Commentary

A 59-year-old man is admitted with abdominal pain. He has a history of pancreatitis. A contrast CT scan is ordered. He reports a history of severe shellfish allergy when the radiology tech checks him in for the procedure. You are paged regarding what to do:

A) Continue with scan as ordered.

B) Switch to MRI scan.

C) Switch to MRI scan with gadolinium.

D) Continue with CT with contrast, give dose of Solu-Medrol.

E) Continue with CT with contrast give IV diphenhydramine.
 

The correct answer here is A, This patient can receive his scan and receive contrast as ordered.

For many years, patients have been asked about shellfish allergy as a proxy for having increased risk when receiving iodine containing contrast. The mistaken thought was that shellfish contains iodine, so allergy to shellfish was likely to portend allergy to iodine.

Allergy to shellfish is caused by individual proteins that are definitely not in iodine-containing contrast.¹ Beaty et al. studied the prevalence of the belief that allergy to shellfish is tied to iodine allergy in a survey given to 231 faculty radiologists and interventional cardiologists.² Almost 70% responded that they inquire about seafood allergy before procedures that require iodine contrast, and 37% reported they would withhold the contrast or premedicate patients if they had a seafood allergy.

In a more recent study, Westermann-Clark and colleagues surveyed 252 health professionals before and after an educational intervention to dispel the myth of shellfish allergy and iodinated contrast reactions.³ Before the intervention, 66% of participants felt it was important to ask about shellfish allergies and 93% felt it was important to ask about iodine allergies; 26% responded that they would withhold iodinated contrast material in patients with a shellfish allergy, and 56% would withhold in patients with an iodine allergy. A total of 62% reported they would premedicate patients with a shellfish allergy and 75% would premedicate patients with an iodine allergy. The numbers declined dramatically after the educational intervention.

Patients who have seafood allergy have a higher rate of reactions to iodinated contrast, but not at a higher rate than do patients with other food allergies or asthma.⁴ Most radiology departments do not screen for other food allergies despite the fact these allergies have the same increased risk as for patients with a seafood/shellfish allergy. These patients are more allergic, and in general, are more likely to have reactions. The American Academy of Allergy, Asthma, and Immunology recommends not routinely ordering low- or iso-osmolar radiocontrast media or pretreating with either antihistamines or steroids in patients with a history of seafood allergy.⁵

• It is unnecessary and unhelpful to ask patients about seafood allergies before ordering radiologic studies involving contrast.
• Iodine allergy does not exist.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Narayan AK et al. Avoiding contrast-enhanced computed tomography scans in patients with shellfish allergies. J Hosp Med. 2016 Jun;11(6):435-7.

2. Beaty AD et al. Seafood allergy and radiocontrast media: Are physicians propagating a myth? Am J Med. 2008 Feb;121(2):158.e1-4.

3. Westermann-Clark E et al. Debunking myths about “allergy” to radiocontrast media in an academic institution. Postgrad Med. 2015 Apr;127(3):295-300.

4. Coakley FV and DM Panicek. Iodine allergy: An oyster without a pearl? AJR Am J Roentgenol. 1997 Oct;169(4):951-2.

5. American Academy of Allergy, Asthma & Immunology recommendations on low- or iso-osmolar radiocontrast media.

6. Schabelman E and M Witting. The relationship of radiocontrast, iodine, and seafood allergies: A medical myth exposed. J Emerg Med. 2010 Nov;39(5):701-7.

7. van Ketel WG and WH van den Berg. Sensitization to povidone-iodine. Dermatol Clin. 1990 Jan;8(1):107-9.

A 59-year-old man is admitted with abdominal pain. He has a history of pancreatitis. A contrast CT scan is ordered. He reports a history of severe shellfish allergy when the radiology tech checks him in for the procedure. You are paged regarding what to do:

A) Continue with scan as ordered.

B) Switch to MRI scan.

C) Switch to MRI scan with gadolinium.

D) Continue with CT with contrast, give dose of Solu-Medrol.

E) Continue with CT with contrast give IV diphenhydramine.
 

The correct answer here is A, This patient can receive his scan and receive contrast as ordered.

For many years, patients have been asked about shellfish allergy as a proxy for having increased risk when receiving iodine containing contrast. The mistaken thought was that shellfish contains iodine, so allergy to shellfish was likely to portend allergy to iodine.

Allergy to shellfish is caused by individual proteins that are definitely not in iodine-containing contrast.¹ Beaty et al. studied the prevalence of the belief that allergy to shellfish is tied to iodine allergy in a survey given to 231 faculty radiologists and interventional cardiologists.² Almost 70% responded that they inquire about seafood allergy before procedures that require iodine contrast, and 37% reported they would withhold the contrast or premedicate patients if they had a seafood allergy.

In a more recent study, Westermann-Clark and colleagues surveyed 252 health professionals before and after an educational intervention to dispel the myth of shellfish allergy and iodinated contrast reactions.³ Before the intervention, 66% of participants felt it was important to ask about shellfish allergies and 93% felt it was important to ask about iodine allergies; 26% responded that they would withhold iodinated contrast material in patients with a shellfish allergy, and 56% would withhold in patients with an iodine allergy. A total of 62% reported they would premedicate patients with a shellfish allergy and 75% would premedicate patients with an iodine allergy. The numbers declined dramatically after the educational intervention.

Patients who have seafood allergy have a higher rate of reactions to iodinated contrast, but not at a higher rate than do patients with other food allergies or asthma.⁴ Most radiology departments do not screen for other food allergies despite the fact these allergies have the same increased risk as for patients with a seafood/shellfish allergy. These patients are more allergic, and in general, are more likely to have reactions. The American Academy of Allergy, Asthma, and Immunology recommends not routinely ordering low- or iso-osmolar radiocontrast media or pretreating with either antihistamines or steroids in patients with a history of seafood allergy.⁵

• It is unnecessary and unhelpful to ask patients about seafood allergies before ordering radiologic studies involving contrast.
• Iodine allergy does not exist.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Narayan AK et al. Avoiding contrast-enhanced computed tomography scans in patients with shellfish allergies. J Hosp Med. 2016 Jun;11(6):435-7.

2. Beaty AD et al. Seafood allergy and radiocontrast media: Are physicians propagating a myth? Am J Med. 2008 Feb;121(2):158.e1-4.

3. Westermann-Clark E et al. Debunking myths about “allergy” to radiocontrast media in an academic institution. Postgrad Med. 2015 Apr;127(3):295-300.

4. Coakley FV and DM Panicek. Iodine allergy: An oyster without a pearl? AJR Am J Roentgenol. 1997 Oct;169(4):951-2.

5. American Academy of Allergy, Asthma & Immunology recommendations on low- or iso-osmolar radiocontrast media.

6. Schabelman E and M Witting. The relationship of radiocontrast, iodine, and seafood allergies: A medical myth exposed. J Emerg Med. 2010 Nov;39(5):701-7.

7. van Ketel WG and WH van den Berg. Sensitization to povidone-iodine. Dermatol Clin. 1990 Jan;8(1):107-9.

A 59-year-old man is admitted with abdominal pain. He has a history of pancreatitis. A contrast CT scan is ordered. He reports a history of severe shellfish allergy when the radiology tech checks him in for the procedure. You are paged regarding what to do:

A) Continue with scan as ordered.

B) Switch to MRI scan.

C) Switch to MRI scan with gadolinium.

D) Continue with CT with contrast, give dose of Solu-Medrol.

E) Continue with CT with contrast give IV diphenhydramine.
 

The correct answer here is A, This patient can receive his scan and receive contrast as ordered.

For many years, patients have been asked about shellfish allergy as a proxy for having increased risk when receiving iodine containing contrast. The mistaken thought was that shellfish contains iodine, so allergy to shellfish was likely to portend allergy to iodine.

Allergy to shellfish is caused by individual proteins that are definitely not in iodine-containing contrast.¹ Beaty et al. studied the prevalence of the belief that allergy to shellfish is tied to iodine allergy in a survey given to 231 faculty radiologists and interventional cardiologists.² Almost 70% responded that they inquire about seafood allergy before procedures that require iodine contrast, and 37% reported they would withhold the contrast or premedicate patients if they had a seafood allergy.

In a more recent study, Westermann-Clark and colleagues surveyed 252 health professionals before and after an educational intervention to dispel the myth of shellfish allergy and iodinated contrast reactions.³ Before the intervention, 66% of participants felt it was important to ask about shellfish allergies and 93% felt it was important to ask about iodine allergies; 26% responded that they would withhold iodinated contrast material in patients with a shellfish allergy, and 56% would withhold in patients with an iodine allergy. A total of 62% reported they would premedicate patients with a shellfish allergy and 75% would premedicate patients with an iodine allergy. The numbers declined dramatically after the educational intervention.

Patients who have seafood allergy have a higher rate of reactions to iodinated contrast, but not at a higher rate than do patients with other food allergies or asthma.⁴ Most radiology departments do not screen for other food allergies despite the fact these allergies have the same increased risk as for patients with a seafood/shellfish allergy. These patients are more allergic, and in general, are more likely to have reactions. The American Academy of Allergy, Asthma, and Immunology recommends not routinely ordering low- or iso-osmolar radiocontrast media or pretreating with either antihistamines or steroids in patients with a history of seafood allergy.⁵

• It is unnecessary and unhelpful to ask patients about seafood allergies before ordering radiologic studies involving contrast.
• Iodine allergy does not exist.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Narayan AK et al. Avoiding contrast-enhanced computed tomography scans in patients with shellfish allergies. J Hosp Med. 2016 Jun;11(6):435-7.

2. Beaty AD et al. Seafood allergy and radiocontrast media: Are physicians propagating a myth? Am J Med. 2008 Feb;121(2):158.e1-4.

3. Westermann-Clark E et al. Debunking myths about “allergy” to radiocontrast media in an academic institution. Postgrad Med. 2015 Apr;127(3):295-300.

4. Coakley FV and DM Panicek. Iodine allergy: An oyster without a pearl? AJR Am J Roentgenol. 1997 Oct;169(4):951-2.

5. American Academy of Allergy, Asthma & Immunology recommendations on low- or iso-osmolar radiocontrast media.

6. Schabelman E and M Witting. The relationship of radiocontrast, iodine, and seafood allergies: A medical myth exposed. J Emerg Med. 2010 Nov;39(5):701-7.

7. van Ketel WG and WH van den Berg. Sensitization to povidone-iodine. Dermatol Clin. 1990 Jan;8(1):107-9.

The United States Declaration of Independence is widely known for the words that begin its second paragraph:

We hold these truths to be self-evident, that all men are created equal, that they are endowed by their Creator with certain unalienable Rights, that among these are Life, Liberty and the pursuit of Happiness.

Those basic rights are accessible and exercised by all healthy US citizens, but for many individuals with psychiatric disorders, those inalienable rights may be elusive. Consider how they are compromised by untreated psychiatric illness.

Life. This is the most basic right. In the United States, healthy individuals cherish being alive, and many take it for granted, unlike the residents of nondemocratic countries, where persons may be killed by dictators for political or other reasons (Stalin and Hitler murdered millions of innocent people). In the past, persons with mental illness were considered possessed by demons and were killed or burned at the stake (as in the Middle Ages). But unfortunately, the current major risk for the loss of life among psychiatric patients is the patients themselves. Suicidal urges, attempts, and completions are of epidemic proportions and continue to rise every year. Our patients end their own lives because their illness prompts them to relinquish their life and to embrace untimely death. And once life is lost, all other rights are abdicated. Suicide attempts are common among patients who are diagnosed with bipolar disorder, major depressive disorder, schizophrenia, anxiety, obsessive-compulsive disorder (OCD), posttraumatic stress disorder, and borderline personality disorder. Sometimes, suicide is unintentional, such as when a patient with a substance use disorder inadvertently overdoses (as in the contemporary opioid epidemic) or ingests drugs laced with a deadly substance. For many untreated patients, life can be so fragile, tenuous, and tragically brief.

Liberty. Healthy citizens in the United States (and other democratic countries) have many liberties: where to live, what to do, where to move, what to say, what to believe, who to assemble with, what to eat or drink, whom to befriend, whom to marry, whether or not to procreate, and what to wear. They can choose to be an activist for any cause, no matter how quaint, or to disfigure their bodies with tattoos or piercings.

In contrast, the liberties of individuals with a psychiatric disorder can be compromised. In fact, patients’ liberties can be seriously shackled by their illness. A person with untreated schizophrenia can be enslaved by fixed irrational beliefs that may constrain their choices or determine how they live or relate to others. Command hallucinations can dictate what a patient should or mustn’t do. Poor reality testing detrimentally limits the options of a person with psychosis. A lack of insight deprives a patient with schizophrenia from rational decision-making. Self-neglect leads to physical, mental, and social deterioration.

For persons with depression, the range of liberties is shattered by social withdrawal, overwhelming guilt, sense of worthlessness, dismal hopelessness, doleful ruminations, and loss of appetite or sleep. The only rights that people with depression may exercise is to injure their body or end their life.

Think also of patients with OCD, who are subjugated by their ongoing obsessions or compulsive rituals; think of those with panic disorder who are unable to leave their home due to agoraphobia or cannot drive freely because of fears related to bridges or tunnels; think of persons who are enchained by their addiction and oppressed by the craving for drugs, food, or gambling. There are few meaningful liberties left for all such patients.

Continue to: Happiness

Happiness. I often wonder if most Americans these days are pursuing pleasure rather than happiness, seeking the momentary thrill and gratification instead of long-lasting happiness and joy. But persons with psychiatric brain disorders have great difficulty pursuing either pleasure or happiness. Anhedonia is a common symptom in schizophrenia and depression, depriving patients from experiencing enjoyable activities (ie, having fun) as they used to do before they got sick. Persons with anxiety have such emotional turmoil, it is hard for them to experience pleasure or happiness when feelings of impending doom permeates their souls. Persons with an addictive disorder are coerced to seek their substance for a momentary reward, only to spend a much longer time craving and seeking their substance of choice again and again. On the other end of the spectrum, for persons with mania, the excessive pursuit of high-risk pleasures can have grave consequences or embarrassment after they recover.

Happiness for patients with mental illness is possible only when they emerge from their illness and are “liberated” from the symptoms that disrupt their lives. As psychiatrists, we don’t just evaluate and treat patients with psychiatric illness—we restore their liberties and ability to pursue happiness and enjoy small pleasures.

The motto on the seal of the American University of Beirut, which I attended in my youth, is “That they may have life, and to have it abundantly.” As I have grown older and wiser, I have come to realize the true meaning of that motto. Life is a right we take for granted, but without it, we cannot exercise the various liberties, or be able to pursue happiness. I exercised my right to become a psychiatrist, and that provided me with lifelong happiness and satisfaction, especially when I prevent the loss of life of my patients, restore their liberty by ridding them of illness, and resurrect their ability to experience pleasure and pursue happiness.

The United States Declaration of Independence is widely known for the words that begin its second paragraph:

We hold these truths to be self-evident, that all men are created equal, that they are endowed by their Creator with certain unalienable Rights, that among these are Life, Liberty and the pursuit of Happiness.

Those basic rights are accessible and exercised by all healthy US citizens, but for many individuals with psychiatric disorders, those inalienable rights may be elusive. Consider how they are compromised by untreated psychiatric illness.

Life. This is the most basic right. In the United States, healthy individuals cherish being alive, and many take it for granted, unlike the residents of nondemocratic countries, where persons may be killed by dictators for political or other reasons (Stalin and Hitler murdered millions of innocent people). In the past, persons with mental illness were considered possessed by demons and were killed or burned at the stake (as in the Middle Ages). But unfortunately, the current major risk for the loss of life among psychiatric patients is the patients themselves. Suicidal urges, attempts, and completions are of epidemic proportions and continue to rise every year. Our patients end their own lives because their illness prompts them to relinquish their life and to embrace untimely death. And once life is lost, all other rights are abdicated. Suicide attempts are common among patients who are diagnosed with bipolar disorder, major depressive disorder, schizophrenia, anxiety, obsessive-compulsive disorder (OCD), posttraumatic stress disorder, and borderline personality disorder. Sometimes, suicide is unintentional, such as when a patient with a substance use disorder inadvertently overdoses (as in the contemporary opioid epidemic) or ingests drugs laced with a deadly substance. For many untreated patients, life can be so fragile, tenuous, and tragically brief.

Liberty. Healthy citizens in the United States (and other democratic countries) have many liberties: where to live, what to do, where to move, what to say, what to believe, who to assemble with, what to eat or drink, whom to befriend, whom to marry, whether or not to procreate, and what to wear. They can choose to be an activist for any cause, no matter how quaint, or to disfigure their bodies with tattoos or piercings.

In contrast, the liberties of individuals with a psychiatric disorder can be compromised. In fact, patients’ liberties can be seriously shackled by their illness. A person with untreated schizophrenia can be enslaved by fixed irrational beliefs that may constrain their choices or determine how they live or relate to others. Command hallucinations can dictate what a patient should or mustn’t do. Poor reality testing detrimentally limits the options of a person with psychosis. A lack of insight deprives a patient with schizophrenia from rational decision-making. Self-neglect leads to physical, mental, and social deterioration.

For persons with depression, the range of liberties is shattered by social withdrawal, overwhelming guilt, sense of worthlessness, dismal hopelessness, doleful ruminations, and loss of appetite or sleep. The only rights that people with depression may exercise is to injure their body or end their life.

Think also of patients with OCD, who are subjugated by their ongoing obsessions or compulsive rituals; think of those with panic disorder who are unable to leave their home due to agoraphobia or cannot drive freely because of fears related to bridges or tunnels; think of persons who are enchained by their addiction and oppressed by the craving for drugs, food, or gambling. There are few meaningful liberties left for all such patients.

Continue to: Happiness

Happiness. I often wonder if most Americans these days are pursuing pleasure rather than happiness, seeking the momentary thrill and gratification instead of long-lasting happiness and joy. But persons with psychiatric brain disorders have great difficulty pursuing either pleasure or happiness. Anhedonia is a common symptom in schizophrenia and depression, depriving patients from experiencing enjoyable activities (ie, having fun) as they used to do before they got sick. Persons with anxiety have such emotional turmoil, it is hard for them to experience pleasure or happiness when feelings of impending doom permeates their souls. Persons with an addictive disorder are coerced to seek their substance for a momentary reward, only to spend a much longer time craving and seeking their substance of choice again and again. On the other end of the spectrum, for persons with mania, the excessive pursuit of high-risk pleasures can have grave consequences or embarrassment after they recover.

Happiness for patients with mental illness is possible only when they emerge from their illness and are “liberated” from the symptoms that disrupt their lives. As psychiatrists, we don’t just evaluate and treat patients with psychiatric illness—we restore their liberties and ability to pursue happiness and enjoy small pleasures.

The motto on the seal of the American University of Beirut, which I attended in my youth, is “That they may have life, and to have it abundantly.” As I have grown older and wiser, I have come to realize the true meaning of that motto. Life is a right we take for granted, but without it, we cannot exercise the various liberties, or be able to pursue happiness. I exercised my right to become a psychiatrist, and that provided me with lifelong happiness and satisfaction, especially when I prevent the loss of life of my patients, restore their liberty by ridding them of illness, and resurrect their ability to experience pleasure and pursue happiness.

The United States Declaration of Independence is widely known for the words that begin its second paragraph:

We hold these truths to be self-evident, that all men are created equal, that they are endowed by their Creator with certain unalienable Rights, that among these are Life, Liberty and the pursuit of Happiness.

Those basic rights are accessible and exercised by all healthy US citizens, but for many individuals with psychiatric disorders, those inalienable rights may be elusive. Consider how they are compromised by untreated psychiatric illness.

Life. This is the most basic right. In the United States, healthy individuals cherish being alive, and many take it for granted, unlike the residents of nondemocratic countries, where persons may be killed by dictators for political or other reasons (Stalin and Hitler murdered millions of innocent people). In the past, persons with mental illness were considered possessed by demons and were killed or burned at the stake (as in the Middle Ages). But unfortunately, the current major risk for the loss of life among psychiatric patients is the patients themselves. Suicidal urges, attempts, and completions are of epidemic proportions and continue to rise every year. Our patients end their own lives because their illness prompts them to relinquish their life and to embrace untimely death. And once life is lost, all other rights are abdicated. Suicide attempts are common among patients who are diagnosed with bipolar disorder, major depressive disorder, schizophrenia, anxiety, obsessive-compulsive disorder (OCD), posttraumatic stress disorder, and borderline personality disorder. Sometimes, suicide is unintentional, such as when a patient with a substance use disorder inadvertently overdoses (as in the contemporary opioid epidemic) or ingests drugs laced with a deadly substance. For many untreated patients, life can be so fragile, tenuous, and tragically brief.

Liberty. Healthy citizens in the United States (and other democratic countries) have many liberties: where to live, what to do, where to move, what to say, what to believe, who to assemble with, what to eat or drink, whom to befriend, whom to marry, whether or not to procreate, and what to wear. They can choose to be an activist for any cause, no matter how quaint, or to disfigure their bodies with tattoos or piercings.

In contrast, the liberties of individuals with a psychiatric disorder can be compromised. In fact, patients’ liberties can be seriously shackled by their illness. A person with untreated schizophrenia can be enslaved by fixed irrational beliefs that may constrain their choices or determine how they live or relate to others. Command hallucinations can dictate what a patient should or mustn’t do. Poor reality testing detrimentally limits the options of a person with psychosis. A lack of insight deprives a patient with schizophrenia from rational decision-making. Self-neglect leads to physical, mental, and social deterioration.

For persons with depression, the range of liberties is shattered by social withdrawal, overwhelming guilt, sense of worthlessness, dismal hopelessness, doleful ruminations, and loss of appetite or sleep. The only rights that people with depression may exercise is to injure their body or end their life.

Think also of patients with OCD, who are subjugated by their ongoing obsessions or compulsive rituals; think of those with panic disorder who are unable to leave their home due to agoraphobia or cannot drive freely because of fears related to bridges or tunnels; think of persons who are enchained by their addiction and oppressed by the craving for drugs, food, or gambling. There are few meaningful liberties left for all such patients.

Continue to: Happiness

Happiness. I often wonder if most Americans these days are pursuing pleasure rather than happiness, seeking the momentary thrill and gratification instead of long-lasting happiness and joy. But persons with psychiatric brain disorders have great difficulty pursuing either pleasure or happiness. Anhedonia is a common symptom in schizophrenia and depression, depriving patients from experiencing enjoyable activities (ie, having fun) as they used to do before they got sick. Persons with anxiety have such emotional turmoil, it is hard for them to experience pleasure or happiness when feelings of impending doom permeates their souls. Persons with an addictive disorder are coerced to seek their substance for a momentary reward, only to spend a much longer time craving and seeking their substance of choice again and again. On the other end of the spectrum, for persons with mania, the excessive pursuit of high-risk pleasures can have grave consequences or embarrassment after they recover.

Happiness for patients with mental illness is possible only when they emerge from their illness and are “liberated” from the symptoms that disrupt their lives. As psychiatrists, we don’t just evaluate and treat patients with psychiatric illness—we restore their liberties and ability to pursue happiness and enjoy small pleasures.

The motto on the seal of the American University of Beirut, which I attended in my youth, is “That they may have life, and to have it abundantly.” As I have grown older and wiser, I have come to realize the true meaning of that motto. Life is a right we take for granted, but without it, we cannot exercise the various liberties, or be able to pursue happiness. I exercised my right to become a psychiatrist, and that provided me with lifelong happiness and satisfaction, especially when I prevent the loss of life of my patients, restore their liberty by ridding them of illness, and resurrect their ability to experience pleasure and pursue happiness.

In late January, the Crohn’s & Colitis Foundation teamed with AGA to present the Crohn’s & Colitis Congress^® in Austin, Tex. Each year, this is the premier gathering for IBD experts and the rest of us to catch up on the substantial progress we are making in treating patients with IBD. This month, we highlight a number of articles from the Congress, including results showing how a focused IBD quality initiative reduced emergency department visits, an article about the effects of IBD on fertility, and the link between stress and ulcerative colitis flares. All of these articles are worth reading, since they can help our care of patients. On agau.gastro.org, you can access slides from the Congress.

Several more articles deserve mention. Three articles from the AGA journals highlight new information about colorectal cancer prevention and the U.S. Multi-Society Task Force on Colorectal Cancer has updated colonoscopy follow-up guidance. In our practice management section, we provide a step-by-step guide to changes in evaluation and management (E/M) coding – these changes are the most impactful since the Medicare E/M documentation specifications first appeared.

We have 2 months left before Digestive Disease Week^® (DDW). Each year, DDW marks the end of our AGA Institute President’s term and the beginning of another’s epoch. Hashem B. El-Serag will pass the gavel to Bishr Omary – both great friends and great gastroenterologists. I am happy to see that Gail Hecht follows me as this year’s AGA Julius Friedenwald Medal recipient (AGA’s highest honor). She, too, is a great friend and role model for me and many others. DDW returns to Chicago in early May, and once again will be the world’s best gathering of physicians and scientists dedicated to digestive diseases.
 

John I. Allen, MD, MBA, AGAF
Editor in Chief

In late January, the Crohn’s & Colitis Foundation teamed with AGA to present the Crohn’s & Colitis Congress^® in Austin, Tex. Each year, this is the premier gathering for IBD experts and the rest of us to catch up on the substantial progress we are making in treating patients with IBD. This month, we highlight a number of articles from the Congress, including results showing how a focused IBD quality initiative reduced emergency department visits, an article about the effects of IBD on fertility, and the link between stress and ulcerative colitis flares. All of these articles are worth reading, since they can help our care of patients. On agau.gastro.org, you can access slides from the Congress.

Several more articles deserve mention. Three articles from the AGA journals highlight new information about colorectal cancer prevention and the U.S. Multi-Society Task Force on Colorectal Cancer has updated colonoscopy follow-up guidance. In our practice management section, we provide a step-by-step guide to changes in evaluation and management (E/M) coding – these changes are the most impactful since the Medicare E/M documentation specifications first appeared.

We have 2 months left before Digestive Disease Week^® (DDW). Each year, DDW marks the end of our AGA Institute President’s term and the beginning of another’s epoch. Hashem B. El-Serag will pass the gavel to Bishr Omary – both great friends and great gastroenterologists. I am happy to see that Gail Hecht follows me as this year’s AGA Julius Friedenwald Medal recipient (AGA’s highest honor). She, too, is a great friend and role model for me and many others. DDW returns to Chicago in early May, and once again will be the world’s best gathering of physicians and scientists dedicated to digestive diseases.
 

John I. Allen, MD, MBA, AGAF
Editor in Chief

In late January, the Crohn’s & Colitis Foundation teamed with AGA to present the Crohn’s & Colitis Congress^® in Austin, Tex. Each year, this is the premier gathering for IBD experts and the rest of us to catch up on the substantial progress we are making in treating patients with IBD. This month, we highlight a number of articles from the Congress, including results showing how a focused IBD quality initiative reduced emergency department visits, an article about the effects of IBD on fertility, and the link between stress and ulcerative colitis flares. All of these articles are worth reading, since they can help our care of patients. On agau.gastro.org, you can access slides from the Congress.

Several more articles deserve mention. Three articles from the AGA journals highlight new information about colorectal cancer prevention and the U.S. Multi-Society Task Force on Colorectal Cancer has updated colonoscopy follow-up guidance. In our practice management section, we provide a step-by-step guide to changes in evaluation and management (E/M) coding – these changes are the most impactful since the Medicare E/M documentation specifications first appeared.

We have 2 months left before Digestive Disease Week^® (DDW). Each year, DDW marks the end of our AGA Institute President’s term and the beginning of another’s epoch. Hashem B. El-Serag will pass the gavel to Bishr Omary – both great friends and great gastroenterologists. I am happy to see that Gail Hecht follows me as this year’s AGA Julius Friedenwald Medal recipient (AGA’s highest honor). She, too, is a great friend and role model for me and many others. DDW returns to Chicago in early May, and once again will be the world’s best gathering of physicians and scientists dedicated to digestive diseases.
 

John I. Allen, MD, MBA, AGAF
Editor in Chief

Two very different specialties, obstetrics (O) and gynecology (G), were fused into one in 1889. It is difficult to conceive that, with the expansion of both specialties in knowledge, procedures, and subspecialties, they still remain as one after 130 years. The American College of Obstetricians and Gynecologists was founded in 1952, and after 68 years no major changes have been made to accept or incorporate that there is a need to consider O and G as two different specialties.

Obstetrics and gynecology are the only specialties dedicated exclusively to women but with a very different purpose: the O is for reproduction, the G is for prevention and management of genital diseases. The specialties of O and G are so different the only thing in common is the patient.

It is time to separate the O from the G.
 

Are we training surgically competent residents?

No, we are not. There is an adequate volume for training and practice in O with close to 3.8 million births a year (the number cited by the Centers for Disease Control and Prevention in 2018). Not surprisingly, there is a need for trainees and also for practitioners in rural areas. As a result, the surgical training and practice in G is not optimal. If the number of hysterectomies was even near that of deliveries, there would be an adequate volume for everyone in training and in practice. But this is not the case.

The Accreditation Council for Graduate Medical Education (ACGME) mandates OG residents to graduate with a minimum of 70 minimally invasive hysterectomies (MIH), including laparoscopic (LH), vaginal (VH), and laparoscopic vaginally assisted (LAVH). In 2017, 51% of graduating residents fell below the minimum of 70 MIH.¹ Because the learning curve of LH ranges from 30 to 80 cases,² it is not surprising most residents feel surgically inadequate at graduation to function independently.
 

Increased procedures and technologies with reduced training hours

Let’s look at hysterectomies. From two techniques, vaginal and abdominal, they have expanded to LH, LAVH, robotic, single-site LH, single-site robotic, and recently single-port robotic. In addition, different and new technologies for hysteroscopy and myomectomy procedures have been developed.

All these operations are supposed to be part of any training program as ACGME demands “OG residents must be able to competently perform all medical, diagnostic, and surgical procedures considered essential for the area of practice.”³ In addition, primary care has been added to OG residency training: “Primary health care management from adolescence through reproductive age to midlife and beyond is integral to any ob.gyn.’s practice” and “Obstetrician-gynecologists are viewed by some entities as being primary care physicians for women, especially as coordinators of care among most reproductive-aged women,” according to ACOG.⁴

All this with reduced training hours.

The number of training hours a week has been reduced to 80, while it used to be over 100 hours. If you do the math, 20 fewer hours a week for 4 years amounts to 4,240 hours, equivalent to 180 days, equal to 6 months.

The present residents must learn more with fewer hours of training. Graduating residents must pass a written and an oral exam for certification and with this are approved to enter the operating room and operate on women without a surgical skills test.
 

A simple test shows that elimination of the O for 1 year improves laparoscopic performance

We compared the time to perform three basic laparoscopic skills by fourth-year OG residents with that of fellows at the end of their first year in a minimally invasive G fellowship.⁵ The mean time for the residents completing the three tasks within the allotted time was 16 minutes, compared with 3.5 minutes for fellows: a four times faster performance.

Are there enough patients to maintain surgical skills after residency?

No, there are not.

Consider the following reality after residency. Decreasing number of surgeries and increasing numbers of OGs results in what you have already guessed: a lower surgical volume per OG.

Since 1979, the number of G surgeries has decreased by almost half (46%) while the number of OGs has doubled (54%) resulting in an 81% decrease of number of surgeries per OG, from 132 in 1979 to 25 in 2007.⁶ For hysterectomies, there has been a continuous yearly decline per G from 28 in 1980 to 9.8 in 2007 and to 8.5 in 2010.^7,8

Would any mother feel comfortable having an obstetrician for her pregnancy and delivery performing only 8.5 deliveries a year?
 

Where do we go from here?

Separate the training and practice of O and G, an initiative already started in some residency programs and in some institutions in the United States. The O and the G both include a medical and a surgical practice.

We need to start accepting there is a need for different practices: medical O, medical G, surgical O, and surgical G. It is not new, it is already happening, it is the case in our institution since inception, and it is expanding across the country because it is needed. Graduating residents recognize this need as noticed by the increasing number seeking subspecialty training, from 7% in 2000 to 19.5% in 2012.⁴

Will this require some patients to drive away from home to obtain the best possible care? Yes. It is not a new concept, and it already is occurring for patients traveling to specialized centers away from home for certain conditions. In some countries, the practice is restricted to only a few centers. In Sweden, for instance, patients diagnosed with gynecologic cancer must travel to one of only seven centers subspecialized in gynecologic malignancies.
 

Conclusion

We need to start someday. We already are late after 130 years. We need to provide optimal care for women. They are our mothers. They deserve it. Let the O deliver O care, let the G provide G care, and we will reap improved results.

Dr. Magrina is with the department of medical and surgical gynecology at the Mayo Clinic in Phoenix. The author has no conflict of interest or financial involvement with this manuscript.

References

1. Am J Obstet Gynecol. 2019 Nov 22. doi: 10.1016/j.ajog.2019.11.1258.

2. Clin Obstet Gynecol. 2011 Sep;54(3):376-81.

3. Accreditation Council for Graduate Medical Education. Program requirements for GME in Obstetrics and Gynecology 2017.

4. “The obstetrician-gynecologist workforce in the United States: Facts, figures, and implications, 2017” (Washington, D.C.: ACOG, 2017).

5. J Minim Invasive Gynecol. 2008 Jul-Aug;15(4):410-3.

6. J Minim Invasive Gynecol. 2014 Jul-Aug;21(4):501-3.

7. National Health Statistics Report. Hysterectomy in the U.S. and oophorectomy 1979-2007. http://www.cdc.gov/nchs/products/nhsr.htm.

8. The Healthcare Cost and Utilization Project – Nationwide Inpatient Sample: Agency for Health Care Research Quality. 2013.






 

Two very different specialties, obstetrics (O) and gynecology (G), were fused into one in 1889. It is difficult to conceive that, with the expansion of both specialties in knowledge, procedures, and subspecialties, they still remain as one after 130 years. The American College of Obstetricians and Gynecologists was founded in 1952, and after 68 years no major changes have been made to accept or incorporate that there is a need to consider O and G as two different specialties.

Obstetrics and gynecology are the only specialties dedicated exclusively to women but with a very different purpose: the O is for reproduction, the G is for prevention and management of genital diseases. The specialties of O and G are so different the only thing in common is the patient.

It is time to separate the O from the G.
 

Are we training surgically competent residents?

No, we are not. There is an adequate volume for training and practice in O with close to 3.8 million births a year (the number cited by the Centers for Disease Control and Prevention in 2018). Not surprisingly, there is a need for trainees and also for practitioners in rural areas. As a result, the surgical training and practice in G is not optimal. If the number of hysterectomies was even near that of deliveries, there would be an adequate volume for everyone in training and in practice. But this is not the case.

The Accreditation Council for Graduate Medical Education (ACGME) mandates OG residents to graduate with a minimum of 70 minimally invasive hysterectomies (MIH), including laparoscopic (LH), vaginal (VH), and laparoscopic vaginally assisted (LAVH). In 2017, 51% of graduating residents fell below the minimum of 70 MIH.¹ Because the learning curve of LH ranges from 30 to 80 cases,² it is not surprising most residents feel surgically inadequate at graduation to function independently.
 

Increased procedures and technologies with reduced training hours

Let’s look at hysterectomies. From two techniques, vaginal and abdominal, they have expanded to LH, LAVH, robotic, single-site LH, single-site robotic, and recently single-port robotic. In addition, different and new technologies for hysteroscopy and myomectomy procedures have been developed.

All these operations are supposed to be part of any training program as ACGME demands “OG residents must be able to competently perform all medical, diagnostic, and surgical procedures considered essential for the area of practice.”³ In addition, primary care has been added to OG residency training: “Primary health care management from adolescence through reproductive age to midlife and beyond is integral to any ob.gyn.’s practice” and “Obstetrician-gynecologists are viewed by some entities as being primary care physicians for women, especially as coordinators of care among most reproductive-aged women,” according to ACOG.⁴

All this with reduced training hours.

The number of training hours a week has been reduced to 80, while it used to be over 100 hours. If you do the math, 20 fewer hours a week for 4 years amounts to 4,240 hours, equivalent to 180 days, equal to 6 months.

The present residents must learn more with fewer hours of training. Graduating residents must pass a written and an oral exam for certification and with this are approved to enter the operating room and operate on women without a surgical skills test.
 

A simple test shows that elimination of the O for 1 year improves laparoscopic performance

We compared the time to perform three basic laparoscopic skills by fourth-year OG residents with that of fellows at the end of their first year in a minimally invasive G fellowship.⁵ The mean time for the residents completing the three tasks within the allotted time was 16 minutes, compared with 3.5 minutes for fellows: a four times faster performance.

Are there enough patients to maintain surgical skills after residency?

No, there are not.

Consider the following reality after residency. Decreasing number of surgeries and increasing numbers of OGs results in what you have already guessed: a lower surgical volume per OG.

Since 1979, the number of G surgeries has decreased by almost half (46%) while the number of OGs has doubled (54%) resulting in an 81% decrease of number of surgeries per OG, from 132 in 1979 to 25 in 2007.⁶ For hysterectomies, there has been a continuous yearly decline per G from 28 in 1980 to 9.8 in 2007 and to 8.5 in 2010.^7,8

Would any mother feel comfortable having an obstetrician for her pregnancy and delivery performing only 8.5 deliveries a year?
 

Where do we go from here?

Separate the training and practice of O and G, an initiative already started in some residency programs and in some institutions in the United States. The O and the G both include a medical and a surgical practice.

We need to start accepting there is a need for different practices: medical O, medical G, surgical O, and surgical G. It is not new, it is already happening, it is the case in our institution since inception, and it is expanding across the country because it is needed. Graduating residents recognize this need as noticed by the increasing number seeking subspecialty training, from 7% in 2000 to 19.5% in 2012.⁴

Will this require some patients to drive away from home to obtain the best possible care? Yes. It is not a new concept, and it already is occurring for patients traveling to specialized centers away from home for certain conditions. In some countries, the practice is restricted to only a few centers. In Sweden, for instance, patients diagnosed with gynecologic cancer must travel to one of only seven centers subspecialized in gynecologic malignancies.
 

Conclusion

We need to start someday. We already are late after 130 years. We need to provide optimal care for women. They are our mothers. They deserve it. Let the O deliver O care, let the G provide G care, and we will reap improved results.

Dr. Magrina is with the department of medical and surgical gynecology at the Mayo Clinic in Phoenix. The author has no conflict of interest or financial involvement with this manuscript.

References

1. Am J Obstet Gynecol. 2019 Nov 22. doi: 10.1016/j.ajog.2019.11.1258.

2. Clin Obstet Gynecol. 2011 Sep;54(3):376-81.

3. Accreditation Council for Graduate Medical Education. Program requirements for GME in Obstetrics and Gynecology 2017.

4. “The obstetrician-gynecologist workforce in the United States: Facts, figures, and implications, 2017” (Washington, D.C.: ACOG, 2017).

5. J Minim Invasive Gynecol. 2008 Jul-Aug;15(4):410-3.

6. J Minim Invasive Gynecol. 2014 Jul-Aug;21(4):501-3.

7. National Health Statistics Report. Hysterectomy in the U.S. and oophorectomy 1979-2007. http://www.cdc.gov/nchs/products/nhsr.htm.

8. The Healthcare Cost and Utilization Project – Nationwide Inpatient Sample: Agency for Health Care Research Quality. 2013.






 

Two very different specialties, obstetrics (O) and gynecology (G), were fused into one in 1889. It is difficult to conceive that, with the expansion of both specialties in knowledge, procedures, and subspecialties, they still remain as one after 130 years. The American College of Obstetricians and Gynecologists was founded in 1952, and after 68 years no major changes have been made to accept or incorporate that there is a need to consider O and G as two different specialties.

Obstetrics and gynecology are the only specialties dedicated exclusively to women but with a very different purpose: the O is for reproduction, the G is for prevention and management of genital diseases. The specialties of O and G are so different the only thing in common is the patient.

It is time to separate the O from the G.
 

Are we training surgically competent residents?

No, we are not. There is an adequate volume for training and practice in O with close to 3.8 million births a year (the number cited by the Centers for Disease Control and Prevention in 2018). Not surprisingly, there is a need for trainees and also for practitioners in rural areas. As a result, the surgical training and practice in G is not optimal. If the number of hysterectomies was even near that of deliveries, there would be an adequate volume for everyone in training and in practice. But this is not the case.

The Accreditation Council for Graduate Medical Education (ACGME) mandates OG residents to graduate with a minimum of 70 minimally invasive hysterectomies (MIH), including laparoscopic (LH), vaginal (VH), and laparoscopic vaginally assisted (LAVH). In 2017, 51% of graduating residents fell below the minimum of 70 MIH.¹ Because the learning curve of LH ranges from 30 to 80 cases,² it is not surprising most residents feel surgically inadequate at graduation to function independently.
 

Increased procedures and technologies with reduced training hours

Let’s look at hysterectomies. From two techniques, vaginal and abdominal, they have expanded to LH, LAVH, robotic, single-site LH, single-site robotic, and recently single-port robotic. In addition, different and new technologies for hysteroscopy and myomectomy procedures have been developed.

All these operations are supposed to be part of any training program as ACGME demands “OG residents must be able to competently perform all medical, diagnostic, and surgical procedures considered essential for the area of practice.”³ In addition, primary care has been added to OG residency training: “Primary health care management from adolescence through reproductive age to midlife and beyond is integral to any ob.gyn.’s practice” and “Obstetrician-gynecologists are viewed by some entities as being primary care physicians for women, especially as coordinators of care among most reproductive-aged women,” according to ACOG.⁴

All this with reduced training hours.

The number of training hours a week has been reduced to 80, while it used to be over 100 hours. If you do the math, 20 fewer hours a week for 4 years amounts to 4,240 hours, equivalent to 180 days, equal to 6 months.

The present residents must learn more with fewer hours of training. Graduating residents must pass a written and an oral exam for certification and with this are approved to enter the operating room and operate on women without a surgical skills test.
 

A simple test shows that elimination of the O for 1 year improves laparoscopic performance

We compared the time to perform three basic laparoscopic skills by fourth-year OG residents with that of fellows at the end of their first year in a minimally invasive G fellowship.⁵ The mean time for the residents completing the three tasks within the allotted time was 16 minutes, compared with 3.5 minutes for fellows: a four times faster performance.

Are there enough patients to maintain surgical skills after residency?

No, there are not.

Consider the following reality after residency. Decreasing number of surgeries and increasing numbers of OGs results in what you have already guessed: a lower surgical volume per OG.

Since 1979, the number of G surgeries has decreased by almost half (46%) while the number of OGs has doubled (54%) resulting in an 81% decrease of number of surgeries per OG, from 132 in 1979 to 25 in 2007.⁶ For hysterectomies, there has been a continuous yearly decline per G from 28 in 1980 to 9.8 in 2007 and to 8.5 in 2010.^7,8

Would any mother feel comfortable having an obstetrician for her pregnancy and delivery performing only 8.5 deliveries a year?
 

Where do we go from here?

Separate the training and practice of O and G, an initiative already started in some residency programs and in some institutions in the United States. The O and the G both include a medical and a surgical practice.

We need to start accepting there is a need for different practices: medical O, medical G, surgical O, and surgical G. It is not new, it is already happening, it is the case in our institution since inception, and it is expanding across the country because it is needed. Graduating residents recognize this need as noticed by the increasing number seeking subspecialty training, from 7% in 2000 to 19.5% in 2012.⁴

Will this require some patients to drive away from home to obtain the best possible care? Yes. It is not a new concept, and it already is occurring for patients traveling to specialized centers away from home for certain conditions. In some countries, the practice is restricted to only a few centers. In Sweden, for instance, patients diagnosed with gynecologic cancer must travel to one of only seven centers subspecialized in gynecologic malignancies.
 

Conclusion

We need to start someday. We already are late after 130 years. We need to provide optimal care for women. They are our mothers. They deserve it. Let the O deliver O care, let the G provide G care, and we will reap improved results.

Dr. Magrina is with the department of medical and surgical gynecology at the Mayo Clinic in Phoenix. The author has no conflict of interest or financial involvement with this manuscript.

References

1. Am J Obstet Gynecol. 2019 Nov 22. doi: 10.1016/j.ajog.2019.11.1258.

2. Clin Obstet Gynecol. 2011 Sep;54(3):376-81.

3. Accreditation Council for Graduate Medical Education. Program requirements for GME in Obstetrics and Gynecology 2017.

4. “The obstetrician-gynecologist workforce in the United States: Facts, figures, and implications, 2017” (Washington, D.C.: ACOG, 2017).

5. J Minim Invasive Gynecol. 2008 Jul-Aug;15(4):410-3.

6. J Minim Invasive Gynecol. 2014 Jul-Aug;21(4):501-3.

7. National Health Statistics Report. Hysterectomy in the U.S. and oophorectomy 1979-2007. http://www.cdc.gov/nchs/products/nhsr.htm.

8. The Healthcare Cost and Utilization Project – Nationwide Inpatient Sample: Agency for Health Care Research Quality. 2013.






 

Prematurity remains the leading cause of neonatal morbidity and mortality, accounting for $26 billion a year in immediate costs, despite the implementation in obstetrics of a host of risk stratification algorithms and strategies for risk reduction, including the use of some medications.

It now is questionable whether injectable 17-alpha hydroxyprogesterone caproate (Makena) truly is efficacious in women who’ve had a prior spontaneous preterm birth (sPTB) – a Food and Drug Administration advisory committee last year recommended withdrawing it from the market based on results of an FDA confirmatory study. Even if the drug were efficacious, only a small percentage of the women who have an sPTB have had a prior one. The majority of sPTB occurs among women without such a history.

Vaginal progesterone appears to confer some protection in women found to have a short cervix during the second trimester, but this approach also has limited reach: Only 9% of women with sPTB had an antecedent short cervix in a 2017 study.¹ Like a history of sPTB, screening for short cervical length is a potentially helpful strategy for risk reduction, but it is not a strategy that will significantly impact the overall rate of prematurity.

We’ve fallen short in our goals to significantly reduce the public health impact of prematurity partly because we still do not understand the exact pathways and mechanisms by which sPTB occurs. The main working paradigm for myself and many other researchers over the past 2 decades has centered on infection in the uterus triggering inflammation, followed by cervical remodeling and ripening. Research in animal models, as well as human clinical trials targeting various infections and inflammation, have led to some insights and discoveries, but no successful interventions.

In the past decade, however, our research framework for understanding sPTB incorporates new questions about immunologic, microbiological, and molecular/cellular events that happen in the cervicovaginal space. We’ve learned more about the cervicovaginal microbiota, and most recently, our research at the University of Pennsylvania has elucidated the role that nonoptimal bacteria play in disrupting the cervical endothelial barrier and initiating the process of cervical remodeling that likely precedes sPTB.

We now know that there is an association between cervicovaginal microbial communities, immune responses, and sPTB. We also know that this association is stronger in black women and may help explain some of the observed racial disparities in sPTB. Although more research is needed to determine specific therapeutic strategies, new doors are open.
 

Host immune-microbial interactions

This new research paradigm has involved stepping back and asking basic questions, such as, what do we really know about the cervicovaginal space? In actuality, we know very little. We know little about the immune function of the vaginal and cervical epithelial cells in pregnancy, for instance, and there is a large gap in knowledge regarding the biomechanics of the cervix – a remarkable organ that can change shape and function in a matter of minutes. Studies on the biomechanics of the cervix during pregnancy and in labor are still in their infancy.

However, lessons can be drawn from research on inflammatory bowel disease and other disorders involving the gut. In the gastrointestinal tract, epithelial cells have been found to act as sentinels, forming a mucosal barrier against bacterial pathogens and secreting various immune factors. Research in this field also has shown that microbes living in the gut produce metabolites; that these microbial metabolites may be the key messengers from the microbial communities to the epithelial barrier; and that the microbes, microbial metabolites, and immune responses are responsible for triggering inflammatory processes in the tissues underneath.

In 2011, Jacques Ravel, PhD, who was part of the National Institutes of Health’s Human Microbiome Project, characterized the vaginal microbiome of reproductive-age women for the first time.² His paper classified the vaginal microbial communities of approximately 400 asymptomatic women of various ethnicities into five “community state types” (CSTs) based on the predominant bacteria found in the cervicovaginal space.³

On the heels of his research, Dr. Ravel and I launched an NIH-funded study involving a prospective cohort of 2,000 women with singleton pregnancies – the Motherhood & Microbiome cohort – to look at the cervicovaginal microbiota, the local immune response, and the risk of sPTB.⁴ Cervicovaginal samples were collected at 16-20 weeks’ gestation and during two subsequent clinical visits. From this cohort, which was composed mostly of African American women (74.5%), we conducted a nested case-controlled study of 103 cases of sPTB and 432 women who delivered at term, matched for race.

We carefully adjudicated the deliveries in our 2,000-person cohort so that we homed in on sPTB as opposed to preterm births that are medically indicated for reasons such as fetal distress or preeclampsia. (Several prior studies looking at the associations between the cervicovaginal microbiome had a heterogeneous phenotyping of PTB that made it hard to draw definitive conclusions.)

Our focus in assessing the microbiome and immunologic profiles was on the samples collected at the earliest time points in pregnancy because we hoped to detect a “signature” that could predict an outcome months later. Indeed, we found that the nonoptimal microbiota, known in microbiological terms as CST IV, was associated with about a 150% increased risk of sPTB. This community comprises a dominant array of anaerobic bacteria and a paucity of Lactobacillus species.

We also found that a larger proportion of African American women, compared with non–African American women, had this nonoptimal microbiota early in pregnancy (40% vs. 15%), which is consistent with previous studies in pregnancy and nonpregnancy showing lower levels of Lactobacillus species in the cervicovaginal microbiome of African American women.

Even more interesting was the finding that, although the rate of sPTB was higher in African American women and the effect of CST IV on sPTB was stronger in these women, the risk of sPTB couldn’t be explained solely by the presence of CST IV. Some women with this nonoptimal microbiome delivered at term, whereas others with more optimal microbiome types had sPTBs. This suggests that other factors contribute to African American women having a nonoptimal microbiota and being especially predisposed to sPTB.

Through the study’s immunologic profiling, we found a significant difference in the cervicovaginal levels of an immune factor, beta-defensin 2, between African American women who delivered at term and those who had a sPTB. Women who had a sPTB, even those who had higher levels of Lactobacillus species, had lower levels of beta-defensin 2. This association was not found in non–African American women.

Beta-defensin 2 is a host-derived antimicrobial peptide that, like other antimicrobial peptides, works at epithelial-mucosal barriers to combat bacteria; we have knowledge of its action from research on the gut, as well as some studies of the vaginal space in nonpregnant women that have focused on sexually transmitted infections.

Most exciting for us was the finding that higher levels of beta-defensin 2 appeared to lower the risk of sPTB in women who had a nonoptimal cervicovaginal microbiota. There’s an interplay between the host and the microbiota, in other words, and it’s one that could be essential to manipulate as we seek to reduce sPTB.
 

The cervical epithelial barrier

In the laboratory, meanwhile, we are learning how certain microbes are mechanistically involved in the pathogenesis of sPTB. Research over the last decade has suggested that disruption or breakdown of the cervical epithelial barrier drives cervical remodeling processes that precede sPTB. The question now is, do cervicovaginal bacteria associated with sPTB, or a nonoptimal cervicovaginal microbiota, cause disruption of the vaginal and cervical epithelial barrier – and how?

Using an in vitro model system, we found that Mobiluncus curtisii/mulieris, the bacterial taxa with the strongest association with sPTB in our Motherhood & Microbiome cohort and one that has long been associated with bacterial vaginosis, had a plethora of effects. It increased cell permeability and the expression of inflammatory mediators associated with cervical epithelial breakdown, and it altered expression of microRNAs that have been associated with sPTB in human studies.

Our study on Mobiluncus has served as proof of concept to us that, not only is the bacteria associated with sPTB, but that there are multiple mechanisms by which it can disrupt the cervicovaginal barrier and lead to cervical remodeling.⁵

The findings echo previous in vitro research on Gardnerella vaginalis, another anaerobic bacterium that has been associated with bacterial vaginosis and adverse obstetric outcomes, including sPTB.⁶ Using similar models, we found that G. vaginalis disrupts the cervical epithelial barrier through diverse mechanisms including the cleavage of certain proteins, the up-regulation of proinflammatory immune mediators, and altered gene expression.

Lactobacillus crispatus, on the other hand, conferred protection to the cervical epithelial barrier in this study by mitigating various G. vaginalis–induced effects.

Learning more about host-microbe interactions and the role of microbial metabolites in these interactions, as well as the role of altered gene expression in cervical function, will help us to more fully understand the biological mechanisms regulating cervicovaginal epithelial cells. At this point, we know that, as in the gut, bacteria commonly found in the cervicovaginal space play a significant role in regulating the function of epithelial cells (in both optimal and nonoptimal microbiota), and that various bacteria associated with sPTB contribute to poor outcomes by breaking down the cervical epithelium.
 

Therapeutic implications

Our growing knowledge of the cervicovaginal microbiota does not yet support screening or any particular interventions. We don’t know, for instance, that administering probiotics or prebiotics orally or vaginally will have any effect on rates of sPTB.

Ongoing research at all levels holds promise, however, for the development of diagnostics to identify women at risk for sPTB, and for the development of therapeutic strategies that aim to modify the microbiome and/or modify the immune response. We know from other areas of medicine that there are realistic ways to modulate the immune response and/or microbiota in a system to alter risk.

We need to more thoroughly understand the risk of particular microbiota and immune response factors – and how they vary by race and ethnicity – and we need to study the cervicovaginal microbiota of women before and during pregnancy to learn whether there is something about pregnancy or even about intercourse that can change one’s microbiome to a less favorable state.

It may well be possible in the near future to identify high-risk states of nonoptimal microbiota before conception – microbiota that, in and of themselves, may not be pathogenic but that become detrimental during pregnancy – and it should be possible to screen women early in pregnancy for microbial or immune signatures or both.

The question often arises in medicine of the validity of screening without having achieved certainty about treatments. However, in obstetrics, where we have different levels of care and the ability to personalize monitoring and care, identifying those at greatest risk still has value. Ultimately, with enough investment in all levels of research (basic, translational, and clinical), we can develop interventions and therapeutics that address a biologically plausible mechanism of sPTB and, as a result, achieve significant reductions in the rate of prematurity.

Dr. Elovitz is the Hilarie L. Morgan and Mitchell L. Morgan President’s Distinguished Professor in Women’s Health, vice chair of translational research, and director of the Maternal and Child Health Research Center, department of obstetrics and gynecology, at the University of Pennsylvania, Philadelphia. She disclosed holding a patent on a method to determine risk of preterm birth that relates to the microbiome. Email her at [email protected].

References

1. JAMA. 2017 Mar 14;317(10):1047-56.

2. NIH Human Microbiome Project. https://hmpdacc.org/.

3. PNAS. 2011 Mar 15;108 (Supplement 1):4680-7.

4. Nat Commun. 2019 Mar 21. doi: 10.1038/s41467-019-09285-9.

5. Anaerobe. 2019 Nov 21. doi: 10.1016/j.anaerobe.2019.102127.

6. Front Microbiol. 2018 Oct 8. doi: 10.3389/fmicb.2018.02181.

Prematurity remains the leading cause of neonatal morbidity and mortality, accounting for $26 billion a year in immediate costs, despite the implementation in obstetrics of a host of risk stratification algorithms and strategies for risk reduction, including the use of some medications.

It now is questionable whether injectable 17-alpha hydroxyprogesterone caproate (Makena) truly is efficacious in women who’ve had a prior spontaneous preterm birth (sPTB) – a Food and Drug Administration advisory committee last year recommended withdrawing it from the market based on results of an FDA confirmatory study. Even if the drug were efficacious, only a small percentage of the women who have an sPTB have had a prior one. The majority of sPTB occurs among women without such a history.

Vaginal progesterone appears to confer some protection in women found to have a short cervix during the second trimester, but this approach also has limited reach: Only 9% of women with sPTB had an antecedent short cervix in a 2017 study.¹ Like a history of sPTB, screening for short cervical length is a potentially helpful strategy for risk reduction, but it is not a strategy that will significantly impact the overall rate of prematurity.

We’ve fallen short in our goals to significantly reduce the public health impact of prematurity partly because we still do not understand the exact pathways and mechanisms by which sPTB occurs. The main working paradigm for myself and many other researchers over the past 2 decades has centered on infection in the uterus triggering inflammation, followed by cervical remodeling and ripening. Research in animal models, as well as human clinical trials targeting various infections and inflammation, have led to some insights and discoveries, but no successful interventions.

In the past decade, however, our research framework for understanding sPTB incorporates new questions about immunologic, microbiological, and molecular/cellular events that happen in the cervicovaginal space. We’ve learned more about the cervicovaginal microbiota, and most recently, our research at the University of Pennsylvania has elucidated the role that nonoptimal bacteria play in disrupting the cervical endothelial barrier and initiating the process of cervical remodeling that likely precedes sPTB.

We now know that there is an association between cervicovaginal microbial communities, immune responses, and sPTB. We also know that this association is stronger in black women and may help explain some of the observed racial disparities in sPTB. Although more research is needed to determine specific therapeutic strategies, new doors are open.
 

Host immune-microbial interactions

This new research paradigm has involved stepping back and asking basic questions, such as, what do we really know about the cervicovaginal space? In actuality, we know very little. We know little about the immune function of the vaginal and cervical epithelial cells in pregnancy, for instance, and there is a large gap in knowledge regarding the biomechanics of the cervix – a remarkable organ that can change shape and function in a matter of minutes. Studies on the biomechanics of the cervix during pregnancy and in labor are still in their infancy.

However, lessons can be drawn from research on inflammatory bowel disease and other disorders involving the gut. In the gastrointestinal tract, epithelial cells have been found to act as sentinels, forming a mucosal barrier against bacterial pathogens and secreting various immune factors. Research in this field also has shown that microbes living in the gut produce metabolites; that these microbial metabolites may be the key messengers from the microbial communities to the epithelial barrier; and that the microbes, microbial metabolites, and immune responses are responsible for triggering inflammatory processes in the tissues underneath.

In 2011, Jacques Ravel, PhD, who was part of the National Institutes of Health’s Human Microbiome Project, characterized the vaginal microbiome of reproductive-age women for the first time.² His paper classified the vaginal microbial communities of approximately 400 asymptomatic women of various ethnicities into five “community state types” (CSTs) based on the predominant bacteria found in the cervicovaginal space.³

On the heels of his research, Dr. Ravel and I launched an NIH-funded study involving a prospective cohort of 2,000 women with singleton pregnancies – the Motherhood & Microbiome cohort – to look at the cervicovaginal microbiota, the local immune response, and the risk of sPTB.⁴ Cervicovaginal samples were collected at 16-20 weeks’ gestation and during two subsequent clinical visits. From this cohort, which was composed mostly of African American women (74.5%), we conducted a nested case-controlled study of 103 cases of sPTB and 432 women who delivered at term, matched for race.

We carefully adjudicated the deliveries in our 2,000-person cohort so that we homed in on sPTB as opposed to preterm births that are medically indicated for reasons such as fetal distress or preeclampsia. (Several prior studies looking at the associations between the cervicovaginal microbiome had a heterogeneous phenotyping of PTB that made it hard to draw definitive conclusions.)

Our focus in assessing the microbiome and immunologic profiles was on the samples collected at the earliest time points in pregnancy because we hoped to detect a “signature” that could predict an outcome months later. Indeed, we found that the nonoptimal microbiota, known in microbiological terms as CST IV, was associated with about a 150% increased risk of sPTB. This community comprises a dominant array of anaerobic bacteria and a paucity of Lactobacillus species.

We also found that a larger proportion of African American women, compared with non–African American women, had this nonoptimal microbiota early in pregnancy (40% vs. 15%), which is consistent with previous studies in pregnancy and nonpregnancy showing lower levels of Lactobacillus species in the cervicovaginal microbiome of African American women.

Even more interesting was the finding that, although the rate of sPTB was higher in African American women and the effect of CST IV on sPTB was stronger in these women, the risk of sPTB couldn’t be explained solely by the presence of CST IV. Some women with this nonoptimal microbiome delivered at term, whereas others with more optimal microbiome types had sPTBs. This suggests that other factors contribute to African American women having a nonoptimal microbiota and being especially predisposed to sPTB.

Through the study’s immunologic profiling, we found a significant difference in the cervicovaginal levels of an immune factor, beta-defensin 2, between African American women who delivered at term and those who had a sPTB. Women who had a sPTB, even those who had higher levels of Lactobacillus species, had lower levels of beta-defensin 2. This association was not found in non–African American women.

Beta-defensin 2 is a host-derived antimicrobial peptide that, like other antimicrobial peptides, works at epithelial-mucosal barriers to combat bacteria; we have knowledge of its action from research on the gut, as well as some studies of the vaginal space in nonpregnant women that have focused on sexually transmitted infections.

Most exciting for us was the finding that higher levels of beta-defensin 2 appeared to lower the risk of sPTB in women who had a nonoptimal cervicovaginal microbiota. There’s an interplay between the host and the microbiota, in other words, and it’s one that could be essential to manipulate as we seek to reduce sPTB.
 

The cervical epithelial barrier

In the laboratory, meanwhile, we are learning how certain microbes are mechanistically involved in the pathogenesis of sPTB. Research over the last decade has suggested that disruption or breakdown of the cervical epithelial barrier drives cervical remodeling processes that precede sPTB. The question now is, do cervicovaginal bacteria associated with sPTB, or a nonoptimal cervicovaginal microbiota, cause disruption of the vaginal and cervical epithelial barrier – and how?

Using an in vitro model system, we found that Mobiluncus curtisii/mulieris, the bacterial taxa with the strongest association with sPTB in our Motherhood & Microbiome cohort and one that has long been associated with bacterial vaginosis, had a plethora of effects. It increased cell permeability and the expression of inflammatory mediators associated with cervical epithelial breakdown, and it altered expression of microRNAs that have been associated with sPTB in human studies.

Our study on Mobiluncus has served as proof of concept to us that, not only is the bacteria associated with sPTB, but that there are multiple mechanisms by which it can disrupt the cervicovaginal barrier and lead to cervical remodeling.⁵

The findings echo previous in vitro research on Gardnerella vaginalis, another anaerobic bacterium that has been associated with bacterial vaginosis and adverse obstetric outcomes, including sPTB.⁶ Using similar models, we found that G. vaginalis disrupts the cervical epithelial barrier through diverse mechanisms including the cleavage of certain proteins, the up-regulation of proinflammatory immune mediators, and altered gene expression.

Lactobacillus crispatus, on the other hand, conferred protection to the cervical epithelial barrier in this study by mitigating various G. vaginalis–induced effects.

Learning more about host-microbe interactions and the role of microbial metabolites in these interactions, as well as the role of altered gene expression in cervical function, will help us to more fully understand the biological mechanisms regulating cervicovaginal epithelial cells. At this point, we know that, as in the gut, bacteria commonly found in the cervicovaginal space play a significant role in regulating the function of epithelial cells (in both optimal and nonoptimal microbiota), and that various bacteria associated with sPTB contribute to poor outcomes by breaking down the cervical epithelium.
 

Therapeutic implications

Our growing knowledge of the cervicovaginal microbiota does not yet support screening or any particular interventions. We don’t know, for instance, that administering probiotics or prebiotics orally or vaginally will have any effect on rates of sPTB.

Ongoing research at all levels holds promise, however, for the development of diagnostics to identify women at risk for sPTB, and for the development of therapeutic strategies that aim to modify the microbiome and/or modify the immune response. We know from other areas of medicine that there are realistic ways to modulate the immune response and/or microbiota in a system to alter risk.

We need to more thoroughly understand the risk of particular microbiota and immune response factors – and how they vary by race and ethnicity – and we need to study the cervicovaginal microbiota of women before and during pregnancy to learn whether there is something about pregnancy or even about intercourse that can change one’s microbiome to a less favorable state.

It may well be possible in the near future to identify high-risk states of nonoptimal microbiota before conception – microbiota that, in and of themselves, may not be pathogenic but that become detrimental during pregnancy – and it should be possible to screen women early in pregnancy for microbial or immune signatures or both.

The question often arises in medicine of the validity of screening without having achieved certainty about treatments. However, in obstetrics, where we have different levels of care and the ability to personalize monitoring and care, identifying those at greatest risk still has value. Ultimately, with enough investment in all levels of research (basic, translational, and clinical), we can develop interventions and therapeutics that address a biologically plausible mechanism of sPTB and, as a result, achieve significant reductions in the rate of prematurity.

Dr. Elovitz is the Hilarie L. Morgan and Mitchell L. Morgan President’s Distinguished Professor in Women’s Health, vice chair of translational research, and director of the Maternal and Child Health Research Center, department of obstetrics and gynecology, at the University of Pennsylvania, Philadelphia. She disclosed holding a patent on a method to determine risk of preterm birth that relates to the microbiome. Email her at [email protected].

References

1. JAMA. 2017 Mar 14;317(10):1047-56.

2. NIH Human Microbiome Project. https://hmpdacc.org/.

3. PNAS. 2011 Mar 15;108 (Supplement 1):4680-7.

4. Nat Commun. 2019 Mar 21. doi: 10.1038/s41467-019-09285-9.

5. Anaerobe. 2019 Nov 21. doi: 10.1016/j.anaerobe.2019.102127.

6. Front Microbiol. 2018 Oct 8. doi: 10.3389/fmicb.2018.02181.

Prematurity remains the leading cause of neonatal morbidity and mortality, accounting for $26 billion a year in immediate costs, despite the implementation in obstetrics of a host of risk stratification algorithms and strategies for risk reduction, including the use of some medications.

It now is questionable whether injectable 17-alpha hydroxyprogesterone caproate (Makena) truly is efficacious in women who’ve had a prior spontaneous preterm birth (sPTB) – a Food and Drug Administration advisory committee last year recommended withdrawing it from the market based on results of an FDA confirmatory study. Even if the drug were efficacious, only a small percentage of the women who have an sPTB have had a prior one. The majority of sPTB occurs among women without such a history.

Vaginal progesterone appears to confer some protection in women found to have a short cervix during the second trimester, but this approach also has limited reach: Only 9% of women with sPTB had an antecedent short cervix in a 2017 study.¹ Like a history of sPTB, screening for short cervical length is a potentially helpful strategy for risk reduction, but it is not a strategy that will significantly impact the overall rate of prematurity.

We’ve fallen short in our goals to significantly reduce the public health impact of prematurity partly because we still do not understand the exact pathways and mechanisms by which sPTB occurs. The main working paradigm for myself and many other researchers over the past 2 decades has centered on infection in the uterus triggering inflammation, followed by cervical remodeling and ripening. Research in animal models, as well as human clinical trials targeting various infections and inflammation, have led to some insights and discoveries, but no successful interventions.

In the past decade, however, our research framework for understanding sPTB incorporates new questions about immunologic, microbiological, and molecular/cellular events that happen in the cervicovaginal space. We’ve learned more about the cervicovaginal microbiota, and most recently, our research at the University of Pennsylvania has elucidated the role that nonoptimal bacteria play in disrupting the cervical endothelial barrier and initiating the process of cervical remodeling that likely precedes sPTB.

We now know that there is an association between cervicovaginal microbial communities, immune responses, and sPTB. We also know that this association is stronger in black women and may help explain some of the observed racial disparities in sPTB. Although more research is needed to determine specific therapeutic strategies, new doors are open.
 

Host immune-microbial interactions

This new research paradigm has involved stepping back and asking basic questions, such as, what do we really know about the cervicovaginal space? In actuality, we know very little. We know little about the immune function of the vaginal and cervical epithelial cells in pregnancy, for instance, and there is a large gap in knowledge regarding the biomechanics of the cervix – a remarkable organ that can change shape and function in a matter of minutes. Studies on the biomechanics of the cervix during pregnancy and in labor are still in their infancy.

However, lessons can be drawn from research on inflammatory bowel disease and other disorders involving the gut. In the gastrointestinal tract, epithelial cells have been found to act as sentinels, forming a mucosal barrier against bacterial pathogens and secreting various immune factors. Research in this field also has shown that microbes living in the gut produce metabolites; that these microbial metabolites may be the key messengers from the microbial communities to the epithelial barrier; and that the microbes, microbial metabolites, and immune responses are responsible for triggering inflammatory processes in the tissues underneath.

In 2011, Jacques Ravel, PhD, who was part of the National Institutes of Health’s Human Microbiome Project, characterized the vaginal microbiome of reproductive-age women for the first time.² His paper classified the vaginal microbial communities of approximately 400 asymptomatic women of various ethnicities into five “community state types” (CSTs) based on the predominant bacteria found in the cervicovaginal space.³

On the heels of his research, Dr. Ravel and I launched an NIH-funded study involving a prospective cohort of 2,000 women with singleton pregnancies – the Motherhood & Microbiome cohort – to look at the cervicovaginal microbiota, the local immune response, and the risk of sPTB.⁴ Cervicovaginal samples were collected at 16-20 weeks’ gestation and during two subsequent clinical visits. From this cohort, which was composed mostly of African American women (74.5%), we conducted a nested case-controlled study of 103 cases of sPTB and 432 women who delivered at term, matched for race.

We carefully adjudicated the deliveries in our 2,000-person cohort so that we homed in on sPTB as opposed to preterm births that are medically indicated for reasons such as fetal distress or preeclampsia. (Several prior studies looking at the associations between the cervicovaginal microbiome had a heterogeneous phenotyping of PTB that made it hard to draw definitive conclusions.)

Our focus in assessing the microbiome and immunologic profiles was on the samples collected at the earliest time points in pregnancy because we hoped to detect a “signature” that could predict an outcome months later. Indeed, we found that the nonoptimal microbiota, known in microbiological terms as CST IV, was associated with about a 150% increased risk of sPTB. This community comprises a dominant array of anaerobic bacteria and a paucity of Lactobacillus species.

We also found that a larger proportion of African American women, compared with non–African American women, had this nonoptimal microbiota early in pregnancy (40% vs. 15%), which is consistent with previous studies in pregnancy and nonpregnancy showing lower levels of Lactobacillus species in the cervicovaginal microbiome of African American women.

Even more interesting was the finding that, although the rate of sPTB was higher in African American women and the effect of CST IV on sPTB was stronger in these women, the risk of sPTB couldn’t be explained solely by the presence of CST IV. Some women with this nonoptimal microbiome delivered at term, whereas others with more optimal microbiome types had sPTBs. This suggests that other factors contribute to African American women having a nonoptimal microbiota and being especially predisposed to sPTB.

Through the study’s immunologic profiling, we found a significant difference in the cervicovaginal levels of an immune factor, beta-defensin 2, between African American women who delivered at term and those who had a sPTB. Women who had a sPTB, even those who had higher levels of Lactobacillus species, had lower levels of beta-defensin 2. This association was not found in non–African American women.

Beta-defensin 2 is a host-derived antimicrobial peptide that, like other antimicrobial peptides, works at epithelial-mucosal barriers to combat bacteria; we have knowledge of its action from research on the gut, as well as some studies of the vaginal space in nonpregnant women that have focused on sexually transmitted infections.

Most exciting for us was the finding that higher levels of beta-defensin 2 appeared to lower the risk of sPTB in women who had a nonoptimal cervicovaginal microbiota. There’s an interplay between the host and the microbiota, in other words, and it’s one that could be essential to manipulate as we seek to reduce sPTB.
 

The cervical epithelial barrier

In the laboratory, meanwhile, we are learning how certain microbes are mechanistically involved in the pathogenesis of sPTB. Research over the last decade has suggested that disruption or breakdown of the cervical epithelial barrier drives cervical remodeling processes that precede sPTB. The question now is, do cervicovaginal bacteria associated with sPTB, or a nonoptimal cervicovaginal microbiota, cause disruption of the vaginal and cervical epithelial barrier – and how?

Using an in vitro model system, we found that Mobiluncus curtisii/mulieris, the bacterial taxa with the strongest association with sPTB in our Motherhood & Microbiome cohort and one that has long been associated with bacterial vaginosis, had a plethora of effects. It increased cell permeability and the expression of inflammatory mediators associated with cervical epithelial breakdown, and it altered expression of microRNAs that have been associated with sPTB in human studies.

Our study on Mobiluncus has served as proof of concept to us that, not only is the bacteria associated with sPTB, but that there are multiple mechanisms by which it can disrupt the cervicovaginal barrier and lead to cervical remodeling.⁵

The findings echo previous in vitro research on Gardnerella vaginalis, another anaerobic bacterium that has been associated with bacterial vaginosis and adverse obstetric outcomes, including sPTB.⁶ Using similar models, we found that G. vaginalis disrupts the cervical epithelial barrier through diverse mechanisms including the cleavage of certain proteins, the up-regulation of proinflammatory immune mediators, and altered gene expression.

Lactobacillus crispatus, on the other hand, conferred protection to the cervical epithelial barrier in this study by mitigating various G. vaginalis–induced effects.

Learning more about host-microbe interactions and the role of microbial metabolites in these interactions, as well as the role of altered gene expression in cervical function, will help us to more fully understand the biological mechanisms regulating cervicovaginal epithelial cells. At this point, we know that, as in the gut, bacteria commonly found in the cervicovaginal space play a significant role in regulating the function of epithelial cells (in both optimal and nonoptimal microbiota), and that various bacteria associated with sPTB contribute to poor outcomes by breaking down the cervical epithelium.
 

Therapeutic implications

Our growing knowledge of the cervicovaginal microbiota does not yet support screening or any particular interventions. We don’t know, for instance, that administering probiotics or prebiotics orally or vaginally will have any effect on rates of sPTB.

Ongoing research at all levels holds promise, however, for the development of diagnostics to identify women at risk for sPTB, and for the development of therapeutic strategies that aim to modify the microbiome and/or modify the immune response. We know from other areas of medicine that there are realistic ways to modulate the immune response and/or microbiota in a system to alter risk.

We need to more thoroughly understand the risk of particular microbiota and immune response factors – and how they vary by race and ethnicity – and we need to study the cervicovaginal microbiota of women before and during pregnancy to learn whether there is something about pregnancy or even about intercourse that can change one’s microbiome to a less favorable state.

It may well be possible in the near future to identify high-risk states of nonoptimal microbiota before conception – microbiota that, in and of themselves, may not be pathogenic but that become detrimental during pregnancy – and it should be possible to screen women early in pregnancy for microbial or immune signatures or both.

The question often arises in medicine of the validity of screening without having achieved certainty about treatments. However, in obstetrics, where we have different levels of care and the ability to personalize monitoring and care, identifying those at greatest risk still has value. Ultimately, with enough investment in all levels of research (basic, translational, and clinical), we can develop interventions and therapeutics that address a biologically plausible mechanism of sPTB and, as a result, achieve significant reductions in the rate of prematurity.

Dr. Elovitz is the Hilarie L. Morgan and Mitchell L. Morgan President’s Distinguished Professor in Women’s Health, vice chair of translational research, and director of the Maternal and Child Health Research Center, department of obstetrics and gynecology, at the University of Pennsylvania, Philadelphia. She disclosed holding a patent on a method to determine risk of preterm birth that relates to the microbiome. Email her at [email protected].

References

1. JAMA. 2017 Mar 14;317(10):1047-56.

2. NIH Human Microbiome Project. https://hmpdacc.org/.

3. PNAS. 2011 Mar 15;108 (Supplement 1):4680-7.

4. Nat Commun. 2019 Mar 21. doi: 10.1038/s41467-019-09285-9.

5. Anaerobe. 2019 Nov 21. doi: 10.1016/j.anaerobe.2019.102127.

6. Front Microbiol. 2018 Oct 8. doi: 10.3389/fmicb.2018.02181.

Preventing infant mortality remains a significant challenge for ob.gyns. Despite the availability of a multitude of preventive and treatment options and some of the best possible medical care offered in the world, the United States lags behind many other developed and developing countries in its rate of infant deaths, which was an estimated 5.8 deaths per 1,000 live births in 2017. We can, and must, do better.

One of the major contributing factors to infant mortality is preterm birth. Defined as birth occurring prior to 37 weeks’ gestation, preterm birth is associated with a myriad of severe neonatal sequelae: low birth weight, bacterial sepsis, neonatal hemorrhage, and respiratory distress syndrome, among others. Therefore, many within the clinical and biomedical research spheres recognize that preventing preterm birth means reducing infant deaths.

However, therein lies the conundrum. We know very little about what causes preterm birth, which renders the current therapeutic strategies – such as use of progesterone supplements or cerclage placement – good for some but not all patients. It is thus vital to continue research to unravel the underlying mechanisms of preterm birth.

A promising area of investigation is the field of microbiome research, which has made great strides in advancing our awareness of the critical role of the millions of organisms living on and within us in maintaining health and fighting disease. For example, we now realize that eradicating all the commensals in our gastrointestinal tract has unintended and very negative consequences and, for patients whose good bacteria have been eliminated, fecal transplant is a therapeutic option. Therefore, it stands to reason that the microbes found in the vagina contribute significantly to women’s overall reproductive health.

The publication of the groundbreaking study characterizing the vaginal microbiome species in reproductive-age women opened new avenues of research into how these organisms contribute to women’s health. Importantly, this work, led initially by Jacques Ravel, PhD, a professor in the department of microbiology & immunology and associate director of the Institute for Genome Sciences at the University of Maryland School of Medicine, has spawned additional investigations into the potential role of the vaginal microbiome in preterm birth.

To provide some insight into the research around how the microorganisms in the vagina may induce or prevent preterm birth is our guest author, Michal A. Elovitz, MD, the Hilarie L. Morgan and Mitchell L. Morgan President’s Distinguished Professor in Women’s Health, vice chair of translational research, and director of the Maternal and Child Health Research Center, department of obstetrics and gynecology, at the University of Pennsylvania, Philadelphia.

Dr. Reece, who specializes in maternal-fetal medicine, is executive vice president for medical affairs at the University of Maryland School of Medicine as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. He is the medical editor of this column. He said he had no relevant financial disclosures. Contact him at [email protected].

Preventing infant mortality remains a significant challenge for ob.gyns. Despite the availability of a multitude of preventive and treatment options and some of the best possible medical care offered in the world, the United States lags behind many other developed and developing countries in its rate of infant deaths, which was an estimated 5.8 deaths per 1,000 live births in 2017. We can, and must, do better.

One of the major contributing factors to infant mortality is preterm birth. Defined as birth occurring prior to 37 weeks’ gestation, preterm birth is associated with a myriad of severe neonatal sequelae: low birth weight, bacterial sepsis, neonatal hemorrhage, and respiratory distress syndrome, among others. Therefore, many within the clinical and biomedical research spheres recognize that preventing preterm birth means reducing infant deaths.

However, therein lies the conundrum. We know very little about what causes preterm birth, which renders the current therapeutic strategies – such as use of progesterone supplements or cerclage placement – good for some but not all patients. It is thus vital to continue research to unravel the underlying mechanisms of preterm birth.

A promising area of investigation is the field of microbiome research, which has made great strides in advancing our awareness of the critical role of the millions of organisms living on and within us in maintaining health and fighting disease. For example, we now realize that eradicating all the commensals in our gastrointestinal tract has unintended and very negative consequences and, for patients whose good bacteria have been eliminated, fecal transplant is a therapeutic option. Therefore, it stands to reason that the microbes found in the vagina contribute significantly to women’s overall reproductive health.

The publication of the groundbreaking study characterizing the vaginal microbiome species in reproductive-age women opened new avenues of research into how these organisms contribute to women’s health. Importantly, this work, led initially by Jacques Ravel, PhD, a professor in the department of microbiology & immunology and associate director of the Institute for Genome Sciences at the University of Maryland School of Medicine, has spawned additional investigations into the potential role of the vaginal microbiome in preterm birth.

To provide some insight into the research around how the microorganisms in the vagina may induce or prevent preterm birth is our guest author, Michal A. Elovitz, MD, the Hilarie L. Morgan and Mitchell L. Morgan President’s Distinguished Professor in Women’s Health, vice chair of translational research, and director of the Maternal and Child Health Research Center, department of obstetrics and gynecology, at the University of Pennsylvania, Philadelphia.

Dr. Reece, who specializes in maternal-fetal medicine, is executive vice president for medical affairs at the University of Maryland School of Medicine as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. He is the medical editor of this column. He said he had no relevant financial disclosures. Contact him at [email protected].

Preventing infant mortality remains a significant challenge for ob.gyns. Despite the availability of a multitude of preventive and treatment options and some of the best possible medical care offered in the world, the United States lags behind many other developed and developing countries in its rate of infant deaths, which was an estimated 5.8 deaths per 1,000 live births in 2017. We can, and must, do better.

One of the major contributing factors to infant mortality is preterm birth. Defined as birth occurring prior to 37 weeks’ gestation, preterm birth is associated with a myriad of severe neonatal sequelae: low birth weight, bacterial sepsis, neonatal hemorrhage, and respiratory distress syndrome, among others. Therefore, many within the clinical and biomedical research spheres recognize that preventing preterm birth means reducing infant deaths.

However, therein lies the conundrum. We know very little about what causes preterm birth, which renders the current therapeutic strategies – such as use of progesterone supplements or cerclage placement – good for some but not all patients. It is thus vital to continue research to unravel the underlying mechanisms of preterm birth.

A promising area of investigation is the field of microbiome research, which has made great strides in advancing our awareness of the critical role of the millions of organisms living on and within us in maintaining health and fighting disease. For example, we now realize that eradicating all the commensals in our gastrointestinal tract has unintended and very negative consequences and, for patients whose good bacteria have been eliminated, fecal transplant is a therapeutic option. Therefore, it stands to reason that the microbes found in the vagina contribute significantly to women’s overall reproductive health.

The publication of the groundbreaking study characterizing the vaginal microbiome species in reproductive-age women opened new avenues of research into how these organisms contribute to women’s health. Importantly, this work, led initially by Jacques Ravel, PhD, a professor in the department of microbiology & immunology and associate director of the Institute for Genome Sciences at the University of Maryland School of Medicine, has spawned additional investigations into the potential role of the vaginal microbiome in preterm birth.

To provide some insight into the research around how the microorganisms in the vagina may induce or prevent preterm birth is our guest author, Michal A. Elovitz, MD, the Hilarie L. Morgan and Mitchell L. Morgan President’s Distinguished Professor in Women’s Health, vice chair of translational research, and director of the Maternal and Child Health Research Center, department of obstetrics and gynecology, at the University of Pennsylvania, Philadelphia.

Dr. Reece, who specializes in maternal-fetal medicine, is executive vice president for medical affairs at the University of Maryland School of Medicine as well as the John Z. and Akiko K. Bowers Distinguished Professor and dean of the school of medicine. He is the medical editor of this column. He said he had no relevant financial disclosures. Contact him at [email protected].

While preparing to write this technology column, I received a great deal of insight from the unlikeliest of sources: my mother-in-law.

Now don’t get me wrong – she’s a truly lovely, intelligent, and capable woman. I have sought her advice often on many things and have always been impressed by her wisdom and pragmatism, but I’ve just never thought of asking her for her opinion on medicine or technology, as I considered her knowledge of both subjects to be limited.

This occasion changed my opinion. In fact, I believe that, as health care IT becomes more complex, people like my mother-in-law may be exactly who we should be looking to for answers.

A few weeks ago, my mother-in-law and I were discussing her recent trip to the doctor. When she mentioned some lab tests, I suggested that we log in to her patient portal to view the results. This elicited several questions and a declaration of frustration.

“Which portal?” she asked. “I have so many and can’t keep all of the websites and passwords straight! Why can’t all of my doctors use the same portal, and why do they all have different password requirements?”

As she spoke these words, I was immediately struck with an unfortunate reality of EHRs: We have done a brilliant job creating state-of-the-art digital castles and have filled them with the data needed to revolutionize care and improve population health – but we haven’t given our patients the keys to get inside.

We must ask ourselves if, in trying to construct fortresses of information around our patients, we have lost sight of the individuals in the center. I believe that we can answer this question and improve the benefits of patient portals, but we all must agree to a few simple steps to streamline the experience for everyone.
 

Make it easy

A study recently published in the Journal of General Internal Medicine surveyed several hospitals on their usage of patient portals. After determining whether or not the institutions had such portals, the authors then investigated to find out what, if any, guidance was provided to patients about how to use them.

Their findings are frustrating, though not surprising. While 89% of hospitals had some form of patient portal, only 65% of those “had links that were easily found, defined as links accessible within two clicks from the home page.”

Furthermore, even in cases where portals were easily found, good instructions on how to use them were missing. Those instructions that did exist centered on rules and restrictions and laying out “terms and conditions” and informing patients on “what not to do,” rather than explaining how to make the most of the experience.

According to the authors, “this focus on curtailing behavior, and the hurdles placed on finding and understanding guidance, suggest that some hospitals may be prioritizing reducing liability over improving the patient experience with portals.”

If we want our patients to use them, portals must be easy to access and intuitive to use. They also must provide value.
 

Make it meaningful

Patient portals have proliferated exponentially over the last 10 years, thanks to government incentive programs. One such program, known as “meaningful use,” is primarily responsible for this, as it made implementation of a patient portal one of its core requirements.

Sadly, in spite of its oft-reviled name, the meaningful use program never defined patient-friendly standards of usability for patient portals. As a result, current portals just aren’t very good. Patients like my mother-in-law find them to be too numerous, too unfriendly to use, and too limited, so they are not being used to their full potential.

In fact, many institutions may choose not to enable all of the available features in order to limit technical issues and reduce the burden on providers. In the study referenced above, only 63% of portals offered the ability for patients to communicate directly with their physicians, and only 43% offered the ability to refill prescriptions.

When enabled, these functions improve patient engagement and efficiency. Without them, patients are less likely to log on, and physicians are forced to rely on less-efficient telephone calls or traditional letters to communicate results to their patients.
 

Put the patient, not the portal, at the center

History has all but forgotten the attempts by tech giants such as Google and Microsoft to create personal health records. While these initially seemed like a wonderful concept, they sadly proved to be a total flop. Some patients embraced the idea, but security concerns and the lack of buy-in from EHR vendors significantly limited their uptake.

They may simply have been ahead of their time.

A decade later, wearable technology and telemedicine are ushering in a new era of patient-centric care. Individuals have been embracing a greater share of the responsibility for their own personal health information, yet most EHRs lack the ability to easily incorporate data acquired outside physicians’ offices.

It’s time for EHR vendors to go all in and change that. Instead of enslaving patients to the tyranny of fragmented health records, they should prioritize the creation of a robust, standardized, and portable health record that travels with the patient, not the other way around.

Have any other ideas on how to improve patient engagement? We’d love to hear about them and share them in a future column.

If you want to contribute but don’t have any ideas, we have a suggestion: Ask your mother-in-law. You may be surprised at what you learn!

Dr. Notte is a family physician and associate chief medical information officer for Abington (Pa.) Hospital–Jefferson Health. Follow him on twitter (@doctornotte). Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the family medicine residency program at Abington Hospital–Jefferson Health.

Reference

Lee JL et al. J Gen Intern Med. 2019 Nov 12. doi: 10.1007/s11606-019-05528-z.

While preparing to write this technology column, I received a great deal of insight from the unlikeliest of sources: my mother-in-law.

Now don’t get me wrong – she’s a truly lovely, intelligent, and capable woman. I have sought her advice often on many things and have always been impressed by her wisdom and pragmatism, but I’ve just never thought of asking her for her opinion on medicine or technology, as I considered her knowledge of both subjects to be limited.

This occasion changed my opinion. In fact, I believe that, as health care IT becomes more complex, people like my mother-in-law may be exactly who we should be looking to for answers.

A few weeks ago, my mother-in-law and I were discussing her recent trip to the doctor. When she mentioned some lab tests, I suggested that we log in to her patient portal to view the results. This elicited several questions and a declaration of frustration.

“Which portal?” she asked. “I have so many and can’t keep all of the websites and passwords straight! Why can’t all of my doctors use the same portal, and why do they all have different password requirements?”

As she spoke these words, I was immediately struck with an unfortunate reality of EHRs: We have done a brilliant job creating state-of-the-art digital castles and have filled them with the data needed to revolutionize care and improve population health – but we haven’t given our patients the keys to get inside.

We must ask ourselves if, in trying to construct fortresses of information around our patients, we have lost sight of the individuals in the center. I believe that we can answer this question and improve the benefits of patient portals, but we all must agree to a few simple steps to streamline the experience for everyone.
 

Make it easy

A study recently published in the Journal of General Internal Medicine surveyed several hospitals on their usage of patient portals. After determining whether or not the institutions had such portals, the authors then investigated to find out what, if any, guidance was provided to patients about how to use them.

Their findings are frustrating, though not surprising. While 89% of hospitals had some form of patient portal, only 65% of those “had links that were easily found, defined as links accessible within two clicks from the home page.”

Furthermore, even in cases where portals were easily found, good instructions on how to use them were missing. Those instructions that did exist centered on rules and restrictions and laying out “terms and conditions” and informing patients on “what not to do,” rather than explaining how to make the most of the experience.

According to the authors, “this focus on curtailing behavior, and the hurdles placed on finding and understanding guidance, suggest that some hospitals may be prioritizing reducing liability over improving the patient experience with portals.”

If we want our patients to use them, portals must be easy to access and intuitive to use. They also must provide value.
 

Make it meaningful

Patient portals have proliferated exponentially over the last 10 years, thanks to government incentive programs. One such program, known as “meaningful use,” is primarily responsible for this, as it made implementation of a patient portal one of its core requirements.

Sadly, in spite of its oft-reviled name, the meaningful use program never defined patient-friendly standards of usability for patient portals. As a result, current portals just aren’t very good. Patients like my mother-in-law find them to be too numerous, too unfriendly to use, and too limited, so they are not being used to their full potential.

In fact, many institutions may choose not to enable all of the available features in order to limit technical issues and reduce the burden on providers. In the study referenced above, only 63% of portals offered the ability for patients to communicate directly with their physicians, and only 43% offered the ability to refill prescriptions.

When enabled, these functions improve patient engagement and efficiency. Without them, patients are less likely to log on, and physicians are forced to rely on less-efficient telephone calls or traditional letters to communicate results to their patients.
 

Put the patient, not the portal, at the center

History has all but forgotten the attempts by tech giants such as Google and Microsoft to create personal health records. While these initially seemed like a wonderful concept, they sadly proved to be a total flop. Some patients embraced the idea, but security concerns and the lack of buy-in from EHR vendors significantly limited their uptake.

They may simply have been ahead of their time.

A decade later, wearable technology and telemedicine are ushering in a new era of patient-centric care. Individuals have been embracing a greater share of the responsibility for their own personal health information, yet most EHRs lack the ability to easily incorporate data acquired outside physicians’ offices.

It’s time for EHR vendors to go all in and change that. Instead of enslaving patients to the tyranny of fragmented health records, they should prioritize the creation of a robust, standardized, and portable health record that travels with the patient, not the other way around.

Have any other ideas on how to improve patient engagement? We’d love to hear about them and share them in a future column.

If you want to contribute but don’t have any ideas, we have a suggestion: Ask your mother-in-law. You may be surprised at what you learn!

Dr. Notte is a family physician and associate chief medical information officer for Abington (Pa.) Hospital–Jefferson Health. Follow him on twitter (@doctornotte). Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the family medicine residency program at Abington Hospital–Jefferson Health.

Reference

Lee JL et al. J Gen Intern Med. 2019 Nov 12. doi: 10.1007/s11606-019-05528-z.

While preparing to write this technology column, I received a great deal of insight from the unlikeliest of sources: my mother-in-law.

Now don’t get me wrong – she’s a truly lovely, intelligent, and capable woman. I have sought her advice often on many things and have always been impressed by her wisdom and pragmatism, but I’ve just never thought of asking her for her opinion on medicine or technology, as I considered her knowledge of both subjects to be limited.

This occasion changed my opinion. In fact, I believe that, as health care IT becomes more complex, people like my mother-in-law may be exactly who we should be looking to for answers.

A few weeks ago, my mother-in-law and I were discussing her recent trip to the doctor. When she mentioned some lab tests, I suggested that we log in to her patient portal to view the results. This elicited several questions and a declaration of frustration.

“Which portal?” she asked. “I have so many and can’t keep all of the websites and passwords straight! Why can’t all of my doctors use the same portal, and why do they all have different password requirements?”

As she spoke these words, I was immediately struck with an unfortunate reality of EHRs: We have done a brilliant job creating state-of-the-art digital castles and have filled them with the data needed to revolutionize care and improve population health – but we haven’t given our patients the keys to get inside.

We must ask ourselves if, in trying to construct fortresses of information around our patients, we have lost sight of the individuals in the center. I believe that we can answer this question and improve the benefits of patient portals, but we all must agree to a few simple steps to streamline the experience for everyone.
 

Make it easy

A study recently published in the Journal of General Internal Medicine surveyed several hospitals on their usage of patient portals. After determining whether or not the institutions had such portals, the authors then investigated to find out what, if any, guidance was provided to patients about how to use them.

Their findings are frustrating, though not surprising. While 89% of hospitals had some form of patient portal, only 65% of those “had links that were easily found, defined as links accessible within two clicks from the home page.”

Furthermore, even in cases where portals were easily found, good instructions on how to use them were missing. Those instructions that did exist centered on rules and restrictions and laying out “terms and conditions” and informing patients on “what not to do,” rather than explaining how to make the most of the experience.

According to the authors, “this focus on curtailing behavior, and the hurdles placed on finding and understanding guidance, suggest that some hospitals may be prioritizing reducing liability over improving the patient experience with portals.”

If we want our patients to use them, portals must be easy to access and intuitive to use. They also must provide value.
 

Make it meaningful

Patient portals have proliferated exponentially over the last 10 years, thanks to government incentive programs. One such program, known as “meaningful use,” is primarily responsible for this, as it made implementation of a patient portal one of its core requirements.

Sadly, in spite of its oft-reviled name, the meaningful use program never defined patient-friendly standards of usability for patient portals. As a result, current portals just aren’t very good. Patients like my mother-in-law find them to be too numerous, too unfriendly to use, and too limited, so they are not being used to their full potential.

In fact, many institutions may choose not to enable all of the available features in order to limit technical issues and reduce the burden on providers. In the study referenced above, only 63% of portals offered the ability for patients to communicate directly with their physicians, and only 43% offered the ability to refill prescriptions.

When enabled, these functions improve patient engagement and efficiency. Without them, patients are less likely to log on, and physicians are forced to rely on less-efficient telephone calls or traditional letters to communicate results to their patients.
 

Put the patient, not the portal, at the center

History has all but forgotten the attempts by tech giants such as Google and Microsoft to create personal health records. While these initially seemed like a wonderful concept, they sadly proved to be a total flop. Some patients embraced the idea, but security concerns and the lack of buy-in from EHR vendors significantly limited their uptake.

They may simply have been ahead of their time.

A decade later, wearable technology and telemedicine are ushering in a new era of patient-centric care. Individuals have been embracing a greater share of the responsibility for their own personal health information, yet most EHRs lack the ability to easily incorporate data acquired outside physicians’ offices.

It’s time for EHR vendors to go all in and change that. Instead of enslaving patients to the tyranny of fragmented health records, they should prioritize the creation of a robust, standardized, and portable health record that travels with the patient, not the other way around.

Have any other ideas on how to improve patient engagement? We’d love to hear about them and share them in a future column.

If you want to contribute but don’t have any ideas, we have a suggestion: Ask your mother-in-law. You may be surprised at what you learn!

Dr. Notte is a family physician and associate chief medical information officer for Abington (Pa.) Hospital–Jefferson Health. Follow him on twitter (@doctornotte). Dr. Skolnik is professor of family and community medicine at Sidney Kimmel Medical College, Philadelphia, and associate director of the family medicine residency program at Abington Hospital–Jefferson Health.

Reference

Lee JL et al. J Gen Intern Med. 2019 Nov 12. doi: 10.1007/s11606-019-05528-z.

Bullying happens to our patients and sometimes to the doctors in the medical community. As psychiatrists, we need to share information on how to spot it and deal with it in the workplace.

SDI Productions/iStock/Getty Images

We can view bullying as the endpoint in a continuum with authority at one end and harassment at the other extreme. Discipline maintains order but those in charge can be misguided or mean spirited.

Bullying is bad and prevalent, but is it inevitable in the workplace? There are three categories: those who get bullied, those who bully, and those who witness bullying. Any one, two, or even all three can apply in a work environment. Some escape the problem, and for them, bullying remains theoretical, a phenomenon to understand.

How do we define bullying? You know it when you see it; bullying interferes with functioning. It includes harsh language, threats, snubbing, screaming, and undermining.
 

Case is illustrative

Helen, a medical consultant on a surgical unit, was reading a chart when another internist arrived for the same purpose. He introduced himself as a new full-time assistant to the head of medical consultations. Helen greeted him and said: “Since I started with this case, I will continue. There was probably an error in the referral process.” Bill looked concerned. “But he has uncontrolled diabetes.” Taken aback, Helen said: “I think I can handle it. I’ve been on the hospital staff for 25 years.”

Then the bullying began. On occasion, Bill and a resident consulted on patients Helen was treating already, as though her input were nonexistent. When Helen inquired about this, rather than attribute it to an error in communication within a large hospital, Bill diminished the value of her input. She asked, “How many medical consultants does a patient need?” She decided to confront Bill and tell him that he had no reason to treat her with disrespect. After that, Bill’s disparaging remarks intensified and he threatened her saying, “I’m not someone you want to go up against.” Bill sent her an email, “You are demeaning and harsh to the staff; if you want to retain your hospital credentials you must change your behavior.” In her response, Helen agreed to meet with Bill and she emailed, “It is not in my nature to mistreat anyone, staff or patient.” The meeting never happened.

Helen sought me out for psychiatric consultation and psychotherapy because she felt demoralized. Confused by Bill’s assault on her reputation, she needed a strategy and confirmation of her worth. We conceived a plan. Helen decided to get busy and get better. She redoubled her efforts to be cordial, and she remained effective with her patients. I suggested that she confide in a trusted senior attending at the hospital, which she did. She aired her insights to him. Excellence mattered and the threats disappeared. Bill had no power over Helen after all. She was a voluntary attending. She never succumbed to despair; rather she converted her response to the threats into useful energy.

When does authority become harassment?

A pecking order exists in every organization because, from the CEO to the janitor, it is necessary to maintain productivity. But when does this hierarchy become abusive? Discipline gets learned early. Those who are familiar with the comic strip “Calvin and Hobbes” by Bill Watterson may remember the 6-year-old boy asserting his intention to stay home from school – only to be forced to the bus stop by his mother. Call that authority, discipline, or even bullying, but it represents a child’s first encounter with obedience despite protest. When authority interferes rather than enhances effectiveness, question the methods used to attain order.

The vulnerable

If you do your job and you do it well, there should be no bullying. It is hard to know why a target gets chosen for harassment. However, some questions may need answering by the target. Does he or she avoid conflict even when there is bad behavior? Does past trauma immobilize him into passivity? Such issues necessitate self examination. Psychotherapy helps to uncover and clear up these issues.

Is bullying a fact of life?

In “Lord of the Flies,” William Golding portrays a fictional group of unsupervised boys abandoned on an island. An initial hierarchy descends into threats and eventual violence. Consider the animal world. In the wild, a wolf pack isolates a caribou from the herd to kill and devour. On a farm, llamas raised for yarn establish which llama is in charge. Those cases illustrate the hierarchy that exists because there is the need for food or reproductive prowess.

In the workplace, isolation of the target is common when authority extends to bullying. According to Robert Sapolsky, PhD, a neuroscientist and author, there are biological underpinnings for group conformity. This implies that colleagues who stand apart feel distress and get relief when they join the ganging up on a target. Those who watch harassment may hide from confronting it or even from pointing it out to protect themselves. As psychiatrists, we need to notice bullying when it occurs so it can be eradicated for the sake of the workplace and the target.
 

How do bullies think?

Challenge the bully at your own peril, because expecting a bully to change is futile. Recall Helen’s confrontation with Bill. It provoked him. His power to harass her came from his perceived position. Bullies regard the pleasant person as weak. Bullies can fall into two categories: Sadists who get pleasure from seeing others suffer, and opportunists. The latter focus only on their goals and disregard concerns expressed by others. Outside of the workplace, they may be reasonable. If workplace morale deteriorates along with productivity, the bully gets ousted. Otherwise, companies usually protect high performers at the expense of targets.

Is bullying different in medicine?

It can happen in a training program. The ingredients for bullying exist, including imbalance of power. Often, there are no witnesses, and there can be lack of accountability because of changing authorities. Just as technology can help make harassment possible, it also enables the target to spot and document inappropriate communications by saving emails and texts. Whenever a need for advancement exists along with changing authority, bullying gets tolerated. Who wants to be derailed by reporting? Those in training have the goal of completing a program. If they report bullying, they fear antagonism and retribution, a personal expense that can deter advancement.

Remedies

Let truth and fairness be your guide. That is easy to say and hard to do, but there are helpful personal and legal resources.

Personal capability

Get busy; get better. That became Helen’s method of choice. She focused on her role and productivity, not on her hurt. Helen shunned victimhood. With the help of psychotherapy and by confiding in a mentor, she prevailed. What works is recalling challenges that were mastered and the qualities that made for success. Acquire skills, build a good reputation, be assertive, not defensive.

The group is powerful, and that means it is important to build alliances above and below in the organizational hierarchy; cultivate friendship with trustworthy people. Occasionally, there is unwarranted ganging up on a manager, bullying from below. It is more likely to happen to a newly appointed supervisor. A way to avert that is to communicate with staff throughout the institution and remain accessible.
 

Legal options

What are legal options to confront bullying? Of note, workplace bullying is not necessarily illegal. According to one employment attorney, “There is no law that prohibits uncivil behavior on the job.” However, under Title VII of the federal law enacted in 1964, there are protected characteristics such as race, color, national origin, sex, age, and disability. The Equal Employment Opportunity Commission enforces Title VII. In cases of assault or stalking, harassment is illegal and criminal.

Some employees report to Human Resources or seek out their company’s employee assistance program. As useful as those options may be, they are part of the company and potentially partial to the administration. There can be incentives to protect those with power against a complainant. For assistance, it is preferable to enlist an outside attorney and a therapist in the community.

Advocacy exists. The Workplace Bullying Institute maintains a website, holds workshops, promotes literature, and offers information. The National Employment Lawyers Association can provide referrals or recommendations that come from other legal sources. Cases rarely reach court because of the expense of a trial; rather, the parties reach a financial settlement. When there is cause, an employment attorney can best pursue justice for the worker.
 

Conclusion

Get busy; get better is the solution to bullying. Avoid victimhood. That means prepare: Update the resume, seek opportunities, and identify allies. Bullies get beaten; as Abraham Lincoln said, “You can fool some of the people some of the time but you can’t fool all of the people all of the time.”

According to the Workplace Bullying Institute, 7 out of 10 bullied workers either resign or get fired. You should leave only when the leaving is better than the staying. Bullying brings out the worst in the workplace. Those who bully isolate the target. Coworkers often shun the target, fearing for their own position; they may even participate in the harassment. Psychiatrists need to remain sensitive to harassment in their own environment and for their patients. We have tools to address bullying in the workplace and a moral responsibility to combat it.
 

References

Workplace Bullying Institute (WBI)

National Employment Lawyers Association (NELA)

“Ozymandias” by Percy Bysshe Shelley

BY BEN HINDELL, PSY.D.

Cyberbullying is willful, repeated harm inflicted with the use of computers, cell phones, and other electronic devices. In some cases, a single message may be viewed by multiple people because the text and pictures are posted elsewhere.

Courtesy Dr. Hindell

Technology makes is possible to harass at any hour. The concept of willful harm is essential. Without interaction between sender and recipient, nuances are lost. Face to face might make a communication benign instead of malevolent or threatening. This has implications for the workplace, where colleagues increasingly communicate by email rather than discuss matters in person or by telephone.
 

Steps for survivors of cyberbullying

• Do not respond immediately to an inflammatory message, post, or email. Gather your thoughts and avoid responding in anger.
• Keep calm and rational, not emotional.
• Try to respond in person and work to avoid a conflict.
• Remember, your interpretation may differ from what was intended.
• Communicate openly and honestly and not defensively.
• Calmly indicate you were offended and you want the comments to stop.
• Move up the chain of command, if comments don’t cease.
• Save all messages and posts as evidence.
• Report the cyberbullying to your employer. Human resources may get involved.
• Detach from the cyberbully, if it continues. Block social media, cell phone messaging, and emails.
• Find support from friends, family, and a psychotherapist, if needed. As a last resort, it may become necessary to enlist an attorney.
• Take the high road; remain calm and professional at work. The bully may be seeking a reaction from the behavior. Prevent it.

All of the elements of workplace bullying apply to cyberbullying, but the latter can be more insidious. Psychiatrists and psychologists are able to support patients who deal with cyberbullying and help them cope successfully.
 

Dr. Cohen is in private practice and is a clinical assistant professor of psychiatry at Weill Cornell Medical Center of New York-Presbyterian Hospital, and psychiatric consultant at the Hospital for Special Surgery, also in New York. She made changes to the patient’s story to protect confidentiality.

Dr. Hindell is a psychologist with the Mental Health Service of Colorado College, Colorado Springs. He also practices psychotherapy in Denver. Dr. Hindell is the son of Dr. Cohen.

Bullying happens to our patients and sometimes to the doctors in the medical community. As psychiatrists, we need to share information on how to spot it and deal with it in the workplace.

SDI Productions/iStock/Getty Images

We can view bullying as the endpoint in a continuum with authority at one end and harassment at the other extreme. Discipline maintains order but those in charge can be misguided or mean spirited.

Bullying is bad and prevalent, but is it inevitable in the workplace? There are three categories: those who get bullied, those who bully, and those who witness bullying. Any one, two, or even all three can apply in a work environment. Some escape the problem, and for them, bullying remains theoretical, a phenomenon to understand.

How do we define bullying? You know it when you see it; bullying interferes with functioning. It includes harsh language, threats, snubbing, screaming, and undermining.
 

Case is illustrative

Helen, a medical consultant on a surgical unit, was reading a chart when another internist arrived for the same purpose. He introduced himself as a new full-time assistant to the head of medical consultations. Helen greeted him and said: “Since I started with this case, I will continue. There was probably an error in the referral process.” Bill looked concerned. “But he has uncontrolled diabetes.” Taken aback, Helen said: “I think I can handle it. I’ve been on the hospital staff for 25 years.”

Then the bullying began. On occasion, Bill and a resident consulted on patients Helen was treating already, as though her input were nonexistent. When Helen inquired about this, rather than attribute it to an error in communication within a large hospital, Bill diminished the value of her input. She asked, “How many medical consultants does a patient need?” She decided to confront Bill and tell him that he had no reason to treat her with disrespect. After that, Bill’s disparaging remarks intensified and he threatened her saying, “I’m not someone you want to go up against.” Bill sent her an email, “You are demeaning and harsh to the staff; if you want to retain your hospital credentials you must change your behavior.” In her response, Helen agreed to meet with Bill and she emailed, “It is not in my nature to mistreat anyone, staff or patient.” The meeting never happened.

Helen sought me out for psychiatric consultation and psychotherapy because she felt demoralized. Confused by Bill’s assault on her reputation, she needed a strategy and confirmation of her worth. We conceived a plan. Helen decided to get busy and get better. She redoubled her efforts to be cordial, and she remained effective with her patients. I suggested that she confide in a trusted senior attending at the hospital, which she did. She aired her insights to him. Excellence mattered and the threats disappeared. Bill had no power over Helen after all. She was a voluntary attending. She never succumbed to despair; rather she converted her response to the threats into useful energy.

When does authority become harassment?

A pecking order exists in every organization because, from the CEO to the janitor, it is necessary to maintain productivity. But when does this hierarchy become abusive? Discipline gets learned early. Those who are familiar with the comic strip “Calvin and Hobbes” by Bill Watterson may remember the 6-year-old boy asserting his intention to stay home from school – only to be forced to the bus stop by his mother. Call that authority, discipline, or even bullying, but it represents a child’s first encounter with obedience despite protest. When authority interferes rather than enhances effectiveness, question the methods used to attain order.

The vulnerable

If you do your job and you do it well, there should be no bullying. It is hard to know why a target gets chosen for harassment. However, some questions may need answering by the target. Does he or she avoid conflict even when there is bad behavior? Does past trauma immobilize him into passivity? Such issues necessitate self examination. Psychotherapy helps to uncover and clear up these issues.

Is bullying a fact of life?

In “Lord of the Flies,” William Golding portrays a fictional group of unsupervised boys abandoned on an island. An initial hierarchy descends into threats and eventual violence. Consider the animal world. In the wild, a wolf pack isolates a caribou from the herd to kill and devour. On a farm, llamas raised for yarn establish which llama is in charge. Those cases illustrate the hierarchy that exists because there is the need for food or reproductive prowess.

In the workplace, isolation of the target is common when authority extends to bullying. According to Robert Sapolsky, PhD, a neuroscientist and author, there are biological underpinnings for group conformity. This implies that colleagues who stand apart feel distress and get relief when they join the ganging up on a target. Those who watch harassment may hide from confronting it or even from pointing it out to protect themselves. As psychiatrists, we need to notice bullying when it occurs so it can be eradicated for the sake of the workplace and the target.
 

How do bullies think?

Challenge the bully at your own peril, because expecting a bully to change is futile. Recall Helen’s confrontation with Bill. It provoked him. His power to harass her came from his perceived position. Bullies regard the pleasant person as weak. Bullies can fall into two categories: Sadists who get pleasure from seeing others suffer, and opportunists. The latter focus only on their goals and disregard concerns expressed by others. Outside of the workplace, they may be reasonable. If workplace morale deteriorates along with productivity, the bully gets ousted. Otherwise, companies usually protect high performers at the expense of targets.

Is bullying different in medicine?

It can happen in a training program. The ingredients for bullying exist, including imbalance of power. Often, there are no witnesses, and there can be lack of accountability because of changing authorities. Just as technology can help make harassment possible, it also enables the target to spot and document inappropriate communications by saving emails and texts. Whenever a need for advancement exists along with changing authority, bullying gets tolerated. Who wants to be derailed by reporting? Those in training have the goal of completing a program. If they report bullying, they fear antagonism and retribution, a personal expense that can deter advancement.

Remedies

Let truth and fairness be your guide. That is easy to say and hard to do, but there are helpful personal and legal resources.

Personal capability

Get busy; get better. That became Helen’s method of choice. She focused on her role and productivity, not on her hurt. Helen shunned victimhood. With the help of psychotherapy and by confiding in a mentor, she prevailed. What works is recalling challenges that were mastered and the qualities that made for success. Acquire skills, build a good reputation, be assertive, not defensive.

The group is powerful, and that means it is important to build alliances above and below in the organizational hierarchy; cultivate friendship with trustworthy people. Occasionally, there is unwarranted ganging up on a manager, bullying from below. It is more likely to happen to a newly appointed supervisor. A way to avert that is to communicate with staff throughout the institution and remain accessible.
 

Legal options

What are legal options to confront bullying? Of note, workplace bullying is not necessarily illegal. According to one employment attorney, “There is no law that prohibits uncivil behavior on the job.” However, under Title VII of the federal law enacted in 1964, there are protected characteristics such as race, color, national origin, sex, age, and disability. The Equal Employment Opportunity Commission enforces Title VII. In cases of assault or stalking, harassment is illegal and criminal.

Some employees report to Human Resources or seek out their company’s employee assistance program. As useful as those options may be, they are part of the company and potentially partial to the administration. There can be incentives to protect those with power against a complainant. For assistance, it is preferable to enlist an outside attorney and a therapist in the community.

Advocacy exists. The Workplace Bullying Institute maintains a website, holds workshops, promotes literature, and offers information. The National Employment Lawyers Association can provide referrals or recommendations that come from other legal sources. Cases rarely reach court because of the expense of a trial; rather, the parties reach a financial settlement. When there is cause, an employment attorney can best pursue justice for the worker.
 

Conclusion

Get busy; get better is the solution to bullying. Avoid victimhood. That means prepare: Update the resume, seek opportunities, and identify allies. Bullies get beaten; as Abraham Lincoln said, “You can fool some of the people some of the time but you can’t fool all of the people all of the time.”

According to the Workplace Bullying Institute, 7 out of 10 bullied workers either resign or get fired. You should leave only when the leaving is better than the staying. Bullying brings out the worst in the workplace. Those who bully isolate the target. Coworkers often shun the target, fearing for their own position; they may even participate in the harassment. Psychiatrists need to remain sensitive to harassment in their own environment and for their patients. We have tools to address bullying in the workplace and a moral responsibility to combat it.
 

References

Workplace Bullying Institute (WBI)

National Employment Lawyers Association (NELA)

“Ozymandias” by Percy Bysshe Shelley

BY BEN HINDELL, PSY.D.

Cyberbullying is willful, repeated harm inflicted with the use of computers, cell phones, and other electronic devices. In some cases, a single message may be viewed by multiple people because the text and pictures are posted elsewhere.

Courtesy Dr. Hindell

Technology makes is possible to harass at any hour. The concept of willful harm is essential. Without interaction between sender and recipient, nuances are lost. Face to face might make a communication benign instead of malevolent or threatening. This has implications for the workplace, where colleagues increasingly communicate by email rather than discuss matters in person or by telephone.
 

Steps for survivors of cyberbullying

• Do not respond immediately to an inflammatory message, post, or email. Gather your thoughts and avoid responding in anger.
• Keep calm and rational, not emotional.
• Try to respond in person and work to avoid a conflict.
• Remember, your interpretation may differ from what was intended.
• Communicate openly and honestly and not defensively.
• Calmly indicate you were offended and you want the comments to stop.
• Move up the chain of command, if comments don’t cease.
• Save all messages and posts as evidence.
• Report the cyberbullying to your employer. Human resources may get involved.
• Detach from the cyberbully, if it continues. Block social media, cell phone messaging, and emails.
• Find support from friends, family, and a psychotherapist, if needed. As a last resort, it may become necessary to enlist an attorney.
• Take the high road; remain calm and professional at work. The bully may be seeking a reaction from the behavior. Prevent it.

All of the elements of workplace bullying apply to cyberbullying, but the latter can be more insidious. Psychiatrists and psychologists are able to support patients who deal with cyberbullying and help them cope successfully.
 

Dr. Cohen is in private practice and is a clinical assistant professor of psychiatry at Weill Cornell Medical Center of New York-Presbyterian Hospital, and psychiatric consultant at the Hospital for Special Surgery, also in New York. She made changes to the patient’s story to protect confidentiality.

Dr. Hindell is a psychologist with the Mental Health Service of Colorado College, Colorado Springs. He also practices psychotherapy in Denver. Dr. Hindell is the son of Dr. Cohen.

Bullying happens to our patients and sometimes to the doctors in the medical community. As psychiatrists, we need to share information on how to spot it and deal with it in the workplace.

SDI Productions/iStock/Getty Images

We can view bullying as the endpoint in a continuum with authority at one end and harassment at the other extreme. Discipline maintains order but those in charge can be misguided or mean spirited.

Bullying is bad and prevalent, but is it inevitable in the workplace? There are three categories: those who get bullied, those who bully, and those who witness bullying. Any one, two, or even all three can apply in a work environment. Some escape the problem, and for them, bullying remains theoretical, a phenomenon to understand.

How do we define bullying? You know it when you see it; bullying interferes with functioning. It includes harsh language, threats, snubbing, screaming, and undermining.
 

Case is illustrative

Helen, a medical consultant on a surgical unit, was reading a chart when another internist arrived for the same purpose. He introduced himself as a new full-time assistant to the head of medical consultations. Helen greeted him and said: “Since I started with this case, I will continue. There was probably an error in the referral process.” Bill looked concerned. “But he has uncontrolled diabetes.” Taken aback, Helen said: “I think I can handle it. I’ve been on the hospital staff for 25 years.”

Then the bullying began. On occasion, Bill and a resident consulted on patients Helen was treating already, as though her input were nonexistent. When Helen inquired about this, rather than attribute it to an error in communication within a large hospital, Bill diminished the value of her input. She asked, “How many medical consultants does a patient need?” She decided to confront Bill and tell him that he had no reason to treat her with disrespect. After that, Bill’s disparaging remarks intensified and he threatened her saying, “I’m not someone you want to go up against.” Bill sent her an email, “You are demeaning and harsh to the staff; if you want to retain your hospital credentials you must change your behavior.” In her response, Helen agreed to meet with Bill and she emailed, “It is not in my nature to mistreat anyone, staff or patient.” The meeting never happened.

Helen sought me out for psychiatric consultation and psychotherapy because she felt demoralized. Confused by Bill’s assault on her reputation, she needed a strategy and confirmation of her worth. We conceived a plan. Helen decided to get busy and get better. She redoubled her efforts to be cordial, and she remained effective with her patients. I suggested that she confide in a trusted senior attending at the hospital, which she did. She aired her insights to him. Excellence mattered and the threats disappeared. Bill had no power over Helen after all. She was a voluntary attending. She never succumbed to despair; rather she converted her response to the threats into useful energy.

When does authority become harassment?

A pecking order exists in every organization because, from the CEO to the janitor, it is necessary to maintain productivity. But when does this hierarchy become abusive? Discipline gets learned early. Those who are familiar with the comic strip “Calvin and Hobbes” by Bill Watterson may remember the 6-year-old boy asserting his intention to stay home from school – only to be forced to the bus stop by his mother. Call that authority, discipline, or even bullying, but it represents a child’s first encounter with obedience despite protest. When authority interferes rather than enhances effectiveness, question the methods used to attain order.

The vulnerable

If you do your job and you do it well, there should be no bullying. It is hard to know why a target gets chosen for harassment. However, some questions may need answering by the target. Does he or she avoid conflict even when there is bad behavior? Does past trauma immobilize him into passivity? Such issues necessitate self examination. Psychotherapy helps to uncover and clear up these issues.

Is bullying a fact of life?

In “Lord of the Flies,” William Golding portrays a fictional group of unsupervised boys abandoned on an island. An initial hierarchy descends into threats and eventual violence. Consider the animal world. In the wild, a wolf pack isolates a caribou from the herd to kill and devour. On a farm, llamas raised for yarn establish which llama is in charge. Those cases illustrate the hierarchy that exists because there is the need for food or reproductive prowess.

In the workplace, isolation of the target is common when authority extends to bullying. According to Robert Sapolsky, PhD, a neuroscientist and author, there are biological underpinnings for group conformity. This implies that colleagues who stand apart feel distress and get relief when they join the ganging up on a target. Those who watch harassment may hide from confronting it or even from pointing it out to protect themselves. As psychiatrists, we need to notice bullying when it occurs so it can be eradicated for the sake of the workplace and the target.
 

How do bullies think?

Challenge the bully at your own peril, because expecting a bully to change is futile. Recall Helen’s confrontation with Bill. It provoked him. His power to harass her came from his perceived position. Bullies regard the pleasant person as weak. Bullies can fall into two categories: Sadists who get pleasure from seeing others suffer, and opportunists. The latter focus only on their goals and disregard concerns expressed by others. Outside of the workplace, they may be reasonable. If workplace morale deteriorates along with productivity, the bully gets ousted. Otherwise, companies usually protect high performers at the expense of targets.

Is bullying different in medicine?

It can happen in a training program. The ingredients for bullying exist, including imbalance of power. Often, there are no witnesses, and there can be lack of accountability because of changing authorities. Just as technology can help make harassment possible, it also enables the target to spot and document inappropriate communications by saving emails and texts. Whenever a need for advancement exists along with changing authority, bullying gets tolerated. Who wants to be derailed by reporting? Those in training have the goal of completing a program. If they report bullying, they fear antagonism and retribution, a personal expense that can deter advancement.

Remedies

Let truth and fairness be your guide. That is easy to say and hard to do, but there are helpful personal and legal resources.

Personal capability

Get busy; get better. That became Helen’s method of choice. She focused on her role and productivity, not on her hurt. Helen shunned victimhood. With the help of psychotherapy and by confiding in a mentor, she prevailed. What works is recalling challenges that were mastered and the qualities that made for success. Acquire skills, build a good reputation, be assertive, not defensive.

The group is powerful, and that means it is important to build alliances above and below in the organizational hierarchy; cultivate friendship with trustworthy people. Occasionally, there is unwarranted ganging up on a manager, bullying from below. It is more likely to happen to a newly appointed supervisor. A way to avert that is to communicate with staff throughout the institution and remain accessible.
 

Legal options

What are legal options to confront bullying? Of note, workplace bullying is not necessarily illegal. According to one employment attorney, “There is no law that prohibits uncivil behavior on the job.” However, under Title VII of the federal law enacted in 1964, there are protected characteristics such as race, color, national origin, sex, age, and disability. The Equal Employment Opportunity Commission enforces Title VII. In cases of assault or stalking, harassment is illegal and criminal.

Some employees report to Human Resources or seek out their company’s employee assistance program. As useful as those options may be, they are part of the company and potentially partial to the administration. There can be incentives to protect those with power against a complainant. For assistance, it is preferable to enlist an outside attorney and a therapist in the community.

Advocacy exists. The Workplace Bullying Institute maintains a website, holds workshops, promotes literature, and offers information. The National Employment Lawyers Association can provide referrals or recommendations that come from other legal sources. Cases rarely reach court because of the expense of a trial; rather, the parties reach a financial settlement. When there is cause, an employment attorney can best pursue justice for the worker.
 

Conclusion

Get busy; get better is the solution to bullying. Avoid victimhood. That means prepare: Update the resume, seek opportunities, and identify allies. Bullies get beaten; as Abraham Lincoln said, “You can fool some of the people some of the time but you can’t fool all of the people all of the time.”

According to the Workplace Bullying Institute, 7 out of 10 bullied workers either resign or get fired. You should leave only when the leaving is better than the staying. Bullying brings out the worst in the workplace. Those who bully isolate the target. Coworkers often shun the target, fearing for their own position; they may even participate in the harassment. Psychiatrists need to remain sensitive to harassment in their own environment and for their patients. We have tools to address bullying in the workplace and a moral responsibility to combat it.
 

References

Workplace Bullying Institute (WBI)

National Employment Lawyers Association (NELA)

“Ozymandias” by Percy Bysshe Shelley

BY BEN HINDELL, PSY.D.

Cyberbullying is willful, repeated harm inflicted with the use of computers, cell phones, and other electronic devices. In some cases, a single message may be viewed by multiple people because the text and pictures are posted elsewhere.

Courtesy Dr. Hindell

Technology makes is possible to harass at any hour. The concept of willful harm is essential. Without interaction between sender and recipient, nuances are lost. Face to face might make a communication benign instead of malevolent or threatening. This has implications for the workplace, where colleagues increasingly communicate by email rather than discuss matters in person or by telephone.
 

Steps for survivors of cyberbullying

• Do not respond immediately to an inflammatory message, post, or email. Gather your thoughts and avoid responding in anger.
• Keep calm and rational, not emotional.
• Try to respond in person and work to avoid a conflict.
• Remember, your interpretation may differ from what was intended.
• Communicate openly and honestly and not defensively.
• Calmly indicate you were offended and you want the comments to stop.
• Move up the chain of command, if comments don’t cease.
• Save all messages and posts as evidence.
• Report the cyberbullying to your employer. Human resources may get involved.
• Detach from the cyberbully, if it continues. Block social media, cell phone messaging, and emails.
• Find support from friends, family, and a psychotherapist, if needed. As a last resort, it may become necessary to enlist an attorney.
• Take the high road; remain calm and professional at work. The bully may be seeking a reaction from the behavior. Prevent it.

All of the elements of workplace bullying apply to cyberbullying, but the latter can be more insidious. Psychiatrists and psychologists are able to support patients who deal with cyberbullying and help them cope successfully.
 

Dr. Cohen is in private practice and is a clinical assistant professor of psychiatry at Weill Cornell Medical Center of New York-Presbyterian Hospital, and psychiatric consultant at the Hospital for Special Surgery, also in New York. She made changes to the patient’s story to protect confidentiality.

Dr. Hindell is a psychologist with the Mental Health Service of Colorado College, Colorado Springs. He also practices psychotherapy in Denver. Dr. Hindell is the son of Dr. Cohen.

There is no Baby Book of Names or hurricane alphabet to readily name diseases and their causal entities. Throughout history and even in the modern era, a host of considerations have intruded on the decision as to what to call these blights upon humanity. Names have varied from inflammatory to misleading, from colloquial to scientific. And when it concerns a new epidemiological entity such as the latest coronavirus outbreak originating in China, health organizations, media, politicians, scientific taxonomy commissions, and the public at large all have a stake in the naming.

Courtesy NIAID-RML

From “Wuhan virus” to “novel coronavirus-2019” to “COVID-19 virus,” the name of the new coronavirus that first appeared in China has been evolving to its now official designation: SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). But where did the final name come from, how does such a name become official, and who makes it so?
 

Virus taxonomy

The Coronavirus Study Group (CSG) of the International Committee on Taxonomy of Viruses (ICTV) named the new coronavirus SARS-CoV-2 based upon its genetic relationship to the original SARS-CoV that caused an outbreak of disease in 2002–2003.

According to the ICTV website, the first internationally organized attempts to introduce order into the bewildering variety of viruses took place at the International Congress of Microbiology held in Moscow in 1966 where a committee was created that later became the ICTV and was given the task of developing a single, universal taxonomic scheme for all the viruses infecting animals, plants, fungi, bacteria, and archaea. The ICTV was created as a committee of the virology division of the International Union of Microbiological Societies and is governed by statutes approved by the virology division. Virus classification and nomenclature are subject to rules set out in an International Code.

These designate that: “The universal virus classification system shall employ the hierarchical levels of realm, subrealm, kingdom, subkingdom, phylum, subphylum, class, subclass, order, suborder, family, subfamily, genus, subgenus and species.”

Many of the topmost areas of classification are based on whether the viruses are DNA or RNA, single or double stranded, and have a simple protein shell or a complex lipoprotein envelope. Other levels of classification include host species, type of replication, and type of diseases they cause, the later exemplified in the SARS designation for this virus.

There are 98 international study groups (SGs) covering all major virus orders, families, and genera that are part of the ICTV, and it was the one dedicated to the single-stranded RNA coronaviruses, the CSG, that came up with the SARS-CoV-2 name and first referenced it in their Feb 11 publication in the Cold Springs Harbor preprint journal bioRxiv.

“Based on phylogeny, taxonomy and established practice, the CSG formally recognizes this virus as a sister to severe acute respiratory syndrome coronaviruses (SARS-CoVs) of the species severe acute respiratory syndrome–related coronavirus and designates it as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2),” they wrote.

According to the National Center for Biotechnology Information Taxonomy Browser, with respect to the original SARS CoV virus, of which this is a relative, the full taxonomic designation is: Viruses, Riboviria, Nidovirales, Cornidovirineae, Coronaviridae, Orthocoronavirinae, Betacoronavirus, Sarbecovirus.
 

The problem with naming names

The World Health Organization currently is not using the official scientific name of the virus, but rather is merely labeling it with regard to the disease: COVID-19, which simply refers to coronavirus disease 2019.

They are following a modern standard by which disease names avoid inflammatory connotations with people and places. Too often in the past from syphilis as the “French pox,” the 1918 influenza as the “Spanish flu,” AIDS as the “gay plague,” Middle East Respiratory Syndrome (MERS), and the currently named “WuFlu,” which made an appearance early in the new outbreak and which is symbolic of a sudden wave of anti-Asian, and specifically Chinese, prejudice.

Chinatown districts even in the United States are being affected economically through unwarranted fear associated with the virus. And there have been equivalently virulent outbreaks of hate speech against Asian individuals in places untouched by the new virus.

However, although SARS-CoV-2 as a name avoids such problems, different considerations led the WHO to reject it in its discussions, determining that its use ties it to tightly to the much more deadly SARS-CoV-1 virus in the public mind, risking greater fear and panic, especially in Asia, where SARS-CoV-1 had the biggest impact.

Back in 1896, William Sykes, MD, writing in the first flush of the triumph of germ theory in modern medicine, attempted to give some guidance to how medical science should best come up with new names of diseases by merging the demands of common parlance with those of taxonomic legitimacy. His “On the Origin and History of Disease-Names,” published in the Lancet, had clearcut advice: “It is vain to attempt to replace a folk name or one widely adopted by the people by a new one deliberately coined by scholars, and this for the following reasons: first, whatever names may be accepted by medical men must be translated by them into the vernacular of their patients, and by a resulting reaction the vernacular name comes to be the commoner one with themselves; and, secondly, there is no continuity or unchangeableness in the terms invented by savants, which are amended, improved upon, and displaced by the next writer on the subject, or, even more absurdly still, by the very inventors themselves in a subsequent publication.”

This is the reason that virus taxonomy provides names based upon unchangeable scientific descriptors of the actual disease causing entity, as illustrated by the decisions of the ICTV. In addition, the genomic sequences being provided by the scientific community are all being organized under the SARS-CoV-2 name and thus are cementing that moniker as the only acceptable scientific one.

Whether the rest of the world universally adopts SARS-CoV-2 as a name is still in question. If the outbreak spreads significantly beyond its current limits, fear and confusion – and simply the need for a more familiar-sounding label – may lead the general public to adopt more colloquial designations than those that science attempts to impose, as Dr. Sykes suggested back in 1896. That remains to be seen.

[email protected]

Mark Lesney is the managing editor of MDedge.com/IDPractioner. He has a PhD in plant virology and a PhD in the history of science, with a focus on the history of biotechnology and medicine. He has served as an adjunct assistant professor of the department of biochemistry and molecular & cellular biology at Georgetown University, Washington.

There is no Baby Book of Names or hurricane alphabet to readily name diseases and their causal entities. Throughout history and even in the modern era, a host of considerations have intruded on the decision as to what to call these blights upon humanity. Names have varied from inflammatory to misleading, from colloquial to scientific. And when it concerns a new epidemiological entity such as the latest coronavirus outbreak originating in China, health organizations, media, politicians, scientific taxonomy commissions, and the public at large all have a stake in the naming.

Courtesy NIAID-RML

From “Wuhan virus” to “novel coronavirus-2019” to “COVID-19 virus,” the name of the new coronavirus that first appeared in China has been evolving to its now official designation: SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). But where did the final name come from, how does such a name become official, and who makes it so?
 

Virus taxonomy

The Coronavirus Study Group (CSG) of the International Committee on Taxonomy of Viruses (ICTV) named the new coronavirus SARS-CoV-2 based upon its genetic relationship to the original SARS-CoV that caused an outbreak of disease in 2002–2003.

According to the ICTV website, the first internationally organized attempts to introduce order into the bewildering variety of viruses took place at the International Congress of Microbiology held in Moscow in 1966 where a committee was created that later became the ICTV and was given the task of developing a single, universal taxonomic scheme for all the viruses infecting animals, plants, fungi, bacteria, and archaea. The ICTV was created as a committee of the virology division of the International Union of Microbiological Societies and is governed by statutes approved by the virology division. Virus classification and nomenclature are subject to rules set out in an International Code.

These designate that: “The universal virus classification system shall employ the hierarchical levels of realm, subrealm, kingdom, subkingdom, phylum, subphylum, class, subclass, order, suborder, family, subfamily, genus, subgenus and species.”

Many of the topmost areas of classification are based on whether the viruses are DNA or RNA, single or double stranded, and have a simple protein shell or a complex lipoprotein envelope. Other levels of classification include host species, type of replication, and type of diseases they cause, the later exemplified in the SARS designation for this virus.

There are 98 international study groups (SGs) covering all major virus orders, families, and genera that are part of the ICTV, and it was the one dedicated to the single-stranded RNA coronaviruses, the CSG, that came up with the SARS-CoV-2 name and first referenced it in their Feb 11 publication in the Cold Springs Harbor preprint journal bioRxiv.

“Based on phylogeny, taxonomy and established practice, the CSG formally recognizes this virus as a sister to severe acute respiratory syndrome coronaviruses (SARS-CoVs) of the species severe acute respiratory syndrome–related coronavirus and designates it as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2),” they wrote.

According to the National Center for Biotechnology Information Taxonomy Browser, with respect to the original SARS CoV virus, of which this is a relative, the full taxonomic designation is: Viruses, Riboviria, Nidovirales, Cornidovirineae, Coronaviridae, Orthocoronavirinae, Betacoronavirus, Sarbecovirus.
 

The problem with naming names

The World Health Organization currently is not using the official scientific name of the virus, but rather is merely labeling it with regard to the disease: COVID-19, which simply refers to coronavirus disease 2019.

They are following a modern standard by which disease names avoid inflammatory connotations with people and places. Too often in the past from syphilis as the “French pox,” the 1918 influenza as the “Spanish flu,” AIDS as the “gay plague,” Middle East Respiratory Syndrome (MERS), and the currently named “WuFlu,” which made an appearance early in the new outbreak and which is symbolic of a sudden wave of anti-Asian, and specifically Chinese, prejudice.

Chinatown districts even in the United States are being affected economically through unwarranted fear associated with the virus. And there have been equivalently virulent outbreaks of hate speech against Asian individuals in places untouched by the new virus.

However, although SARS-CoV-2 as a name avoids such problems, different considerations led the WHO to reject it in its discussions, determining that its use ties it to tightly to the much more deadly SARS-CoV-1 virus in the public mind, risking greater fear and panic, especially in Asia, where SARS-CoV-1 had the biggest impact.

Back in 1896, William Sykes, MD, writing in the first flush of the triumph of germ theory in modern medicine, attempted to give some guidance to how medical science should best come up with new names of diseases by merging the demands of common parlance with those of taxonomic legitimacy. His “On the Origin and History of Disease-Names,” published in the Lancet, had clearcut advice: “It is vain to attempt to replace a folk name or one widely adopted by the people by a new one deliberately coined by scholars, and this for the following reasons: first, whatever names may be accepted by medical men must be translated by them into the vernacular of their patients, and by a resulting reaction the vernacular name comes to be the commoner one with themselves; and, secondly, there is no continuity or unchangeableness in the terms invented by savants, which are amended, improved upon, and displaced by the next writer on the subject, or, even more absurdly still, by the very inventors themselves in a subsequent publication.”

This is the reason that virus taxonomy provides names based upon unchangeable scientific descriptors of the actual disease causing entity, as illustrated by the decisions of the ICTV. In addition, the genomic sequences being provided by the scientific community are all being organized under the SARS-CoV-2 name and thus are cementing that moniker as the only acceptable scientific one.

Whether the rest of the world universally adopts SARS-CoV-2 as a name is still in question. If the outbreak spreads significantly beyond its current limits, fear and confusion – and simply the need for a more familiar-sounding label – may lead the general public to adopt more colloquial designations than those that science attempts to impose, as Dr. Sykes suggested back in 1896. That remains to be seen.

[email protected]

Mark Lesney is the managing editor of MDedge.com/IDPractioner. He has a PhD in plant virology and a PhD in the history of science, with a focus on the history of biotechnology and medicine. He has served as an adjunct assistant professor of the department of biochemistry and molecular & cellular biology at Georgetown University, Washington.

There is no Baby Book of Names or hurricane alphabet to readily name diseases and their causal entities. Throughout history and even in the modern era, a host of considerations have intruded on the decision as to what to call these blights upon humanity. Names have varied from inflammatory to misleading, from colloquial to scientific. And when it concerns a new epidemiological entity such as the latest coronavirus outbreak originating in China, health organizations, media, politicians, scientific taxonomy commissions, and the public at large all have a stake in the naming.

Courtesy NIAID-RML

From “Wuhan virus” to “novel coronavirus-2019” to “COVID-19 virus,” the name of the new coronavirus that first appeared in China has been evolving to its now official designation: SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2). But where did the final name come from, how does such a name become official, and who makes it so?
 

Virus taxonomy

The Coronavirus Study Group (CSG) of the International Committee on Taxonomy of Viruses (ICTV) named the new coronavirus SARS-CoV-2 based upon its genetic relationship to the original SARS-CoV that caused an outbreak of disease in 2002–2003.

According to the ICTV website, the first internationally organized attempts to introduce order into the bewildering variety of viruses took place at the International Congress of Microbiology held in Moscow in 1966 where a committee was created that later became the ICTV and was given the task of developing a single, universal taxonomic scheme for all the viruses infecting animals, plants, fungi, bacteria, and archaea. The ICTV was created as a committee of the virology division of the International Union of Microbiological Societies and is governed by statutes approved by the virology division. Virus classification and nomenclature are subject to rules set out in an International Code.

These designate that: “The universal virus classification system shall employ the hierarchical levels of realm, subrealm, kingdom, subkingdom, phylum, subphylum, class, subclass, order, suborder, family, subfamily, genus, subgenus and species.”

Many of the topmost areas of classification are based on whether the viruses are DNA or RNA, single or double stranded, and have a simple protein shell or a complex lipoprotein envelope. Other levels of classification include host species, type of replication, and type of diseases they cause, the later exemplified in the SARS designation for this virus.

There are 98 international study groups (SGs) covering all major virus orders, families, and genera that are part of the ICTV, and it was the one dedicated to the single-stranded RNA coronaviruses, the CSG, that came up with the SARS-CoV-2 name and first referenced it in their Feb 11 publication in the Cold Springs Harbor preprint journal bioRxiv.

“Based on phylogeny, taxonomy and established practice, the CSG formally recognizes this virus as a sister to severe acute respiratory syndrome coronaviruses (SARS-CoVs) of the species severe acute respiratory syndrome–related coronavirus and designates it as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2),” they wrote.

According to the National Center for Biotechnology Information Taxonomy Browser, with respect to the original SARS CoV virus, of which this is a relative, the full taxonomic designation is: Viruses, Riboviria, Nidovirales, Cornidovirineae, Coronaviridae, Orthocoronavirinae, Betacoronavirus, Sarbecovirus.
 

The problem with naming names

The World Health Organization currently is not using the official scientific name of the virus, but rather is merely labeling it with regard to the disease: COVID-19, which simply refers to coronavirus disease 2019.

They are following a modern standard by which disease names avoid inflammatory connotations with people and places. Too often in the past from syphilis as the “French pox,” the 1918 influenza as the “Spanish flu,” AIDS as the “gay plague,” Middle East Respiratory Syndrome (MERS), and the currently named “WuFlu,” which made an appearance early in the new outbreak and which is symbolic of a sudden wave of anti-Asian, and specifically Chinese, prejudice.

Chinatown districts even in the United States are being affected economically through unwarranted fear associated with the virus. And there have been equivalently virulent outbreaks of hate speech against Asian individuals in places untouched by the new virus.

However, although SARS-CoV-2 as a name avoids such problems, different considerations led the WHO to reject it in its discussions, determining that its use ties it to tightly to the much more deadly SARS-CoV-1 virus in the public mind, risking greater fear and panic, especially in Asia, where SARS-CoV-1 had the biggest impact.

Back in 1896, William Sykes, MD, writing in the first flush of the triumph of germ theory in modern medicine, attempted to give some guidance to how medical science should best come up with new names of diseases by merging the demands of common parlance with those of taxonomic legitimacy. His “On the Origin and History of Disease-Names,” published in the Lancet, had clearcut advice: “It is vain to attempt to replace a folk name or one widely adopted by the people by a new one deliberately coined by scholars, and this for the following reasons: first, whatever names may be accepted by medical men must be translated by them into the vernacular of their patients, and by a resulting reaction the vernacular name comes to be the commoner one with themselves; and, secondly, there is no continuity or unchangeableness in the terms invented by savants, which are amended, improved upon, and displaced by the next writer on the subject, or, even more absurdly still, by the very inventors themselves in a subsequent publication.”

This is the reason that virus taxonomy provides names based upon unchangeable scientific descriptors of the actual disease causing entity, as illustrated by the decisions of the ICTV. In addition, the genomic sequences being provided by the scientific community are all being organized under the SARS-CoV-2 name and thus are cementing that moniker as the only acceptable scientific one.

Whether the rest of the world universally adopts SARS-CoV-2 as a name is still in question. If the outbreak spreads significantly beyond its current limits, fear and confusion – and simply the need for a more familiar-sounding label – may lead the general public to adopt more colloquial designations than those that science attempts to impose, as Dr. Sykes suggested back in 1896. That remains to be seen.

[email protected]

Mark Lesney is the managing editor of MDedge.com/IDPractioner. He has a PhD in plant virology and a PhD in the history of science, with a focus on the history of biotechnology and medicine. He has served as an adjunct assistant professor of the department of biochemistry and molecular & cellular biology at Georgetown University, Washington.