHIKV could cause persistent arthritis symptoms is through the presence of persistent CHIKV or viral antigens at low enough levels in the synovial tissue that it is undetectable in the synovial fluid, Dr. Chang and her associates suggested. There is also a possibility of epigenetic changes to the host DNA, altering host gene transcription. Other epigenetic changes, like epigenetic imprinting, could be possible in macrophages, leading to more aggressive cell behavior, they said. Unlikelier scenarios would be the presence of seronegative RA in these patients or, alternatively, the presence of seronegative RA indicating prior infection with CHIKV or other arthritogenic viruses.

Whatever mechanisms are causing CHIKV-associated arthritis, “these study findings may have important clinical relevance for CHIKV in the Americas. Since there is no current standard of care guidance for the treatment of CHIKV arthritis, some patients are currently being treated with immunosuppressant medications such as methotrexate, hydroxychloroquine, etanercept, adalimumab, sulfasalazine, fingolimod, abatacept, and tofacitinib,” Dr. Chang and her colleagues wrote. “This practice could be potentially harmful in the setting of replicating virus in the synovium as it could permit reemergence of a systemic viral infection.”

The CAMA study has several important limitations , the investigators said, the first being that during collection of synovial fluid, 0-20 mL of saline solution were used to flush the joints, which could have affected the ability to detect virus in the samples. In an attempt to mitigate this, the researchers cultured 0.5-1.5 mL of sampled synovial fluid to expand any replication-competent virus present in the sample, used two complementary PCR assays to detect nucleic acids, and a proteomic approach to look for viral proteins.

The researchers acknowledged that despite these measures, “proving the absence of a target is difficult, and we recognize that it is possible that our approach failed to detect low-level viral antigen; however, our orthogonal approach clearly demonstrates that if viral antigen exists in the synovial fluid, it is at extremely low levels.” They advised that future studies may want to use synovial biopsies rather than extracted fluid.

The investigators also did not include patients who had previously been infected by CHIKV without chronic arthritis. This issue was compounded by the lack of age- and sex-matched healthy controls.

All researchers involved in the studies reported no financial conflicts of interest. The studies were supported by various grants from the National Institutes of Health and the Rheumatology Research Foundation.

[email protected]

SOURCE: Chang A et al. Arthritis Rheumatol. 2017 Dec 20. doi: 10.1002/art.40383 and Chang A et al. Arthritis Rheumatol. 2017 Dec 20. doi: 10.1002/art.40384

 

SAN DIEGO – The presence of Corynebacterium in the gut microbiome of people with two G alleles at the rs356219 single nucleotide polymorphism locus of the alpha-synuclein gene was associated with 100% probability of having Parkinson’s disease in a study conducted by the NeuroGenetics Research Consortium.

If the finding is replicated, it means that Corynebacterium is the trigger for Parkinson’s disease (PD) in people with the GG genotype. The GG signature at rs356219 is the strongest genetic risk factor for PD identified to date, but it’s not necessarily strong enough to cause the disease on its own. “It definitely needs a trigger,” and there’s a good chance that Corynebacterium is it, said senior investigator Haydeh Payami, PhD, professor of neurology and genomics at the University of Alabama, Birmingham.

Kuo Chun Hung/Thinkstock

It’s a potentially huge finding that begins to unravel the link between the dozens of genetic risk factors for PD and environmental triggers that push people over the edge. “Corynebacterium isn’t the only bug. I think there are other bugs that go with other” genetic risk factors. Eventually, “we are going to map this whole thing out: Which bugs go with which genetic susceptibilities, and which genetic susceptibilities are triggered by” other things in the environment, such as pesticides, Dr. Payami, leader of the multicenter neurogenetics research collaboration, said in an interview.

Her team genotyped SNCA rs356219 from blood samples in 197 middle-aged PD patients and 115 age-matched controls. They also extracted DNA from stool samples to see what bacteria were in their gut and then looked for interactions between rs356219 genotype, gut microbiome, and PD risk.

The medical literature has been full of hints for a while now that PD might be set off by something going wrong in the gastrointestinal tract. Colonic inflammation, alpha-synuclein pathology in the gut, and dysbiosis of the gut microbiome in PD are among the many clues. The goal of the work was to find the link between PD and its GI aberrations.

Ninety genera were identified in the stool samples, but “no matter how you looked at the data, whichever method you used, one [genus] kept coming up” for interaction with the rs356219 genotype, “and that was Corynebacterium,” Dr. Payami said.

As in past studies, the rs356219 AA genotype did not increase the odds of PD, and there was no difference in microbiome abundance between PD patients and controls. The GA genotype increased the odds slightly without Corynebacterium, but it increased the odds more than fivefold when Corynebacterium was in the gut (odds ratio, 5.9; P = .04). If people had GG plus Corynebacterium, however, “you nailed it,” Dr. Payami said: The odds of developing PD were infinite (P = .0003).

Corynebacterium was more abundant in GA subjects with PD than GA subjects without PD, but it was by far the most abundant in GG subjects, and every person who had the GG genotype and gut Corynebacterium also had PD.

Corynebacterium are gram-positive, aerobic bacilli commonly found on the skin. Some members of the genus are opportunistic pathogens. It’s not clear how they get incorporated into the gut microbiome, or if they can be wiped out selectively in the gut with antibiotics or probiotics.

Perhaps Corynebacterium in the GI tract induces expression of alpha-synuclein protein, a major component of PD Lewy bodies that’s known to travel from the gut to the brain. Maybe the amount expressed depends on how many Gs people have in rs356219. Perhaps “if you have two Gs, you get so much alpha-synuclein that’s there’s no turning back, and it’s enough to cause PD,” Dr. Payami said.

The study was led by Zachary Wallen, a PhD candidate in Dr. Payami’s lab, and presented by him at the annual meeting of the American Neurological Association. The work was supported by the National Institutes of Health. Dr. Payami and Mr. Wallen had no industry disclosures.

[email protected]

SOURCE: Wallen Z et al. ANA 2017 abstract number S268

 

SAN DIEGO – The presence of Corynebacterium in the gut microbiome of people with two G alleles at the rs356219 single nucleotide polymorphism locus of the alpha-synuclein gene was associated with 100% probability of having Parkinson’s disease in a study conducted by the NeuroGenetics Research Consortium.

If the finding is replicated, it means that Corynebacterium is the trigger for Parkinson’s disease (PD) in people with the GG genotype. The GG signature at rs356219 is the strongest genetic risk factor for PD identified to date, but it’s not necessarily strong enough to cause the disease on its own. “It definitely needs a trigger,” and there’s a good chance that Corynebacterium is it, said senior investigator Haydeh Payami, PhD, professor of neurology and genomics at the University of Alabama, Birmingham.

Kuo Chun Hung/Thinkstock

It’s a potentially huge finding that begins to unravel the link between the dozens of genetic risk factors for PD and environmental triggers that push people over the edge. “Corynebacterium isn’t the only bug. I think there are other bugs that go with other” genetic risk factors. Eventually, “we are going to map this whole thing out: Which bugs go with which genetic susceptibilities, and which genetic susceptibilities are triggered by” other things in the environment, such as pesticides, Dr. Payami, leader of the multicenter neurogenetics research collaboration, said in an interview.

Her team genotyped SNCA rs356219 from blood samples in 197 middle-aged PD patients and 115 age-matched controls. They also extracted DNA from stool samples to see what bacteria were in their gut and then looked for interactions between rs356219 genotype, gut microbiome, and PD risk.

The medical literature has been full of hints for a while now that PD might be set off by something going wrong in the gastrointestinal tract. Colonic inflammation, alpha-synuclein pathology in the gut, and dysbiosis of the gut microbiome in PD are among the many clues. The goal of the work was to find the link between PD and its GI aberrations.

Ninety genera were identified in the stool samples, but “no matter how you looked at the data, whichever method you used, one [genus] kept coming up” for interaction with the rs356219 genotype, “and that was Corynebacterium,” Dr. Payami said.

As in past studies, the rs356219 AA genotype did not increase the odds of PD, and there was no difference in microbiome abundance between PD patients and controls. The GA genotype increased the odds slightly without Corynebacterium, but it increased the odds more than fivefold when Corynebacterium was in the gut (odds ratio, 5.9; P = .04). If people had GG plus Corynebacterium, however, “you nailed it,” Dr. Payami said: The odds of developing PD were infinite (P = .0003).

Corynebacterium was more abundant in GA subjects with PD than GA subjects without PD, but it was by far the most abundant in GG subjects, and every person who had the GG genotype and gut Corynebacterium also had PD.

Corynebacterium are gram-positive, aerobic bacilli commonly found on the skin. Some members of the genus are opportunistic pathogens. It’s not clear how they get incorporated into the gut microbiome, or if they can be wiped out selectively in the gut with antibiotics or probiotics.

Perhaps Corynebacterium in the GI tract induces expression of alpha-synuclein protein, a major component of PD Lewy bodies that’s known to travel from the gut to the brain. Maybe the amount expressed depends on how many Gs people have in rs356219. Perhaps “if you have two Gs, you get so much alpha-synuclein that’s there’s no turning back, and it’s enough to cause PD,” Dr. Payami said.

The study was led by Zachary Wallen, a PhD candidate in Dr. Payami’s lab, and presented by him at the annual meeting of the American Neurological Association. The work was supported by the National Institutes of Health. Dr. Payami and Mr. Wallen had no industry disclosures.

[email protected]

SOURCE: Wallen Z et al. ANA 2017 abstract number S268

 

SAN DIEGO – The presence of Corynebacterium in the gut microbiome of people with two G alleles at the rs356219 single nucleotide polymorphism locus of the alpha-synuclein gene was associated with 100% probability of having Parkinson’s disease in a study conducted by the NeuroGenetics Research Consortium.

If the finding is replicated, it means that Corynebacterium is the trigger for Parkinson’s disease (PD) in people with the GG genotype. The GG signature at rs356219 is the strongest genetic risk factor for PD identified to date, but it’s not necessarily strong enough to cause the disease on its own. “It definitely needs a trigger,” and there’s a good chance that Corynebacterium is it, said senior investigator Haydeh Payami, PhD, professor of neurology and genomics at the University of Alabama, Birmingham.

Kuo Chun Hung/Thinkstock

It’s a potentially huge finding that begins to unravel the link between the dozens of genetic risk factors for PD and environmental triggers that push people over the edge. “Corynebacterium isn’t the only bug. I think there are other bugs that go with other” genetic risk factors. Eventually, “we are going to map this whole thing out: Which bugs go with which genetic susceptibilities, and which genetic susceptibilities are triggered by” other things in the environment, such as pesticides, Dr. Payami, leader of the multicenter neurogenetics research collaboration, said in an interview.

Her team genotyped SNCA rs356219 from blood samples in 197 middle-aged PD patients and 115 age-matched controls. They also extracted DNA from stool samples to see what bacteria were in their gut and then looked for interactions between rs356219 genotype, gut microbiome, and PD risk.

The medical literature has been full of hints for a while now that PD might be set off by something going wrong in the gastrointestinal tract. Colonic inflammation, alpha-synuclein pathology in the gut, and dysbiosis of the gut microbiome in PD are among the many clues. The goal of the work was to find the link between PD and its GI aberrations.

Ninety genera were identified in the stool samples, but “no matter how you looked at the data, whichever method you used, one [genus] kept coming up” for interaction with the rs356219 genotype, “and that was Corynebacterium,” Dr. Payami said.

As in past studies, the rs356219 AA genotype did not increase the odds of PD, and there was no difference in microbiome abundance between PD patients and controls. The GA genotype increased the odds slightly without Corynebacterium, but it increased the odds more than fivefold when Corynebacterium was in the gut (odds ratio, 5.9; P = .04). If people had GG plus Corynebacterium, however, “you nailed it,” Dr. Payami said: The odds of developing PD were infinite (P = .0003).

Corynebacterium was more abundant in GA subjects with PD than GA subjects without PD, but it was by far the most abundant in GG subjects, and every person who had the GG genotype and gut Corynebacterium also had PD.

Corynebacterium are gram-positive, aerobic bacilli commonly found on the skin. Some members of the genus are opportunistic pathogens. It’s not clear how they get incorporated into the gut microbiome, or if they can be wiped out selectively in the gut with antibiotics or probiotics.

Perhaps Corynebacterium in the GI tract induces expression of alpha-synuclein protein, a major component of PD Lewy bodies that’s known to travel from the gut to the brain. Maybe the amount expressed depends on how many Gs people have in rs356219. Perhaps “if you have two Gs, you get so much alpha-synuclein that’s there’s no turning back, and it’s enough to cause PD,” Dr. Payami said.

The study was led by Zachary Wallen, a PhD candidate in Dr. Payami’s lab, and presented by him at the annual meeting of the American Neurological Association. The work was supported by the National Institutes of Health. Dr. Payami and Mr. Wallen had no industry disclosures.

[email protected]

SOURCE: Wallen Z et al. ANA 2017 abstract number S268

SAN DIEGO – By standardizing antibiotic treatment for simple and uncomplicated staphylococcal bloodstream infections (BSI), an algorithm effectively shortens therapy and simplifies decision making, according to results of a multinational randomized trial.

“The data from the study confirm that the algorithm achieves more with less and verify that shorter antibiotic courses are sufficient,” reported Thomas L. Holland, MD, an infectious disease specialist at Duke University Hospital in Durham, N.C.

CDC/Janice Haney Carr

Several cases of complicated staphylococcal BSI found their way into the study despite selection criteria designed to enroll only uncomplicated cases. This was inevitable because not all cases destined to become complicated can be identified initially, but outcomes overall still remained similar between the algorithm and standard of care (SOC) groups.

In this study, the patients randomized to algorithm treatment received vancomycin (or daptomycin in allergic or intolerant patients), which was administered for periods of duration based on clinical features. In those randomized to SOC, the choice and duration of antibiotics were left to the discretion of the treating physician without restrictions.

In those with simple staphylococcal BSI, the algorithm called for no further antibiotics beyond what had already been administered empirically prior to randomization. Key features of simple coagulase-negative staphylococcal (CONS) BSIs include absence of fever or evidence of metastatic infection, as well as no more than one positive follow-up blood culture. The key features of simple Staphylococcus aureus BSI are similar. However, no positive blood cultures are required for S. aureus BSI to be classified as simple.

“In the algorithm arm, no antibiotics were given to those with simple staphylococcal BSI unless antibiotics had been given prior to randomization,” Dr. Holland explained, but he acknowledged that empiric antibiotics prior to randomization reflect “clinical reality.”

In those with uncomplicated rather than simple staphylococcal BSI, vancomycin was given for 5 days to those with CONS BSI and for 14 days to those with S. aureus BSI. In those who were randomized and then subsequently found to have a complicated infection, defined as multiple positive blood cultures or evidence of metastatic infection, patients received as few as 7 days or as many as 28 days of antibiotics, “reflecting the heterogeneity of these infections,” Dr. Holland reported at an annual scientific meeting on infectious diseases.

The coprimary endpoints were treatment success at test of cure and treatment safety, both of which were adjudicated by an external committee consisting of infectious disease specialists blinded to the therapy.

There were 509 patients from 16 sites in both the United States and Spain. CONS BSIs represented approximately 75% of patients in both arms. The complicated staphylococcal infections, which also were evenly distributed in the two arms, were included in the intention-to-treat analysis. Of complicated staphylococcal infections in this study, the pathogen was CONS in 34 instances and S. aureus in 37.

Treatment success was achieved in 82.0% and 81.5% of patients in the algorithm and SOC arms, respectively. Significant adverse events occurred in 32.9% and 28.3% of patients, respectively. Neither difference approached statistical significance.

“In other words, the algorithm was as effective and safe as standard of care,” Dr. Holland confirmed.

However, the median duration of treatment was reduced substantially for those randomized to the algorithm arm, compared with that seen in the standard of care arm. Among evaluable patients without complicated BSI, the mean duration of therapy was 4.4 days in the algorithm group vs. 6.2 days in the SOC group (P = .003). Most of this nearly 2-day reduction in treatment was achieved in uncomplicated CONS BSI patients. In this group, the mean days of treatment were 5.3 days and 8.4 days for the algorithm and SOC groups, respectively. In the uncomplicated S. aureus group, the reduction (from 15.9 to 15.3 days) was not significant.

“The study has several messages. For one, it suggests that patients who meet the criteria of simple staphylococcal BSI can be managed safely with monitoring alone. In addition, this study “provides the best evidence to date that 14 days of vancomycin from the first negative blood culture is sufficient in uncomplicated S. aureus bloodstream infections,” Dr. Holland stated.

“For many, these data will validate what they are already doing,” said Dr. Holland, who reported that the algorithm is now being applied routinely at his institution. “The value is that we now have a randomized trial to demonstrate that shorter therapy can be provided in uncomplicated staphylococcal blood stream infections without increasing risk of serious adverse events.”

[email protected]

SAN DIEGO – By standardizing antibiotic treatment for simple and uncomplicated staphylococcal bloodstream infections (BSI), an algorithm effectively shortens therapy and simplifies decision making, according to results of a multinational randomized trial.

“The data from the study confirm that the algorithm achieves more with less and verify that shorter antibiotic courses are sufficient,” reported Thomas L. Holland, MD, an infectious disease specialist at Duke University Hospital in Durham, N.C.

CDC/Janice Haney Carr

Several cases of complicated staphylococcal BSI found their way into the study despite selection criteria designed to enroll only uncomplicated cases. This was inevitable because not all cases destined to become complicated can be identified initially, but outcomes overall still remained similar between the algorithm and standard of care (SOC) groups.

In this study, the patients randomized to algorithm treatment received vancomycin (or daptomycin in allergic or intolerant patients), which was administered for periods of duration based on clinical features. In those randomized to SOC, the choice and duration of antibiotics were left to the discretion of the treating physician without restrictions.

In those with simple staphylococcal BSI, the algorithm called for no further antibiotics beyond what had already been administered empirically prior to randomization. Key features of simple coagulase-negative staphylococcal (CONS) BSIs include absence of fever or evidence of metastatic infection, as well as no more than one positive follow-up blood culture. The key features of simple Staphylococcus aureus BSI are similar. However, no positive blood cultures are required for S. aureus BSI to be classified as simple.

“In the algorithm arm, no antibiotics were given to those with simple staphylococcal BSI unless antibiotics had been given prior to randomization,” Dr. Holland explained, but he acknowledged that empiric antibiotics prior to randomization reflect “clinical reality.”

In those with uncomplicated rather than simple staphylococcal BSI, vancomycin was given for 5 days to those with CONS BSI and for 14 days to those with S. aureus BSI. In those who were randomized and then subsequently found to have a complicated infection, defined as multiple positive blood cultures or evidence of metastatic infection, patients received as few as 7 days or as many as 28 days of antibiotics, “reflecting the heterogeneity of these infections,” Dr. Holland reported at an annual scientific meeting on infectious diseases.

The coprimary endpoints were treatment success at test of cure and treatment safety, both of which were adjudicated by an external committee consisting of infectious disease specialists blinded to the therapy.

There were 509 patients from 16 sites in both the United States and Spain. CONS BSIs represented approximately 75% of patients in both arms. The complicated staphylococcal infections, which also were evenly distributed in the two arms, were included in the intention-to-treat analysis. Of complicated staphylococcal infections in this study, the pathogen was CONS in 34 instances and S. aureus in 37.

Treatment success was achieved in 82.0% and 81.5% of patients in the algorithm and SOC arms, respectively. Significant adverse events occurred in 32.9% and 28.3% of patients, respectively. Neither difference approached statistical significance.

“In other words, the algorithm was as effective and safe as standard of care,” Dr. Holland confirmed.

However, the median duration of treatment was reduced substantially for those randomized to the algorithm arm, compared with that seen in the standard of care arm. Among evaluable patients without complicated BSI, the mean duration of therapy was 4.4 days in the algorithm group vs. 6.2 days in the SOC group (P = .003). Most of this nearly 2-day reduction in treatment was achieved in uncomplicated CONS BSI patients. In this group, the mean days of treatment were 5.3 days and 8.4 days for the algorithm and SOC groups, respectively. In the uncomplicated S. aureus group, the reduction (from 15.9 to 15.3 days) was not significant.

“The study has several messages. For one, it suggests that patients who meet the criteria of simple staphylococcal BSI can be managed safely with monitoring alone. In addition, this study “provides the best evidence to date that 14 days of vancomycin from the first negative blood culture is sufficient in uncomplicated S. aureus bloodstream infections,” Dr. Holland stated.

“For many, these data will validate what they are already doing,” said Dr. Holland, who reported that the algorithm is now being applied routinely at his institution. “The value is that we now have a randomized trial to demonstrate that shorter therapy can be provided in uncomplicated staphylococcal blood stream infections without increasing risk of serious adverse events.”

[email protected]

SAN DIEGO – By standardizing antibiotic treatment for simple and uncomplicated staphylococcal bloodstream infections (BSI), an algorithm effectively shortens therapy and simplifies decision making, according to results of a multinational randomized trial.

“The data from the study confirm that the algorithm achieves more with less and verify that shorter antibiotic courses are sufficient,” reported Thomas L. Holland, MD, an infectious disease specialist at Duke University Hospital in Durham, N.C.

CDC/Janice Haney Carr

Several cases of complicated staphylococcal BSI found their way into the study despite selection criteria designed to enroll only uncomplicated cases. This was inevitable because not all cases destined to become complicated can be identified initially, but outcomes overall still remained similar between the algorithm and standard of care (SOC) groups.

In this study, the patients randomized to algorithm treatment received vancomycin (or daptomycin in allergic or intolerant patients), which was administered for periods of duration based on clinical features. In those randomized to SOC, the choice and duration of antibiotics were left to the discretion of the treating physician without restrictions.

In those with simple staphylococcal BSI, the algorithm called for no further antibiotics beyond what had already been administered empirically prior to randomization. Key features of simple coagulase-negative staphylococcal (CONS) BSIs include absence of fever or evidence of metastatic infection, as well as no more than one positive follow-up blood culture. The key features of simple Staphylococcus aureus BSI are similar. However, no positive blood cultures are required for S. aureus BSI to be classified as simple.

“In the algorithm arm, no antibiotics were given to those with simple staphylococcal BSI unless antibiotics had been given prior to randomization,” Dr. Holland explained, but he acknowledged that empiric antibiotics prior to randomization reflect “clinical reality.”

In those with uncomplicated rather than simple staphylococcal BSI, vancomycin was given for 5 days to those with CONS BSI and for 14 days to those with S. aureus BSI. In those who were randomized and then subsequently found to have a complicated infection, defined as multiple positive blood cultures or evidence of metastatic infection, patients received as few as 7 days or as many as 28 days of antibiotics, “reflecting the heterogeneity of these infections,” Dr. Holland reported at an annual scientific meeting on infectious diseases.

The coprimary endpoints were treatment success at test of cure and treatment safety, both of which were adjudicated by an external committee consisting of infectious disease specialists blinded to the therapy.

There were 509 patients from 16 sites in both the United States and Spain. CONS BSIs represented approximately 75% of patients in both arms. The complicated staphylococcal infections, which also were evenly distributed in the two arms, were included in the intention-to-treat analysis. Of complicated staphylococcal infections in this study, the pathogen was CONS in 34 instances and S. aureus in 37.

Treatment success was achieved in 82.0% and 81.5% of patients in the algorithm and SOC arms, respectively. Significant adverse events occurred in 32.9% and 28.3% of patients, respectively. Neither difference approached statistical significance.

“In other words, the algorithm was as effective and safe as standard of care,” Dr. Holland confirmed.

However, the median duration of treatment was reduced substantially for those randomized to the algorithm arm, compared with that seen in the standard of care arm. Among evaluable patients without complicated BSI, the mean duration of therapy was 4.4 days in the algorithm group vs. 6.2 days in the SOC group (P = .003). Most of this nearly 2-day reduction in treatment was achieved in uncomplicated CONS BSI patients. In this group, the mean days of treatment were 5.3 days and 8.4 days for the algorithm and SOC groups, respectively. In the uncomplicated S. aureus group, the reduction (from 15.9 to 15.3 days) was not significant.

“The study has several messages. For one, it suggests that patients who meet the criteria of simple staphylococcal BSI can be managed safely with monitoring alone. In addition, this study “provides the best evidence to date that 14 days of vancomycin from the first negative blood culture is sufficient in uncomplicated S. aureus bloodstream infections,” Dr. Holland stated.

“For many, these data will validate what they are already doing,” said Dr. Holland, who reported that the algorithm is now being applied routinely at his institution. “The value is that we now have a randomized trial to demonstrate that shorter therapy can be provided in uncomplicated staphylococcal blood stream infections without increasing risk of serious adverse events.”

[email protected]

 

SAN DIEGO – Add neurologic issues to the growing list of medical problems faced by survivors of Ebola virus.

Among 153 Liberian patients about a year out from their acute illness, “there were only a handful who didn’t have” some lingering neurologic problem. “The most commonly reported ongoing symptoms were headache and memory loss. A couple of people had seizures possibly related to Ebola.” Depression, anxiety, and posttraumatic stress disorder were common, said neurologist Jeanne Billioux, MD, a clinical fellow at the National Institute of Neurological Disorders and Stroke, Bethesda, Md.

Almost two-thirds of the patients had abnormal neurologic exams. The most common findings were tremors, pathological reflexes, mild dysmetria, and abnormalities of eye pursuits and saccades, plus nystagmus. The findings were statistically significant, compared with 81 close contacts, generally household members, who served as controls in the ongoing natural history study, which was presented at the annual meeting of the American Neurological Association.

“It was really surprising to me that” so many “people had abnormal neurologic exams.” For the most part, “they weren’t overtly abnormal compared to the controls, but you could tell the difference. They mentated more slowly, had issues with cranial nerves, and things like that. They couldn’t function the way they did before. We did not realize Ebola affected the CNS as much as it does,” Dr. Billioux said.

What’s become clear in the wake of the recent outbreak in West Africa, by far the worst to date with over 28,000 cases and more than 11,000 deaths, is that there is a post-Ebola syndrome that includes ophthalmologic, cardiac, and rheumatologic problems. It now appears that “neurologic sequelae are a part of it,” as well, she said.

The natural history study – dubbed the Partnership for Research on Ebola Virus in Liberia (PREVAIL III) – is a collaboration between the National Institutes of Health and the Ministry of Health of Liberia, one of the hardest-hit countries; the neurology investigation is just one component of the study, which includes about 1,500 patients overall.

Serology testing confirmed that cases truly did have Ebola, and the controls did not. After the first evaluation a year or so after the acute illness, patients have been followed up every 6 months, with some out to about 3 years.

Although patients aren’t back to normal, the good news is that their symptoms and exams are improving. “We started with only 6 who had no symptoms; now we have 15. Headaches are getting better; memory is getting better. It’s wonderful,” Dr. Billioux said.

The patients were asked to recall their acute symptoms during their first study visit. Many reported headaches, weakness, altered mental status, and cranial nerve symptoms. About 2% described convulsions or strokelike symptoms, and about 25% described symptoms consistent with meningitis.

It’s unclear how the virus affected the CNS, which isn’t considered to be a target organ. Perhaps fluid loss from severe diarrhea led to cerebral hypoperfusion. The cytokine storm during the acute phase might also have played a role. The virus has, however, been isolated from cerebral spinal fluid and, although uncommon, there are the reports of meningitis symptoms, so perhaps it does have direct CNS effects. Much remains to be learned.

Both cases and controls were a mean of about 35 years old, and evenly split between the sexes; 108 patients (70.6%) spent more than 2 weeks in an Ebola treatment unit.

The work was funded by the National Institutes of Health. Dr. Billioux had no disclosures.

[email protected]

 

SAN DIEGO – Add neurologic issues to the growing list of medical problems faced by survivors of Ebola virus.

Among 153 Liberian patients about a year out from their acute illness, “there were only a handful who didn’t have” some lingering neurologic problem. “The most commonly reported ongoing symptoms were headache and memory loss. A couple of people had seizures possibly related to Ebola.” Depression, anxiety, and posttraumatic stress disorder were common, said neurologist Jeanne Billioux, MD, a clinical fellow at the National Institute of Neurological Disorders and Stroke, Bethesda, Md.

Almost two-thirds of the patients had abnormal neurologic exams. The most common findings were tremors, pathological reflexes, mild dysmetria, and abnormalities of eye pursuits and saccades, plus nystagmus. The findings were statistically significant, compared with 81 close contacts, generally household members, who served as controls in the ongoing natural history study, which was presented at the annual meeting of the American Neurological Association.

“It was really surprising to me that” so many “people had abnormal neurologic exams.” For the most part, “they weren’t overtly abnormal compared to the controls, but you could tell the difference. They mentated more slowly, had issues with cranial nerves, and things like that. They couldn’t function the way they did before. We did not realize Ebola affected the CNS as much as it does,” Dr. Billioux said.

What’s become clear in the wake of the recent outbreak in West Africa, by far the worst to date with over 28,000 cases and more than 11,000 deaths, is that there is a post-Ebola syndrome that includes ophthalmologic, cardiac, and rheumatologic problems. It now appears that “neurologic sequelae are a part of it,” as well, she said.

The natural history study – dubbed the Partnership for Research on Ebola Virus in Liberia (PREVAIL III) – is a collaboration between the National Institutes of Health and the Ministry of Health of Liberia, one of the hardest-hit countries; the neurology investigation is just one component of the study, which includes about 1,500 patients overall.

Serology testing confirmed that cases truly did have Ebola, and the controls did not. After the first evaluation a year or so after the acute illness, patients have been followed up every 6 months, with some out to about 3 years.

Although patients aren’t back to normal, the good news is that their symptoms and exams are improving. “We started with only 6 who had no symptoms; now we have 15. Headaches are getting better; memory is getting better. It’s wonderful,” Dr. Billioux said.

The patients were asked to recall their acute symptoms during their first study visit. Many reported headaches, weakness, altered mental status, and cranial nerve symptoms. About 2% described convulsions or strokelike symptoms, and about 25% described symptoms consistent with meningitis.

It’s unclear how the virus affected the CNS, which isn’t considered to be a target organ. Perhaps fluid loss from severe diarrhea led to cerebral hypoperfusion. The cytokine storm during the acute phase might also have played a role. The virus has, however, been isolated from cerebral spinal fluid and, although uncommon, there are the reports of meningitis symptoms, so perhaps it does have direct CNS effects. Much remains to be learned.

Both cases and controls were a mean of about 35 years old, and evenly split between the sexes; 108 patients (70.6%) spent more than 2 weeks in an Ebola treatment unit.

The work was funded by the National Institutes of Health. Dr. Billioux had no disclosures.

[email protected]

 

SAN DIEGO – Add neurologic issues to the growing list of medical problems faced by survivors of Ebola virus.

Among 153 Liberian patients about a year out from their acute illness, “there were only a handful who didn’t have” some lingering neurologic problem. “The most commonly reported ongoing symptoms were headache and memory loss. A couple of people had seizures possibly related to Ebola.” Depression, anxiety, and posttraumatic stress disorder were common, said neurologist Jeanne Billioux, MD, a clinical fellow at the National Institute of Neurological Disorders and Stroke, Bethesda, Md.

Almost two-thirds of the patients had abnormal neurologic exams. The most common findings were tremors, pathological reflexes, mild dysmetria, and abnormalities of eye pursuits and saccades, plus nystagmus. The findings were statistically significant, compared with 81 close contacts, generally household members, who served as controls in the ongoing natural history study, which was presented at the annual meeting of the American Neurological Association.

“It was really surprising to me that” so many “people had abnormal neurologic exams.” For the most part, “they weren’t overtly abnormal compared to the controls, but you could tell the difference. They mentated more slowly, had issues with cranial nerves, and things like that. They couldn’t function the way they did before. We did not realize Ebola affected the CNS as much as it does,” Dr. Billioux said.

What’s become clear in the wake of the recent outbreak in West Africa, by far the worst to date with over 28,000 cases and more than 11,000 deaths, is that there is a post-Ebola syndrome that includes ophthalmologic, cardiac, and rheumatologic problems. It now appears that “neurologic sequelae are a part of it,” as well, she said.

The natural history study – dubbed the Partnership for Research on Ebola Virus in Liberia (PREVAIL III) – is a collaboration between the National Institutes of Health and the Ministry of Health of Liberia, one of the hardest-hit countries; the neurology investigation is just one component of the study, which includes about 1,500 patients overall.

Serology testing confirmed that cases truly did have Ebola, and the controls did not. After the first evaluation a year or so after the acute illness, patients have been followed up every 6 months, with some out to about 3 years.

Although patients aren’t back to normal, the good news is that their symptoms and exams are improving. “We started with only 6 who had no symptoms; now we have 15. Headaches are getting better; memory is getting better. It’s wonderful,” Dr. Billioux said.

The patients were asked to recall their acute symptoms during their first study visit. Many reported headaches, weakness, altered mental status, and cranial nerve symptoms. About 2% described convulsions or strokelike symptoms, and about 25% described symptoms consistent with meningitis.

It’s unclear how the virus affected the CNS, which isn’t considered to be a target organ. Perhaps fluid loss from severe diarrhea led to cerebral hypoperfusion. The cytokine storm during the acute phase might also have played a role. The virus has, however, been isolated from cerebral spinal fluid and, although uncommon, there are the reports of meningitis symptoms, so perhaps it does have direct CNS effects. Much remains to be learned.

Both cases and controls were a mean of about 35 years old, and evenly split between the sexes; 108 patients (70.6%) spent more than 2 weeks in an Ebola treatment unit.

The work was funded by the National Institutes of Health. Dr. Billioux had no disclosures.

[email protected]

SAN DIEGO – Antibiotic prescriptions written by dentists make a substantial but largely unrecognized contribution to the risk of community-acquired Clostridium difficile (CA-CDI) infections, according to results of a public health initiative that was presented at an annual scientific meeting on infectious diseases.

When nearly 1,000 cases of CA-CDI suspected of being the result of antibiotic exposure were evaluated, it was found that 15% of the prescriptions were written by dentists, often for indications that are counter to current guidelines, reported Maria Bye, MPH, an officer in the Infectious Disease Epidemiology, Prevention, and Control Division of the Minnesota Department of Health, St. Paul.

“Everyone plays a role in antibiotic stewardship. Dentists should be following the guidelines for antibiotic prophylaxis and counsel patients about the risk and symptoms of C. diff and other complications,” Ms. Bye said. She said that up until now “dentists have largely been left out of the conversation.”

In another finding from this study relevant to infection control, a substantial proportion of dentist-prescribed antibiotics associated with CA-CDI were not in the medical record. Rather, they were discovered in interviews conducted to isolate risk factors. “This is concerning since clinicians unaware of these exposures will not think about CA-CDI or other complications of antibiotic use, possibly delaying therapy,” Ms. Bye said.

The importance of dental antibiotic prescriptions in CA-CDI was identified in an ongoing infectious disease program managed by the Minnesota Department of Health in collaboration with the Centers for Disease Control and Prevention. In the years 2009-2015, medical records and interviews were conducted to identify risk factors in 1,626 confirmed cases of CA-CDI in five Minnesota counties. All cases were among patients without an overnight stay in a health care facility in the previous 12 weeks, which was an exclusion criterion.

After the review of medical records and patient interviews, 926 (57%) of the CA-CDI cases were deemed likely to be related to antibiotic exposure. Of these antibiotic exposures, 136 (15%) were from prescriptions written by dentists, a figure reached only when patients were interviewed. According to Ms. Bye, 34% of the antibiotics prescribed by dentists were not in the medical record.

There were also notable differences in antibiotic exposures stemming from dentist prescriptions relative to prescriptions from other sources. Perhaps most significantly, dental-related antibiotic prescriptions were far more likely to be for clindamycin (50% vs. 10%; P less than .001), which is commonly associated with increased risk of C. difficile, according to Ms. Bye. Fluoroquinolones (6% vs. 19%; P less than .001) and cephalosporins (7% vs. 30%; P less than .001) were significantly less likely to be prescribed by dentists. Patients who developed CA-CDI associated with antibiotics prescribed by dentists were also significantly older than were those receiving antibiotics from another source (mean age 57 years vs. 45 years; P less than .001).

For the first years of this analysis, information on the indication for dentist-prescribed antibiotics was not collected, but these data were collected beginning in 2015. In the data collected so far, a substantial proportion of prescriptions were written for prophylaxis against systemic infections, including prevention of endocarditis or infection of prosthetic joints. However, few of these prescriptions were indicated.

“The American Dental Association stated that antibiotic prophylaxis is not generally recommended in patients with prosthetic joints,” said Ms. Bye, noting that this is consistent with similar statements issued by the American Academy of Orthopedic Surgery. In 2007, the American Heart Association narrowed its recommendations for prophylactic antibiotics to patients at the highest risk of adverse consequences from endocarditis.

Of the four patients who received prophylactic antibiotics from their dentists for a cardiovascular or orthopedic indication, only one met current criteria, Ms. Bye reported.

The contribution of antibiotic exposures from dentist prescriptions to CA-CDI should not be surprising, according to Ms. Bye. In the United States, dentists prescribe 10% of all outpatient antibiotics. Although there are many valid indications for these prescriptions, Ms. Bye cited a survey that found that the proportion of dentists familiar with current guidelines and the risks of adverse events produced by antibiotics, including CA-CDI, is less than 50%.

“Dentists need to be included in antibiotic stewardship programs,” she advised. This will include educating dentists about the indications for antibiotic prophylaxis for medical conditions. She also suggested that clinicians should routinely ask patients about whether they have received antibiotics from a dentist so that this information gets into the medical record.

The event was the combined annual meetings of the Infectious Diseases Society of America, the Society for Healthcare Epidemiology of America, the HIV Medicine Association, and the Pediatric Infectious Diseases Society.

 

[email protected]

SAN DIEGO – Antibiotic prescriptions written by dentists make a substantial but largely unrecognized contribution to the risk of community-acquired Clostridium difficile (CA-CDI) infections, according to results of a public health initiative that was presented at an annual scientific meeting on infectious diseases.

When nearly 1,000 cases of CA-CDI suspected of being the result of antibiotic exposure were evaluated, it was found that 15% of the prescriptions were written by dentists, often for indications that are counter to current guidelines, reported Maria Bye, MPH, an officer in the Infectious Disease Epidemiology, Prevention, and Control Division of the Minnesota Department of Health, St. Paul.

“Everyone plays a role in antibiotic stewardship. Dentists should be following the guidelines for antibiotic prophylaxis and counsel patients about the risk and symptoms of C. diff and other complications,” Ms. Bye said. She said that up until now “dentists have largely been left out of the conversation.”

In another finding from this study relevant to infection control, a substantial proportion of dentist-prescribed antibiotics associated with CA-CDI were not in the medical record. Rather, they were discovered in interviews conducted to isolate risk factors. “This is concerning since clinicians unaware of these exposures will not think about CA-CDI or other complications of antibiotic use, possibly delaying therapy,” Ms. Bye said.

The importance of dental antibiotic prescriptions in CA-CDI was identified in an ongoing infectious disease program managed by the Minnesota Department of Health in collaboration with the Centers for Disease Control and Prevention. In the years 2009-2015, medical records and interviews were conducted to identify risk factors in 1,626 confirmed cases of CA-CDI in five Minnesota counties. All cases were among patients without an overnight stay in a health care facility in the previous 12 weeks, which was an exclusion criterion.

After the review of medical records and patient interviews, 926 (57%) of the CA-CDI cases were deemed likely to be related to antibiotic exposure. Of these antibiotic exposures, 136 (15%) were from prescriptions written by dentists, a figure reached only when patients were interviewed. According to Ms. Bye, 34% of the antibiotics prescribed by dentists were not in the medical record.

There were also notable differences in antibiotic exposures stemming from dentist prescriptions relative to prescriptions from other sources. Perhaps most significantly, dental-related antibiotic prescriptions were far more likely to be for clindamycin (50% vs. 10%; P less than .001), which is commonly associated with increased risk of C. difficile, according to Ms. Bye. Fluoroquinolones (6% vs. 19%; P less than .001) and cephalosporins (7% vs. 30%; P less than .001) were significantly less likely to be prescribed by dentists. Patients who developed CA-CDI associated with antibiotics prescribed by dentists were also significantly older than were those receiving antibiotics from another source (mean age 57 years vs. 45 years; P less than .001).

For the first years of this analysis, information on the indication for dentist-prescribed antibiotics was not collected, but these data were collected beginning in 2015. In the data collected so far, a substantial proportion of prescriptions were written for prophylaxis against systemic infections, including prevention of endocarditis or infection of prosthetic joints. However, few of these prescriptions were indicated.

“The American Dental Association stated that antibiotic prophylaxis is not generally recommended in patients with prosthetic joints,” said Ms. Bye, noting that this is consistent with similar statements issued by the American Academy of Orthopedic Surgery. In 2007, the American Heart Association narrowed its recommendations for prophylactic antibiotics to patients at the highest risk of adverse consequences from endocarditis.

Of the four patients who received prophylactic antibiotics from their dentists for a cardiovascular or orthopedic indication, only one met current criteria, Ms. Bye reported.

The contribution of antibiotic exposures from dentist prescriptions to CA-CDI should not be surprising, according to Ms. Bye. In the United States, dentists prescribe 10% of all outpatient antibiotics. Although there are many valid indications for these prescriptions, Ms. Bye cited a survey that found that the proportion of dentists familiar with current guidelines and the risks of adverse events produced by antibiotics, including CA-CDI, is less than 50%.

“Dentists need to be included in antibiotic stewardship programs,” she advised. This will include educating dentists about the indications for antibiotic prophylaxis for medical conditions. She also suggested that clinicians should routinely ask patients about whether they have received antibiotics from a dentist so that this information gets into the medical record.

The event was the combined annual meetings of the Infectious Diseases Society of America, the Society for Healthcare Epidemiology of America, the HIV Medicine Association, and the Pediatric Infectious Diseases Society.

 

[email protected]

SAN DIEGO – Antibiotic prescriptions written by dentists make a substantial but largely unrecognized contribution to the risk of community-acquired Clostridium difficile (CA-CDI) infections, according to results of a public health initiative that was presented at an annual scientific meeting on infectious diseases.

When nearly 1,000 cases of CA-CDI suspected of being the result of antibiotic exposure were evaluated, it was found that 15% of the prescriptions were written by dentists, often for indications that are counter to current guidelines, reported Maria Bye, MPH, an officer in the Infectious Disease Epidemiology, Prevention, and Control Division of the Minnesota Department of Health, St. Paul.

“Everyone plays a role in antibiotic stewardship. Dentists should be following the guidelines for antibiotic prophylaxis and counsel patients about the risk and symptoms of C. diff and other complications,” Ms. Bye said. She said that up until now “dentists have largely been left out of the conversation.”

In another finding from this study relevant to infection control, a substantial proportion of dentist-prescribed antibiotics associated with CA-CDI were not in the medical record. Rather, they were discovered in interviews conducted to isolate risk factors. “This is concerning since clinicians unaware of these exposures will not think about CA-CDI or other complications of antibiotic use, possibly delaying therapy,” Ms. Bye said.

The importance of dental antibiotic prescriptions in CA-CDI was identified in an ongoing infectious disease program managed by the Minnesota Department of Health in collaboration with the Centers for Disease Control and Prevention. In the years 2009-2015, medical records and interviews were conducted to identify risk factors in 1,626 confirmed cases of CA-CDI in five Minnesota counties. All cases were among patients without an overnight stay in a health care facility in the previous 12 weeks, which was an exclusion criterion.

After the review of medical records and patient interviews, 926 (57%) of the CA-CDI cases were deemed likely to be related to antibiotic exposure. Of these antibiotic exposures, 136 (15%) were from prescriptions written by dentists, a figure reached only when patients were interviewed. According to Ms. Bye, 34% of the antibiotics prescribed by dentists were not in the medical record.

There were also notable differences in antibiotic exposures stemming from dentist prescriptions relative to prescriptions from other sources. Perhaps most significantly, dental-related antibiotic prescriptions were far more likely to be for clindamycin (50% vs. 10%; P less than .001), which is commonly associated with increased risk of C. difficile, according to Ms. Bye. Fluoroquinolones (6% vs. 19%; P less than .001) and cephalosporins (7% vs. 30%; P less than .001) were significantly less likely to be prescribed by dentists. Patients who developed CA-CDI associated with antibiotics prescribed by dentists were also significantly older than were those receiving antibiotics from another source (mean age 57 years vs. 45 years; P less than .001).

For the first years of this analysis, information on the indication for dentist-prescribed antibiotics was not collected, but these data were collected beginning in 2015. In the data collected so far, a substantial proportion of prescriptions were written for prophylaxis against systemic infections, including prevention of endocarditis or infection of prosthetic joints. However, few of these prescriptions were indicated.

“The American Dental Association stated that antibiotic prophylaxis is not generally recommended in patients with prosthetic joints,” said Ms. Bye, noting that this is consistent with similar statements issued by the American Academy of Orthopedic Surgery. In 2007, the American Heart Association narrowed its recommendations for prophylactic antibiotics to patients at the highest risk of adverse consequences from endocarditis.

Of the four patients who received prophylactic antibiotics from their dentists for a cardiovascular or orthopedic indication, only one met current criteria, Ms. Bye reported.

The contribution of antibiotic exposures from dentist prescriptions to CA-CDI should not be surprising, according to Ms. Bye. In the United States, dentists prescribe 10% of all outpatient antibiotics. Although there are many valid indications for these prescriptions, Ms. Bye cited a survey that found that the proportion of dentists familiar with current guidelines and the risks of adverse events produced by antibiotics, including CA-CDI, is less than 50%.

“Dentists need to be included in antibiotic stewardship programs,” she advised. This will include educating dentists about the indications for antibiotic prophylaxis for medical conditions. She also suggested that clinicians should routinely ask patients about whether they have received antibiotics from a dentist so that this information gets into the medical record.

The event was the combined annual meetings of the Infectious Diseases Society of America, the Society for Healthcare Epidemiology of America, the HIV Medicine Association, and the Pediatric Infectious Diseases Society.

 

[email protected]

 

SAN DIEGO – Typhus in many forms, particularly scrub typhus, has reemerged worldwide, but none of these rickettsial infections poses a significant public health threat if promptly diagnosed, according to an update presented at an annual scientific meeting on infectious diseases.

Scrub typhus, which is spread by several species of trombiculid mites or chiggers, poses a large threat in regard to typhus epidemics, particularly in Asia, but sporadic cases of different types of typhus are being seen everywhere, including in the United States, according to George M. Varghese, MD, department of infectious diseases, Christian Medical College, Vellore, India.

“The typhus diseases are clinically similar but epidemiologically and etiologically distinct,” reported Dr. Varghese, “but doxycycline is the drug of choice for almost all of the rickettsial infections.”

The bacteria responsible for scrub typhus is Orientia tsutsugamushi, which is no longer included in the genus Rickettsia, but Dr. Varghese, who has published frequently on the epidemiology of scrub typhus, said that it is still appropriately grouped among rickettsial infections. It shares many features with the other rickettsioses, which were considered to be fading but are now resurging after the large epidemics that occurred prior to the introduction of antibiotics.

In the World Wars, Rickettsia prowazekii – which is carried and spread by body lice – was the most well known typhus threat. According to Dr. Varghese, this bacterium may have killed more soldiers in these conflicts than did firearms. Although R. prowazekii has not disappeared as a source of typhus outbreaks, particularly in South America and Africa, there are current epidemics produced from rickettsial infections carried by fleas, such as R. typhi, or ticks, like R. rickettsii, or mice, like R. felis.

For clinical detection of these forms of typhus, there are differences. Although all are associated with a rapid onset of fever, headache, and myalgia, subtle signs can be helpful in making a diagnosis while waiting for laboratory confirmation. For example, scrub typhus, unlike Rocky Mountain Fever, which is caused by tick bites, does not generally include a rash. Rather, eschars, which are small patches of necrotic skin, are far more characteristic.

“Serological tests are the most common diagnostic tool for typhus, but serology may not allow early diagnosis. You can obtain a false positive in the early stages of disease,” Dr. Varghese warned. To speed the diagnosis, he said that looking for the clinical clues characteristic of the suspected form of typhus, such as the scrub typhus-associated eschar, “is valuable.” However, he also emphasized that even with positive serology results, “good epidemiology and history is helpful for laboratory interpretation.”

A variety of serological tests can identify typhus pathogens, but ELISA is now the most widely used, according to Dr. Varghese, noting that this test offers a sensitivity of 93% and a specificity of 91%. Both are higher than those provided by alternatives. As a result of improved sensitivity of diagnostic tests, prevalence rates of some forms of typhus have proved to be unexpectedly high. For example, in a study undertaken in his region of India, the seroprevalence of scrub typhus was 31.8% (Trop Med Int Health. 2017;22:576-82. doi: 10.1111/tmi.12853).

Of unmet needs in the clinical management of typhus, Dr. Varghese listed better strategies for point-of-care diagnosis and treatment and better data on how to manage patients who are severely ill. Advanced disease, which is common to rural areas with limited access to health care, is the source of almost all typhus mortality, according to Dr. Varghese. He described a trial now being initiated in severe disease that will compare intravenous doxycycline to IV azithromycin and to a combination of both IV doxycycline and azithromycin.

Although Dr. Varghese cautioned that reports of resistant typhus infections, particularly in Thailand, might prove to be the next big clinical challenge in typhus, he said that progress is being made toward reducing the burden of this disease in his area of the world. In a disease associated with a mortality of 50% if left untreated, he attributes gains to earlier diagnosis and prompt treatment.

At his medical center, “we have been working with this disease for a decade and a half,” he said, referring to scrub typhus. “When we started off, the mortality was around 15% after diagnosis. Today, the mortality is about 5%-7%.”

Dr. Varghese reported that he has no financial relationships relevant to this topic. The event was the combined annual meetings of the Infectious Diseases Society of America, the Society for Healthcare Epidemiology of America, the HIV Medicine Association, and the Pediatric Infectious Diseases Society.

 

SAN DIEGO – Typhus in many forms, particularly scrub typhus, has reemerged worldwide, but none of these rickettsial infections poses a significant public health threat if promptly diagnosed, according to an update presented at an annual scientific meeting on infectious diseases.

Scrub typhus, which is spread by several species of trombiculid mites or chiggers, poses a large threat in regard to typhus epidemics, particularly in Asia, but sporadic cases of different types of typhus are being seen everywhere, including in the United States, according to George M. Varghese, MD, department of infectious diseases, Christian Medical College, Vellore, India.

“The typhus diseases are clinically similar but epidemiologically and etiologically distinct,” reported Dr. Varghese, “but doxycycline is the drug of choice for almost all of the rickettsial infections.”

The bacteria responsible for scrub typhus is Orientia tsutsugamushi, which is no longer included in the genus Rickettsia, but Dr. Varghese, who has published frequently on the epidemiology of scrub typhus, said that it is still appropriately grouped among rickettsial infections. It shares many features with the other rickettsioses, which were considered to be fading but are now resurging after the large epidemics that occurred prior to the introduction of antibiotics.

In the World Wars, Rickettsia prowazekii – which is carried and spread by body lice – was the most well known typhus threat. According to Dr. Varghese, this bacterium may have killed more soldiers in these conflicts than did firearms. Although R. prowazekii has not disappeared as a source of typhus outbreaks, particularly in South America and Africa, there are current epidemics produced from rickettsial infections carried by fleas, such as R. typhi, or ticks, like R. rickettsii, or mice, like R. felis.

For clinical detection of these forms of typhus, there are differences. Although all are associated with a rapid onset of fever, headache, and myalgia, subtle signs can be helpful in making a diagnosis while waiting for laboratory confirmation. For example, scrub typhus, unlike Rocky Mountain Fever, which is caused by tick bites, does not generally include a rash. Rather, eschars, which are small patches of necrotic skin, are far more characteristic.

“Serological tests are the most common diagnostic tool for typhus, but serology may not allow early diagnosis. You can obtain a false positive in the early stages of disease,” Dr. Varghese warned. To speed the diagnosis, he said that looking for the clinical clues characteristic of the suspected form of typhus, such as the scrub typhus-associated eschar, “is valuable.” However, he also emphasized that even with positive serology results, “good epidemiology and history is helpful for laboratory interpretation.”

A variety of serological tests can identify typhus pathogens, but ELISA is now the most widely used, according to Dr. Varghese, noting that this test offers a sensitivity of 93% and a specificity of 91%. Both are higher than those provided by alternatives. As a result of improved sensitivity of diagnostic tests, prevalence rates of some forms of typhus have proved to be unexpectedly high. For example, in a study undertaken in his region of India, the seroprevalence of scrub typhus was 31.8% (Trop Med Int Health. 2017;22:576-82. doi: 10.1111/tmi.12853).

Of unmet needs in the clinical management of typhus, Dr. Varghese listed better strategies for point-of-care diagnosis and treatment and better data on how to manage patients who are severely ill. Advanced disease, which is common to rural areas with limited access to health care, is the source of almost all typhus mortality, according to Dr. Varghese. He described a trial now being initiated in severe disease that will compare intravenous doxycycline to IV azithromycin and to a combination of both IV doxycycline and azithromycin.

Although Dr. Varghese cautioned that reports of resistant typhus infections, particularly in Thailand, might prove to be the next big clinical challenge in typhus, he said that progress is being made toward reducing the burden of this disease in his area of the world. In a disease associated with a mortality of 50% if left untreated, he attributes gains to earlier diagnosis and prompt treatment.

At his medical center, “we have been working with this disease for a decade and a half,” he said, referring to scrub typhus. “When we started off, the mortality was around 15% after diagnosis. Today, the mortality is about 5%-7%.”

Dr. Varghese reported that he has no financial relationships relevant to this topic. The event was the combined annual meetings of the Infectious Diseases Society of America, the Society for Healthcare Epidemiology of America, the HIV Medicine Association, and the Pediatric Infectious Diseases Society.

 

SAN DIEGO – Typhus in many forms, particularly scrub typhus, has reemerged worldwide, but none of these rickettsial infections poses a significant public health threat if promptly diagnosed, according to an update presented at an annual scientific meeting on infectious diseases.

Scrub typhus, which is spread by several species of trombiculid mites or chiggers, poses a large threat in regard to typhus epidemics, particularly in Asia, but sporadic cases of different types of typhus are being seen everywhere, including in the United States, according to George M. Varghese, MD, department of infectious diseases, Christian Medical College, Vellore, India.

“The typhus diseases are clinically similar but epidemiologically and etiologically distinct,” reported Dr. Varghese, “but doxycycline is the drug of choice for almost all of the rickettsial infections.”

The bacteria responsible for scrub typhus is Orientia tsutsugamushi, which is no longer included in the genus Rickettsia, but Dr. Varghese, who has published frequently on the epidemiology of scrub typhus, said that it is still appropriately grouped among rickettsial infections. It shares many features with the other rickettsioses, which were considered to be fading but are now resurging after the large epidemics that occurred prior to the introduction of antibiotics.

In the World Wars, Rickettsia prowazekii – which is carried and spread by body lice – was the most well known typhus threat. According to Dr. Varghese, this bacterium may have killed more soldiers in these conflicts than did firearms. Although R. prowazekii has not disappeared as a source of typhus outbreaks, particularly in South America and Africa, there are current epidemics produced from rickettsial infections carried by fleas, such as R. typhi, or ticks, like R. rickettsii, or mice, like R. felis.

For clinical detection of these forms of typhus, there are differences. Although all are associated with a rapid onset of fever, headache, and myalgia, subtle signs can be helpful in making a diagnosis while waiting for laboratory confirmation. For example, scrub typhus, unlike Rocky Mountain Fever, which is caused by tick bites, does not generally include a rash. Rather, eschars, which are small patches of necrotic skin, are far more characteristic.

“Serological tests are the most common diagnostic tool for typhus, but serology may not allow early diagnosis. You can obtain a false positive in the early stages of disease,” Dr. Varghese warned. To speed the diagnosis, he said that looking for the clinical clues characteristic of the suspected form of typhus, such as the scrub typhus-associated eschar, “is valuable.” However, he also emphasized that even with positive serology results, “good epidemiology and history is helpful for laboratory interpretation.”

A variety of serological tests can identify typhus pathogens, but ELISA is now the most widely used, according to Dr. Varghese, noting that this test offers a sensitivity of 93% and a specificity of 91%. Both are higher than those provided by alternatives. As a result of improved sensitivity of diagnostic tests, prevalence rates of some forms of typhus have proved to be unexpectedly high. For example, in a study undertaken in his region of India, the seroprevalence of scrub typhus was 31.8% (Trop Med Int Health. 2017;22:576-82. doi: 10.1111/tmi.12853).

Of unmet needs in the clinical management of typhus, Dr. Varghese listed better strategies for point-of-care diagnosis and treatment and better data on how to manage patients who are severely ill. Advanced disease, which is common to rural areas with limited access to health care, is the source of almost all typhus mortality, according to Dr. Varghese. He described a trial now being initiated in severe disease that will compare intravenous doxycycline to IV azithromycin and to a combination of both IV doxycycline and azithromycin.

Although Dr. Varghese cautioned that reports of resistant typhus infections, particularly in Thailand, might prove to be the next big clinical challenge in typhus, he said that progress is being made toward reducing the burden of this disease in his area of the world. In a disease associated with a mortality of 50% if left untreated, he attributes gains to earlier diagnosis and prompt treatment.

At his medical center, “we have been working with this disease for a decade and a half,” he said, referring to scrub typhus. “When we started off, the mortality was around 15% after diagnosis. Today, the mortality is about 5%-7%.”

Dr. Varghese reported that he has no financial relationships relevant to this topic. The event was the combined annual meetings of the Infectious Diseases Society of America, the Society for Healthcare Epidemiology of America, the HIV Medicine Association, and the Pediatric Infectious Diseases Society.

 

IDWeek 2017 kicks off Oct. 3 at the San Diego Convention Center, with a focus on pandemic preparedness and other challenges facing infectious diseases clinicians and researchers in the 21st century.

Premeeting workshops and symposia occupy most of the first 2 days of the event, with highlights including a session on managing infections in opioid users and a “late breaker” symposium addressing the latest on the H7N9 outbreak in China, the current findings and recommendations regarding Candida auris, and the epidemiology of the recent Legionella outbreaks in the United States. Another late breaker session focuses on the recent spate of hepatitis A outbreaks, including one in conference host city San Diego, primarily among the homeless population.

IDWeek is the combined annual meeting of the Infectious Diseases Society of America (IDSA), the Society for Healthcare Epidemiology of America (SHEA), the HIV Medicine Association (HIVMA), and the Pediatric Infectious Diseases Society (PIDS). The first IDWeek was held in 2012.

The IDWeek symposia, oral abstract sessions, and poster abstract sessions are the highlights, but the interactive “pro/con” debate sessions should be entertaining and informative. Topics include “Should Your ASP Include the ICU?” and “Is SAAR Ready for Primetime?” Another interactive session – “Diagnostic Clinical Cases” – brings a panel of ID experts together to identify the etiology of challenging clinical cases and to describe diagnostic testing strategies for such cases. Other “pro/con” debates will include a discussion on mandating an annual influenza vaccine for health care workers in acute care settings, and an assessment of the risks and benefits of active surveillance, compared with immediate surgery for persons with a spinal epidural abscess.

One intriguing interactive session – aptly-titled “Nightmare Bugs” – will investigate the problems posed by multidrug-resistant organisms and the need for new antimicrobials to defeat them.

There are many sessions and posters addressing evergreen clinical topics for ID clinicians, such as antimicrobial resistance, antibiotic stewardship, surgical site infections, bacteremia and sepsis, Clostridium difficile, hepatitis care, and HIV care. But the education committee at IDWeek always manages to touch on topics in the news. For instance, one late breaker session will feature a discussion of the nexus between the opioid crisis and infectious diseases, the outbreak of cholera in Yemen, and the epidemiology of the yellow fever outbreak in Brazil.

Featured speakers at the event include James M. Hughes, MD, professor of medicine at Emory University, Atlanta, who will discuss the importance of a One Health approach to emerging microbial threats, and Connie Celum, MD, MPH, professor of global health and medicine, University of Washington, Seattle, who intends to describe the progress in effective HIV prevention interventions and lessons learned in implementation. Neil O. Fishman, MD, of the University of Pennsylvania Perelman School of Medicine, is delivering the annual SHEA lecture at IDWeek, and will explain how ID physicians and epidemiologists can promote interventions to achieve high reliability in health care. Renowned ID researcher Janet Englund, MD, of Seattle Children’s Hospital, will discuss the potential future therapies to prevent or treat respiratory viral infections in high-risk pediatric patients.

The 2017 conference will close with a three-part plenary – “21^st Century Cures” – featuring ID luminaries Christopher Karp, MD, of the Bill & Melinda Gates Foundation, James E. Crowe Jr., MD, of Vanderbilt University Medical Center in Nashville, Tenn., and David Thomas, MD, MPH, of Johns Hopkins University in Baltimore.

[email protected]

On Twitter @richpizzi

 

IDWeek 2017 kicks off Oct. 3 at the San Diego Convention Center, with a focus on pandemic preparedness and other challenges facing infectious diseases clinicians and researchers in the 21st century.

Premeeting workshops and symposia occupy most of the first 2 days of the event, with highlights including a session on managing infections in opioid users and a “late breaker” symposium addressing the latest on the H7N9 outbreak in China, the current findings and recommendations regarding Candida auris, and the epidemiology of the recent Legionella outbreaks in the United States. Another late breaker session focuses on the recent spate of hepatitis A outbreaks, including one in conference host city San Diego, primarily among the homeless population.

IDWeek is the combined annual meeting of the Infectious Diseases Society of America (IDSA), the Society for Healthcare Epidemiology of America (SHEA), the HIV Medicine Association (HIVMA), and the Pediatric Infectious Diseases Society (PIDS). The first IDWeek was held in 2012.

The IDWeek symposia, oral abstract sessions, and poster abstract sessions are the highlights, but the interactive “pro/con” debate sessions should be entertaining and informative. Topics include “Should Your ASP Include the ICU?” and “Is SAAR Ready for Primetime?” Another interactive session – “Diagnostic Clinical Cases” – brings a panel of ID experts together to identify the etiology of challenging clinical cases and to describe diagnostic testing strategies for such cases. Other “pro/con” debates will include a discussion on mandating an annual influenza vaccine for health care workers in acute care settings, and an assessment of the risks and benefits of active surveillance, compared with immediate surgery for persons with a spinal epidural abscess.

One intriguing interactive session – aptly-titled “Nightmare Bugs” – will investigate the problems posed by multidrug-resistant organisms and the need for new antimicrobials to defeat them.

There are many sessions and posters addressing evergreen clinical topics for ID clinicians, such as antimicrobial resistance, antibiotic stewardship, surgical site infections, bacteremia and sepsis, Clostridium difficile, hepatitis care, and HIV care. But the education committee at IDWeek always manages to touch on topics in the news. For instance, one late breaker session will feature a discussion of the nexus between the opioid crisis and infectious diseases, the outbreak of cholera in Yemen, and the epidemiology of the yellow fever outbreak in Brazil.

Featured speakers at the event include James M. Hughes, MD, professor of medicine at Emory University, Atlanta, who will discuss the importance of a One Health approach to emerging microbial threats, and Connie Celum, MD, MPH, professor of global health and medicine, University of Washington, Seattle, who intends to describe the progress in effective HIV prevention interventions and lessons learned in implementation. Neil O. Fishman, MD, of the University of Pennsylvania Perelman School of Medicine, is delivering the annual SHEA lecture at IDWeek, and will explain how ID physicians and epidemiologists can promote interventions to achieve high reliability in health care. Renowned ID researcher Janet Englund, MD, of Seattle Children’s Hospital, will discuss the potential future therapies to prevent or treat respiratory viral infections in high-risk pediatric patients.

The 2017 conference will close with a three-part plenary – “21^st Century Cures” – featuring ID luminaries Christopher Karp, MD, of the Bill & Melinda Gates Foundation, James E. Crowe Jr., MD, of Vanderbilt University Medical Center in Nashville, Tenn., and David Thomas, MD, MPH, of Johns Hopkins University in Baltimore.

[email protected]

On Twitter @richpizzi

 

IDWeek 2017 kicks off Oct. 3 at the San Diego Convention Center, with a focus on pandemic preparedness and other challenges facing infectious diseases clinicians and researchers in the 21st century.

Premeeting workshops and symposia occupy most of the first 2 days of the event, with highlights including a session on managing infections in opioid users and a “late breaker” symposium addressing the latest on the H7N9 outbreak in China, the current findings and recommendations regarding Candida auris, and the epidemiology of the recent Legionella outbreaks in the United States. Another late breaker session focuses on the recent spate of hepatitis A outbreaks, including one in conference host city San Diego, primarily among the homeless population.

IDWeek is the combined annual meeting of the Infectious Diseases Society of America (IDSA), the Society for Healthcare Epidemiology of America (SHEA), the HIV Medicine Association (HIVMA), and the Pediatric Infectious Diseases Society (PIDS). The first IDWeek was held in 2012.

The IDWeek symposia, oral abstract sessions, and poster abstract sessions are the highlights, but the interactive “pro/con” debate sessions should be entertaining and informative. Topics include “Should Your ASP Include the ICU?” and “Is SAAR Ready for Primetime?” Another interactive session – “Diagnostic Clinical Cases” – brings a panel of ID experts together to identify the etiology of challenging clinical cases and to describe diagnostic testing strategies for such cases. Other “pro/con” debates will include a discussion on mandating an annual influenza vaccine for health care workers in acute care settings, and an assessment of the risks and benefits of active surveillance, compared with immediate surgery for persons with a spinal epidural abscess.

One intriguing interactive session – aptly-titled “Nightmare Bugs” – will investigate the problems posed by multidrug-resistant organisms and the need for new antimicrobials to defeat them.

There are many sessions and posters addressing evergreen clinical topics for ID clinicians, such as antimicrobial resistance, antibiotic stewardship, surgical site infections, bacteremia and sepsis, Clostridium difficile, hepatitis care, and HIV care. But the education committee at IDWeek always manages to touch on topics in the news. For instance, one late breaker session will feature a discussion of the nexus between the opioid crisis and infectious diseases, the outbreak of cholera in Yemen, and the epidemiology of the yellow fever outbreak in Brazil.

Featured speakers at the event include James M. Hughes, MD, professor of medicine at Emory University, Atlanta, who will discuss the importance of a One Health approach to emerging microbial threats, and Connie Celum, MD, MPH, professor of global health and medicine, University of Washington, Seattle, who intends to describe the progress in effective HIV prevention interventions and lessons learned in implementation. Neil O. Fishman, MD, of the University of Pennsylvania Perelman School of Medicine, is delivering the annual SHEA lecture at IDWeek, and will explain how ID physicians and epidemiologists can promote interventions to achieve high reliability in health care. Renowned ID researcher Janet Englund, MD, of Seattle Children’s Hospital, will discuss the potential future therapies to prevent or treat respiratory viral infections in high-risk pediatric patients.

The 2017 conference will close with a three-part plenary – “21^st Century Cures” – featuring ID luminaries Christopher Karp, MD, of the Bill & Melinda Gates Foundation, James E. Crowe Jr., MD, of Vanderbilt University Medical Center in Nashville, Tenn., and David Thomas, MD, MPH, of Johns Hopkins University in Baltimore.

[email protected]

On Twitter @richpizzi