Betsy Bates

SANTA BARBARA, CALIF. — Enhanced survival of the smallest of premature infants presents special challenges to dermatologists tasked with caring for conditions arising from incomplete development of the skin.

Skin is a relatively early player in fetal development, with an epidermis present at 36 days that consists of a basal layer and a superficial peridermal layer. Ectodermal tissue gradually appears during organogenesis, and the stratum corneum begins to form around hair follicles at 14 weeks.

But the bridging of these cells into functional skin that includes an epidermal layer does not occur until 22–24 weeks' gestation, an age when preemies now survive at many institutions, said Dr. Lawrence F. Eichenfield, chief of pediatric and adolescent dermatology at Rady Children's Hospital, San Diego.

Complications associated with extreme prematurity of the skin can continue to be seen in babies born at 29- or 30-weeks' gestation or even beyond.

“The timing of this is interesting. What we see with very premature infant skin is skin that doesn't quite have the thickness, doesn't have the adhesion [of] mature skin,” explained Dr. Eichenfield at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

Translucent premature skin may be incapable of fully performing critical functions, leaving infants susceptible to fluid electrolyte loss, temperature dysregulation, injuries, infections, and increased uptake of potentially toxic agents.

One unusual physical consequence of underdeveloped skin is anetoderma of prematurity, characterized by tissue paper-like depressed brown scars or outpouchings of skin.

Although these lesions may not appear to be associated with overt trauma, they tellingly appear in areas where leads or adhesives have been placed, and most likely represent postinflammatory hyperpigmentation, said Dr. Eichenfield. “Look at the pattern of the lesions” to deduce their origin, he suggested.

Quite commonly, erosions and crusts that would be “banal” in other settings can become profound problems in extremely premature infants. For example, the tape used to adhere umbilical lines may erode the skin and lead to significant secondary infections.

The suction pressure produced when leads are removed can lead to ecchymosis in immature skin, or the ecchymosis can be a sign of invasive fungal infection. All too often, it can be hard to distinguish the two, said Dr. Eichenfield, also a professor of pediatrics and medicine at the University of California, San Diego.

One sign not to miss is diffuse superficial crusting around the umbilical line or elsewhere, which can be a tip off to invasion and colonization with cutaneous candidiasis. “This is important, because it is a significant player in mortality in the [neonatal] ICU,” he said.

Another critical troika of symptoms includes pustules/papules, ecchymosis, and crusts. When these three signs are present, opportunistic fungal infections should be a “very, very strong consideration,” stressed Dr. Eichenfield.

Aspergillus and Rhizopus are only two of hundreds of fungi that may infect premature infants opportunistically, with extremely high rates of associated morbidity and mortality. “If you take care of it with debridement and systemic antifungals quickly, [while it remains confined to the skin], you save the child's life,” he said.

Risk factors for fungal infection in preemies include corticosteroid and antibiotic use, adhesive tape, and hospital construction: the latter currently a major issue in California, since hospitals are racing to conform with state earthquake retrofitting standards. At Rady Children's Hospital, four or five cases of Aspergillus-associated fungal infections have been diagnosed in the past year or so, as construction progresses on the building and the surrounding medical complex, he noted.

Tape used for umbilical lines may erode skin and lead to secondary infections. DR. EICHENFIELD

SANTA BARBARA, CALIF. — Enhanced survival of the smallest of premature infants presents special challenges to dermatologists tasked with caring for conditions arising from incomplete development of the skin.

Skin is a relatively early player in fetal development, with an epidermis present at 36 days that consists of a basal layer and a superficial peridermal layer. Ectodermal tissue gradually appears during organogenesis, and the stratum corneum begins to form around hair follicles at 14 weeks.

But the bridging of these cells into functional skin that includes an epidermal layer does not occur until 22–24 weeks' gestation, an age when preemies now survive at many institutions, said Dr. Lawrence F. Eichenfield, chief of pediatric and adolescent dermatology at Rady Children's Hospital, San Diego.

Complications associated with extreme prematurity of the skin can continue to be seen in babies born at 29- or 30-weeks' gestation or even beyond.

“The timing of this is interesting. What we see with very premature infant skin is skin that doesn't quite have the thickness, doesn't have the adhesion [of] mature skin,” explained Dr. Eichenfield at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

Translucent premature skin may be incapable of fully performing critical functions, leaving infants susceptible to fluid electrolyte loss, temperature dysregulation, injuries, infections, and increased uptake of potentially toxic agents.

One unusual physical consequence of underdeveloped skin is anetoderma of prematurity, characterized by tissue paper-like depressed brown scars or outpouchings of skin.

Although these lesions may not appear to be associated with overt trauma, they tellingly appear in areas where leads or adhesives have been placed, and most likely represent postinflammatory hyperpigmentation, said Dr. Eichenfield. “Look at the pattern of the lesions” to deduce their origin, he suggested.

Quite commonly, erosions and crusts that would be “banal” in other settings can become profound problems in extremely premature infants. For example, the tape used to adhere umbilical lines may erode the skin and lead to significant secondary infections.

The suction pressure produced when leads are removed can lead to ecchymosis in immature skin, or the ecchymosis can be a sign of invasive fungal infection. All too often, it can be hard to distinguish the two, said Dr. Eichenfield, also a professor of pediatrics and medicine at the University of California, San Diego.

One sign not to miss is diffuse superficial crusting around the umbilical line or elsewhere, which can be a tip off to invasion and colonization with cutaneous candidiasis. “This is important, because it is a significant player in mortality in the [neonatal] ICU,” he said.

Another critical troika of symptoms includes pustules/papules, ecchymosis, and crusts. When these three signs are present, opportunistic fungal infections should be a “very, very strong consideration,” stressed Dr. Eichenfield.

Aspergillus and Rhizopus are only two of hundreds of fungi that may infect premature infants opportunistically, with extremely high rates of associated morbidity and mortality. “If you take care of it with debridement and systemic antifungals quickly, [while it remains confined to the skin], you save the child's life,” he said.

Risk factors for fungal infection in preemies include corticosteroid and antibiotic use, adhesive tape, and hospital construction: the latter currently a major issue in California, since hospitals are racing to conform with state earthquake retrofitting standards. At Rady Children's Hospital, four or five cases of Aspergillus-associated fungal infections have been diagnosed in the past year or so, as construction progresses on the building and the surrounding medical complex, he noted.

Tape used for umbilical lines may erode skin and lead to secondary infections. DR. EICHENFIELD

SANTA BARBARA, CALIF. — Enhanced survival of the smallest of premature infants presents special challenges to dermatologists tasked with caring for conditions arising from incomplete development of the skin.

Skin is a relatively early player in fetal development, with an epidermis present at 36 days that consists of a basal layer and a superficial peridermal layer. Ectodermal tissue gradually appears during organogenesis, and the stratum corneum begins to form around hair follicles at 14 weeks.

But the bridging of these cells into functional skin that includes an epidermal layer does not occur until 22–24 weeks' gestation, an age when preemies now survive at many institutions, said Dr. Lawrence F. Eichenfield, chief of pediatric and adolescent dermatology at Rady Children's Hospital, San Diego.

Complications associated with extreme prematurity of the skin can continue to be seen in babies born at 29- or 30-weeks' gestation or even beyond.

“The timing of this is interesting. What we see with very premature infant skin is skin that doesn't quite have the thickness, doesn't have the adhesion [of] mature skin,” explained Dr. Eichenfield at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

Translucent premature skin may be incapable of fully performing critical functions, leaving infants susceptible to fluid electrolyte loss, temperature dysregulation, injuries, infections, and increased uptake of potentially toxic agents.

One unusual physical consequence of underdeveloped skin is anetoderma of prematurity, characterized by tissue paper-like depressed brown scars or outpouchings of skin.

Although these lesions may not appear to be associated with overt trauma, they tellingly appear in areas where leads or adhesives have been placed, and most likely represent postinflammatory hyperpigmentation, said Dr. Eichenfield. “Look at the pattern of the lesions” to deduce their origin, he suggested.

Quite commonly, erosions and crusts that would be “banal” in other settings can become profound problems in extremely premature infants. For example, the tape used to adhere umbilical lines may erode the skin and lead to significant secondary infections.

The suction pressure produced when leads are removed can lead to ecchymosis in immature skin, or the ecchymosis can be a sign of invasive fungal infection. All too often, it can be hard to distinguish the two, said Dr. Eichenfield, also a professor of pediatrics and medicine at the University of California, San Diego.

One sign not to miss is diffuse superficial crusting around the umbilical line or elsewhere, which can be a tip off to invasion and colonization with cutaneous candidiasis. “This is important, because it is a significant player in mortality in the [neonatal] ICU,” he said.

Another critical troika of symptoms includes pustules/papules, ecchymosis, and crusts. When these three signs are present, opportunistic fungal infections should be a “very, very strong consideration,” stressed Dr. Eichenfield.

Aspergillus and Rhizopus are only two of hundreds of fungi that may infect premature infants opportunistically, with extremely high rates of associated morbidity and mortality. “If you take care of it with debridement and systemic antifungals quickly, [while it remains confined to the skin], you save the child's life,” he said.

Risk factors for fungal infection in preemies include corticosteroid and antibiotic use, adhesive tape, and hospital construction: the latter currently a major issue in California, since hospitals are racing to conform with state earthquake retrofitting standards. At Rady Children's Hospital, four or five cases of Aspergillus-associated fungal infections have been diagnosed in the past year or so, as construction progresses on the building and the surrounding medical complex, he noted.

Tape used for umbilical lines may erode skin and lead to secondary infections. DR. EICHENFIELD

SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained at a recent dermatology meeting.

“It is a different organism,” Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

For starters, the two forms of MRSA attack different populations.

Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, quite obviously, is hospitalization. Infections are most commonly seen in the intensive care unit, although they are known to spread rapidly throughout health care institutions.

Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.

For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution.

Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population, extending to children as well as adults.

“The problem has moved far outside these original risk groups to almost everyone,” said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center (LAC+USC Medical Center).

For example, the LAC+USC Medical Center and the University of California, Los Angeles, Medical Center—institutions that draw from profoundly disparate socioeconomic populations in Los Angeles—both have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.

Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.

Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.

It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins that are not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.

The genetic differences are not surprising, considering the disparate nature of the infections, said Dr. Holtom. HA-MRSA does not spread in the community setting. Other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population. “Maybe it's because—unlike in the hospital where the patient is awash in an antibiotic-saturated environment—when [the patient goes] home there are no antibiotics that drive the growth of MRSA, or at least kill other organisms and allow [MRSA] to have a better environmental niche.”

ELSEVIER GLOBAL MEDICAL NEWS

SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained at a recent dermatology meeting.

“It is a different organism,” Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

For starters, the two forms of MRSA attack different populations.

Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, quite obviously, is hospitalization. Infections are most commonly seen in the intensive care unit, although they are known to spread rapidly throughout health care institutions.

Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.

For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution.

Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population, extending to children as well as adults.

“The problem has moved far outside these original risk groups to almost everyone,” said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center (LAC+USC Medical Center).

For example, the LAC+USC Medical Center and the University of California, Los Angeles, Medical Center—institutions that draw from profoundly disparate socioeconomic populations in Los Angeles—both have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.

Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.

Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.

It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins that are not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.

The genetic differences are not surprising, considering the disparate nature of the infections, said Dr. Holtom. HA-MRSA does not spread in the community setting. Other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population. “Maybe it's because—unlike in the hospital where the patient is awash in an antibiotic-saturated environment—when [the patient goes] home there are no antibiotics that drive the growth of MRSA, or at least kill other organisms and allow [MRSA] to have a better environmental niche.”

ELSEVIER GLOBAL MEDICAL NEWS

SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained at a recent dermatology meeting.

“It is a different organism,” Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

For starters, the two forms of MRSA attack different populations.

Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, quite obviously, is hospitalization. Infections are most commonly seen in the intensive care unit, although they are known to spread rapidly throughout health care institutions.

Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.

For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution.

Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population, extending to children as well as adults.

“The problem has moved far outside these original risk groups to almost everyone,” said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center (LAC+USC Medical Center).

For example, the LAC+USC Medical Center and the University of California, Los Angeles, Medical Center—institutions that draw from profoundly disparate socioeconomic populations in Los Angeles—both have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.

Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.

Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.

It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins that are not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.

The genetic differences are not surprising, considering the disparate nature of the infections, said Dr. Holtom. HA-MRSA does not spread in the community setting. Other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population. “Maybe it's because—unlike in the hospital where the patient is awash in an antibiotic-saturated environment—when [the patient goes] home there are no antibiotics that drive the growth of MRSA, or at least kill other organisms and allow [MRSA] to have a better environmental niche.”

ELSEVIER GLOBAL MEDICAL NEWS

SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained.

“It is a different organism,” Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

For starters, the two forms of MRSA attack different populations.

Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, obviously, is hospitalization. Infections are most commonly seen in the ICU, although they are known to spread rapidly throughout institutions.

Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.

For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution.

Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population.

“The problem has moved far outside these original risk groups to almost everyone,” said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center.

For example, both his institution and the University of California, Los Angeles, Medical Center, which draw from profoundly disparate socioeconomic populations in Los Angeles, have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.

Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.

Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.

It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins that are not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.

The genetic differences are not surprising, considering the disparate nature of the infections, Dr. Holtom said.

“The one thing that has been very interesting about HA-MRSA for all of these years is that it does not spread in the community setting,” he noted.

He theorized that other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population.

ELSEVIER GLOBAL MEDICAL NEWS

SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained.

“It is a different organism,” Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

For starters, the two forms of MRSA attack different populations.

Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, obviously, is hospitalization. Infections are most commonly seen in the ICU, although they are known to spread rapidly throughout institutions.

Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.

For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution.

Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population.

“The problem has moved far outside these original risk groups to almost everyone,” said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center.

For example, both his institution and the University of California, Los Angeles, Medical Center, which draw from profoundly disparate socioeconomic populations in Los Angeles, have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.

Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.

Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.

It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins that are not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.

The genetic differences are not surprising, considering the disparate nature of the infections, Dr. Holtom said.

“The one thing that has been very interesting about HA-MRSA for all of these years is that it does not spread in the community setting,” he noted.

He theorized that other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population.

ELSEVIER GLOBAL MEDICAL NEWS

SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained.

“It is a different organism,” Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

For starters, the two forms of MRSA attack different populations.

Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, obviously, is hospitalization. Infections are most commonly seen in the ICU, although they are known to spread rapidly throughout institutions.

Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.

For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution.

Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population.

“The problem has moved far outside these original risk groups to almost everyone,” said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center.

For example, both his institution and the University of California, Los Angeles, Medical Center, which draw from profoundly disparate socioeconomic populations in Los Angeles, have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.

Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.

Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.

It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins that are not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.

The genetic differences are not surprising, considering the disparate nature of the infections, Dr. Holtom said.

“The one thing that has been very interesting about HA-MRSA for all of these years is that it does not spread in the community setting,” he noted.

He theorized that other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population.

ELSEVIER GLOBAL MEDICAL NEWS

SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained at a dermatology meeting.

"It is a different organism," Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

For starters, the two forms of MRSA attack different populations.

Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, quite obviously, is hospitalization. Infections are most commonly seen in the intensive care unit, although they are known to spread rapidly throughout health care institutions.

Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.

For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution. Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population, extending to children as well as adults.

"The problem has moved far outside these original risk groups to almost everyone," said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center (LAC+USC Medical Center).

For example, the LAC+USC Medical Center and the University of California, Los Angeles, Medical Center—institutions that draw from profoundly disparate socioeconomic populations—both have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.

Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.

Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.

It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.

"The one thing that has been very interesting about HA-MRSA for all of these years is that it does not spread in the community setting," he noted.

Dr. Holtom theorized that other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population.

"Maybe it's because—unlike in the hospital where the patient is awash in an antibiotic-saturated environment—when [the patient goes] home there are no antibiotics that drive the growth of MRSA, or at least kill other organisms and allow [MRSA] to have a better environmental niche," he speculated.

ELSEVIER GLOBAL MEDICAL NEWS

SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained at a dermatology meeting.

"It is a different organism," Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

For starters, the two forms of MRSA attack different populations.

Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, quite obviously, is hospitalization. Infections are most commonly seen in the intensive care unit, although they are known to spread rapidly throughout health care institutions.

Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.

For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution. Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population, extending to children as well as adults.

"The problem has moved far outside these original risk groups to almost everyone," said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center (LAC+USC Medical Center).

For example, the LAC+USC Medical Center and the University of California, Los Angeles, Medical Center—institutions that draw from profoundly disparate socioeconomic populations—both have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.

Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.

Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.

It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.

"The one thing that has been very interesting about HA-MRSA for all of these years is that it does not spread in the community setting," he noted.

Dr. Holtom theorized that other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population.

"Maybe it's because—unlike in the hospital where the patient is awash in an antibiotic-saturated environment—when [the patient goes] home there are no antibiotics that drive the growth of MRSA, or at least kill other organisms and allow [MRSA] to have a better environmental niche," he speculated.

ELSEVIER GLOBAL MEDICAL NEWS

SANTA BARBARA, CALIF. — Community-acquired methicillin-resistant Staphylococcus aureus is unlike its hospital-acquired cousin epidemiologically, clinically, and genetically, an infectious disease specialist explained at a dermatology meeting.

"It is a different organism," Dr. Paul Holtom said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

For starters, the two forms of MRSA attack different populations.

Risk factors for hospital-acquired (HA) MRSA have not changed appreciably in the roughly 20 years since its emergence. The first risk factor, quite obviously, is hospitalization. Infections are most commonly seen in the intensive care unit, although they are known to spread rapidly throughout health care institutions.

Within the hospitalized population, risk factors include use of fluoroquinolones, enteral feeding, surgery, previous hospitalization, and extended lengths of stay.

For community-acquired (CA) MRSA, early lists of potential risk factors included intravenous drug use, homosexuality (men having sex with men), homelessness or marginal housing, and being in a correctional institution. Athletes with skin-to-skin contact were then added to the risk pool, but it soon became clear that the risk was widespread in the healthy population, extending to children as well as adults.

"The problem has moved far outside these original risk groups to almost everyone," said Dr. Holtom, director of the infectious disease clinic fellowship program and hospital epidemiologist at the Los Angeles County Hospital/University of Southern California Medical Center (LAC+USC Medical Center).

For example, the LAC+USC Medical Center and the University of California, Los Angeles, Medical Center—institutions that draw from profoundly disparate socioeconomic populations—both have CA-MRSA rates of greater than 70% in patients presenting to the emergency departments with skin and soft tissue infections.

Genetic testing reveals that CA-MRSA is indeed a distinct entity, rather than an HA-MRSA that has spread to the nonhospital world, Dr. Holtom said.

Hospital-acquired MRSA contains a special mecA gene that codes for penicillin-binding protein (PBP) 2a, which is an important binding site for penicillins and related antibiotic classes. Specifically, the staphylococcus cassette chromosome (SCC) mec types found in HA-MRSA are types I, II, and III, with type II dominating.

It's a different story for CA-MRSA, which is characterized by SCCmec types IV and sometimes V, which carry genes for a variety of toxins not seen in HA-MRSA, including the Panton-Valentine leukocidin toxin known for generating a prolific inflammatory response and skin necrosis.

"The one thing that has been very interesting about HA-MRSA for all of these years is that it does not spread in the community setting," he noted.

Dr. Holtom theorized that other organisms may have a competitive advantage in non-health care settings, or that HA-MRSA may spread too slowly in the immunocompetent population.

"Maybe it's because—unlike in the hospital where the patient is awash in an antibiotic-saturated environment—when [the patient goes] home there are no antibiotics that drive the growth of MRSA, or at least kill other organisms and allow [MRSA] to have a better environmental niche," he speculated.

ELSEVIER GLOBAL MEDICAL NEWS

SANTA BARBARA, CALIF. — Resist temptation.

When the patient looks good, but the syringe in your hand still contains leftover Restylane or Juvéderm, "Put it down," advised Dr. Allan Wirtzer, a dermatologist in private practice in Sherman Oaks, Calif.

"Don't feel that you have to use an entire syringe on these patients."

"[Don't say,] I'll find a place to put it." You don't have to put it anywhere, he said during a panel on aesthetic complications during the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

Dr. Wirtzer said most of the cases he sees for correction of aesthetic filler procedures boil down to technique error. "Many times, people are injecting too much, too superficial, too soon, and sometimes, it's just a poor choice of material," he said.

Filler materials are expensive, so some physicians want to inject every drop. But overfilled cheeks, nodular lips, and bumpy chins do not lead to patients satisfied that they got their money's worth, he said.

Overtreating a patient with permanent fillers doesn't last forever. "But you can see the results of overtreatment even with Restylane or Perlane or Radiesse for months and months, and these patients are not going to be happy," he said.

Silicone fillers are not for beginners. "If you don't have years of experience with long-term fillers and short-term fillers, don't go near silicone," Dr. Wirtzer said.

Among his other tips:

▸ Inject deeply, using as few needle sticks as possible.

▸ To avoid drift with Radiesse, massage "a great deal." Around the orbicularis muscle, stay very medial so that the facial muscles used in smiling do not create forces that push the material to the outside edges of the lips.

▸ When using Restylane, avoid bulges by injecting below the orbital ridge.

▸ Minimize pain with ice and topical and local anesthetics.

▸ Invest in $3 handheld squeeze balls, which create a distraction for the patient during filler injections.

▸ If you see a blanch and realize you have an infarction in a vessel, "vigorously massage the hell out of it."

Above all, be meticulous in preprocedure discussions with patients about expected sequelae of the treatment, Dr. Wirtzer advised. "When you discuss that a person's going to get red or going to get swollen, this isn't [seen as] a complication; it's a natural event that follows the treatment."

If it is discussed only after the fact, however, it is seen by the patient as an "excuse" meant to explain away a perceived complication, he said.

Dr. Wirtzer disclosed that he serves as a consultant to Medicis Pharmaceutical Corp., maker of Restylane, and Aventis Dermatology, maker of Sculptra.

'You can see the results of overtreatment … for months and months, and these patients are not going to be happy.' DR. WIRTZER

SANTA BARBARA, CALIF. — Resist temptation.

When the patient looks good, but the syringe in your hand still contains leftover Restylane or Juvéderm, "Put it down," advised Dr. Allan Wirtzer, a dermatologist in private practice in Sherman Oaks, Calif.

"Don't feel that you have to use an entire syringe on these patients."

"[Don't say,] I'll find a place to put it." You don't have to put it anywhere, he said during a panel on aesthetic complications during the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

Dr. Wirtzer said most of the cases he sees for correction of aesthetic filler procedures boil down to technique error. "Many times, people are injecting too much, too superficial, too soon, and sometimes, it's just a poor choice of material," he said.

Filler materials are expensive, so some physicians want to inject every drop. But overfilled cheeks, nodular lips, and bumpy chins do not lead to patients satisfied that they got their money's worth, he said.

Overtreating a patient with permanent fillers doesn't last forever. "But you can see the results of overtreatment even with Restylane or Perlane or Radiesse for months and months, and these patients are not going to be happy," he said.

Silicone fillers are not for beginners. "If you don't have years of experience with long-term fillers and short-term fillers, don't go near silicone," Dr. Wirtzer said.

Among his other tips:

▸ Inject deeply, using as few needle sticks as possible.

▸ To avoid drift with Radiesse, massage "a great deal." Around the orbicularis muscle, stay very medial so that the facial muscles used in smiling do not create forces that push the material to the outside edges of the lips.

▸ When using Restylane, avoid bulges by injecting below the orbital ridge.

▸ Minimize pain with ice and topical and local anesthetics.

▸ Invest in $3 handheld squeeze balls, which create a distraction for the patient during filler injections.

▸ If you see a blanch and realize you have an infarction in a vessel, "vigorously massage the hell out of it."

Above all, be meticulous in preprocedure discussions with patients about expected sequelae of the treatment, Dr. Wirtzer advised. "When you discuss that a person's going to get red or going to get swollen, this isn't [seen as] a complication; it's a natural event that follows the treatment."

If it is discussed only after the fact, however, it is seen by the patient as an "excuse" meant to explain away a perceived complication, he said.

Dr. Wirtzer disclosed that he serves as a consultant to Medicis Pharmaceutical Corp., maker of Restylane, and Aventis Dermatology, maker of Sculptra.

'You can see the results of overtreatment … for months and months, and these patients are not going to be happy.' DR. WIRTZER

SANTA BARBARA, CALIF. — Resist temptation.

When the patient looks good, but the syringe in your hand still contains leftover Restylane or Juvéderm, "Put it down," advised Dr. Allan Wirtzer, a dermatologist in private practice in Sherman Oaks, Calif.

"Don't feel that you have to use an entire syringe on these patients."

"[Don't say,] I'll find a place to put it." You don't have to put it anywhere, he said during a panel on aesthetic complications during the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

Dr. Wirtzer said most of the cases he sees for correction of aesthetic filler procedures boil down to technique error. "Many times, people are injecting too much, too superficial, too soon, and sometimes, it's just a poor choice of material," he said.

Filler materials are expensive, so some physicians want to inject every drop. But overfilled cheeks, nodular lips, and bumpy chins do not lead to patients satisfied that they got their money's worth, he said.

Overtreating a patient with permanent fillers doesn't last forever. "But you can see the results of overtreatment even with Restylane or Perlane or Radiesse for months and months, and these patients are not going to be happy," he said.

Silicone fillers are not for beginners. "If you don't have years of experience with long-term fillers and short-term fillers, don't go near silicone," Dr. Wirtzer said.

Among his other tips:

▸ Inject deeply, using as few needle sticks as possible.

▸ To avoid drift with Radiesse, massage "a great deal." Around the orbicularis muscle, stay very medial so that the facial muscles used in smiling do not create forces that push the material to the outside edges of the lips.

▸ When using Restylane, avoid bulges by injecting below the orbital ridge.

▸ Minimize pain with ice and topical and local anesthetics.

▸ Invest in $3 handheld squeeze balls, which create a distraction for the patient during filler injections.

▸ If you see a blanch and realize you have an infarction in a vessel, "vigorously massage the hell out of it."

Above all, be meticulous in preprocedure discussions with patients about expected sequelae of the treatment, Dr. Wirtzer advised. "When you discuss that a person's going to get red or going to get swollen, this isn't [seen as] a complication; it's a natural event that follows the treatment."

If it is discussed only after the fact, however, it is seen by the patient as an "excuse" meant to explain away a perceived complication, he said.

Dr. Wirtzer disclosed that he serves as a consultant to Medicis Pharmaceutical Corp., maker of Restylane, and Aventis Dermatology, maker of Sculptra.

'You can see the results of overtreatment … for months and months, and these patients are not going to be happy.' DR. WIRTZER

SANTA BARBARA, CALIF. — A “care collision” with vitamin D proponents can be avoided by ensuring that patients receive supplements to compensate for their lack of exposure to ultraviolet light, a California-based dermatologist suggested.

“Patients are getting this mixed message about whether they are supposed to go out in the sun or not go out in the sun. There's a lot of confusion,” said Dr. Jeffrey Ashley, a dermatologist in private practice who also directs the nonprofit organization Sun Safety for Kids.

While Boston University endocrinologist Dr. Michael Holick recommended intentional sun exposure or time in the tanning booth in his book “The UV Advantage” (Ibooks Inc., 2004), many dermatologists insist on sun protection, despite evidence of the multifaceted benefits of vitamin D sufficiency, he said.

Inadequate vitamin D is a leading contributor to osteoporosis, diagnosed in 10–12 million Americans, according to Dr. Ashley. It has been proved directly or indirectly to control the expression of more than 200 genes, including regulation of cellular proliferation, differentiation, apoptosis, and angiogenesis.

And current studies are examining its association with recurrent melanoma and cancers of the colon, breast, pancreas, prostate, and ovary, as well as autoimmune diseases, cardiovascular diseases, hypertension, and even schizophrenia.

“I think the bottom line is, until we have more evidence about this, we need to err on the safe side … and make sure our patients have sufficient levels of vitamin D,” he said during the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

“Who should you suspect of being vitamin D deficient in your practice?”

The standard answer: elderly people, whose thin skin does not contain as much vitamin D precursor; people with dark skin tones, who require sixfold as much UV light to produce vitamin D; obese patients, because vitamin D is sequestered in adipose tissue; and breastfed babies, who receive little vitamin D from their mothers' milk.

However, not everyone who is vitamin D deficient fits the classic profile, as evidenced by a recent study of skateboarders in Hawaii, a quarter of whom had blood levels less than 30 ng/mL and 10% of whom had levels less than 10 ng/mL—a level associated with rickets (J. Clin. Endocrin. Metab. 2007;92:2130-5).

When he began routinely ordering vitamin D blood level tests, Dr. Ashley was surprised to find many patients with at-risk blood levels of lower than 20 ng/mL and a number of elderly patients with levels so low they equated to adult rickets, at less than 10 ng/mL.

He recommends that his sun-safe patients make sure they are taking 1,000 IU per day of cholecalciferol (vitamin D3). His patients have welcomed the information, he said, since it addresses conflicting information they have heard about touted benefits of unprotected exposure to the sun.

“I think we've reached the point where there's a care collision between those of us really concerned about skin cancer prevention in the one corner, and [in the other corner] those whose primary concern is maintaining vitamin D sufficiency in the population,” he said.

The American Academy of Dermatology maintains that a well-balanced diet and incidental sun exposure are sufficient to fulfill vitamin D needs, said Dr. Ashley.

“I take exception to that,” he said. Spending time in the sun to obtain ideal levels of vitamin D is an “inaccurate, unreliable, complicated” proposition, because people absorb and metabolize ultraviolet light differently.

Through diet alone, patients would have to eat wild salmon daily to get 1,000 IU of vitamin D—the level recommended by the Canadian Cancer Society and many nutritionists and endocrinologists.

Dr. Ashley now orders vitamin D blood level tests for every patient each winter, unless his or her primary care physicians have already done so. He tells patients, “If we can keep your level up in winter, you'll probably be okay all year-round.”

While he recommends supplementation daily for all of his patients, he is particularly careful about monitoring those whose blood levels fall below what he considers to be the “preferred range for optimal benefit”: 32–60 ng/mL, he said.

Dr. Ashley had no conflicts of interest to disclose.

SANTA BARBARA, CALIF. — A “care collision” with vitamin D proponents can be avoided by ensuring that patients receive supplements to compensate for their lack of exposure to ultraviolet light, a California-based dermatologist suggested.

“Patients are getting this mixed message about whether they are supposed to go out in the sun or not go out in the sun. There's a lot of confusion,” said Dr. Jeffrey Ashley, a dermatologist in private practice who also directs the nonprofit organization Sun Safety for Kids.

While Boston University endocrinologist Dr. Michael Holick recommended intentional sun exposure or time in the tanning booth in his book “The UV Advantage” (Ibooks Inc., 2004), many dermatologists insist on sun protection, despite evidence of the multifaceted benefits of vitamin D sufficiency, he said.

Inadequate vitamin D is a leading contributor to osteoporosis, diagnosed in 10–12 million Americans, according to Dr. Ashley. It has been proved directly or indirectly to control the expression of more than 200 genes, including regulation of cellular proliferation, differentiation, apoptosis, and angiogenesis.

And current studies are examining its association with recurrent melanoma and cancers of the colon, breast, pancreas, prostate, and ovary, as well as autoimmune diseases, cardiovascular diseases, hypertension, and even schizophrenia.

“I think the bottom line is, until we have more evidence about this, we need to err on the safe side … and make sure our patients have sufficient levels of vitamin D,” he said during the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

“Who should you suspect of being vitamin D deficient in your practice?”

The standard answer: elderly people, whose thin skin does not contain as much vitamin D precursor; people with dark skin tones, who require sixfold as much UV light to produce vitamin D; obese patients, because vitamin D is sequestered in adipose tissue; and breastfed babies, who receive little vitamin D from their mothers' milk.

However, not everyone who is vitamin D deficient fits the classic profile, as evidenced by a recent study of skateboarders in Hawaii, a quarter of whom had blood levels less than 30 ng/mL and 10% of whom had levels less than 10 ng/mL—a level associated with rickets (J. Clin. Endocrin. Metab. 2007;92:2130-5).

When he began routinely ordering vitamin D blood level tests, Dr. Ashley was surprised to find many patients with at-risk blood levels of lower than 20 ng/mL and a number of elderly patients with levels so low they equated to adult rickets, at less than 10 ng/mL.

He recommends that his sun-safe patients make sure they are taking 1,000 IU per day of cholecalciferol (vitamin D3). His patients have welcomed the information, he said, since it addresses conflicting information they have heard about touted benefits of unprotected exposure to the sun.

“I think we've reached the point where there's a care collision between those of us really concerned about skin cancer prevention in the one corner, and [in the other corner] those whose primary concern is maintaining vitamin D sufficiency in the population,” he said.

The American Academy of Dermatology maintains that a well-balanced diet and incidental sun exposure are sufficient to fulfill vitamin D needs, said Dr. Ashley.

“I take exception to that,” he said. Spending time in the sun to obtain ideal levels of vitamin D is an “inaccurate, unreliable, complicated” proposition, because people absorb and metabolize ultraviolet light differently.

Through diet alone, patients would have to eat wild salmon daily to get 1,000 IU of vitamin D—the level recommended by the Canadian Cancer Society and many nutritionists and endocrinologists.

Dr. Ashley now orders vitamin D blood level tests for every patient each winter, unless his or her primary care physicians have already done so. He tells patients, “If we can keep your level up in winter, you'll probably be okay all year-round.”

While he recommends supplementation daily for all of his patients, he is particularly careful about monitoring those whose blood levels fall below what he considers to be the “preferred range for optimal benefit”: 32–60 ng/mL, he said.

Dr. Ashley had no conflicts of interest to disclose.

SANTA BARBARA, CALIF. — A “care collision” with vitamin D proponents can be avoided by ensuring that patients receive supplements to compensate for their lack of exposure to ultraviolet light, a California-based dermatologist suggested.

“Patients are getting this mixed message about whether they are supposed to go out in the sun or not go out in the sun. There's a lot of confusion,” said Dr. Jeffrey Ashley, a dermatologist in private practice who also directs the nonprofit organization Sun Safety for Kids.

While Boston University endocrinologist Dr. Michael Holick recommended intentional sun exposure or time in the tanning booth in his book “The UV Advantage” (Ibooks Inc., 2004), many dermatologists insist on sun protection, despite evidence of the multifaceted benefits of vitamin D sufficiency, he said.

Inadequate vitamin D is a leading contributor to osteoporosis, diagnosed in 10–12 million Americans, according to Dr. Ashley. It has been proved directly or indirectly to control the expression of more than 200 genes, including regulation of cellular proliferation, differentiation, apoptosis, and angiogenesis.

And current studies are examining its association with recurrent melanoma and cancers of the colon, breast, pancreas, prostate, and ovary, as well as autoimmune diseases, cardiovascular diseases, hypertension, and even schizophrenia.

“I think the bottom line is, until we have more evidence about this, we need to err on the safe side … and make sure our patients have sufficient levels of vitamin D,” he said during the annual meeting of the California Society of Dermatology and Dermatologic Surgery.

“Who should you suspect of being vitamin D deficient in your practice?”

The standard answer: elderly people, whose thin skin does not contain as much vitamin D precursor; people with dark skin tones, who require sixfold as much UV light to produce vitamin D; obese patients, because vitamin D is sequestered in adipose tissue; and breastfed babies, who receive little vitamin D from their mothers' milk.

However, not everyone who is vitamin D deficient fits the classic profile, as evidenced by a recent study of skateboarders in Hawaii, a quarter of whom had blood levels less than 30 ng/mL and 10% of whom had levels less than 10 ng/mL—a level associated with rickets (J. Clin. Endocrin. Metab. 2007;92:2130-5).

When he began routinely ordering vitamin D blood level tests, Dr. Ashley was surprised to find many patients with at-risk blood levels of lower than 20 ng/mL and a number of elderly patients with levels so low they equated to adult rickets, at less than 10 ng/mL.

He recommends that his sun-safe patients make sure they are taking 1,000 IU per day of cholecalciferol (vitamin D3). His patients have welcomed the information, he said, since it addresses conflicting information they have heard about touted benefits of unprotected exposure to the sun.

“I think we've reached the point where there's a care collision between those of us really concerned about skin cancer prevention in the one corner, and [in the other corner] those whose primary concern is maintaining vitamin D sufficiency in the population,” he said.

The American Academy of Dermatology maintains that a well-balanced diet and incidental sun exposure are sufficient to fulfill vitamin D needs, said Dr. Ashley.

“I take exception to that,” he said. Spending time in the sun to obtain ideal levels of vitamin D is an “inaccurate, unreliable, complicated” proposition, because people absorb and metabolize ultraviolet light differently.

Through diet alone, patients would have to eat wild salmon daily to get 1,000 IU of vitamin D—the level recommended by the Canadian Cancer Society and many nutritionists and endocrinologists.

Dr. Ashley now orders vitamin D blood level tests for every patient each winter, unless his or her primary care physicians have already done so. He tells patients, “If we can keep your level up in winter, you'll probably be okay all year-round.”

While he recommends supplementation daily for all of his patients, he is particularly careful about monitoring those whose blood levels fall below what he considers to be the “preferred range for optimal benefit”: 32–60 ng/mL, he said.

Dr. Ashley had no conflicts of interest to disclose.

DENVER — Apnea risk may be lower than previously believed in otherwise normal infants with bronchiolitis. Early studies included many children with serious comorbid conditions that may have compounded their apnea risk, a systematic review of studies concluded.

Hospitalization rates for children with bronchiolitis have risen 250% in the more than 30 years since publication of a noteworthy article that cited an apnea rate of 20% in children with respiratory syncytial virus (RSV), Dr. Shawn L. Ralston said at a meeting on pediatric hospital medicine.

Hospitalization for RSV-related bronchiolitis is so pervasive that up to one in five hospital admissions of infants is due to the diagnosis. However, severity and death rates have not changed since the 1970s, suggesting some children may be hospitalized unnecessarily, aid Dr. Ralston, a pediatric hospitalist at the University of Texas Health Science Center at San Antonio. She presented the results at a meeting sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.

Dr. Ralston reviewed the literature to determine apnea rates in children with RSV and bronchiolitis. From eight retrospective studies, she identified 3,623 patients as having bronchiolitis. Of those, 310 (8.5%) were deemed to have apnea either observed or indicated by a parent or health care worker report. In 1,402 cases in which gestational age at birth was clearly documented, just 4.7% of full term babies (defined as 38 weeks or greater) with bronchiolitis had associated apnea, she reported.

These rates are far lower than those reported in a series of studies, beginning with one published in 1977 by Denver physician Frederic W. Bruhn (J. Pediatr. 1977;90:382–6) that identified apnea in 56 of 274 infants less than 6 months old who were diagnosed with RSV, a rate of 20.4%.

Other studies during the 1980s had heterogeneous apnea rates ranging from 10% to 20% and left an overall impression that apnea was very common in children with RSV and bronchiolitis.

A closer look at pertinent studies found wide disparities in design, inclusion criteria, and stratification of data. The most striking methodological problem was that studies with high apnea rates failed to exclude children with underlying illnesses and conditions.

The studies also tended to deemphasize the role of patient age and gestational age at birth, which appear to be important risk factors, with the youngest babies being at the highest risk.

DENVER — Apnea risk may be lower than previously believed in otherwise normal infants with bronchiolitis. Early studies included many children with serious comorbid conditions that may have compounded their apnea risk, a systematic review of studies concluded.

Hospitalization rates for children with bronchiolitis have risen 250% in the more than 30 years since publication of a noteworthy article that cited an apnea rate of 20% in children with respiratory syncytial virus (RSV), Dr. Shawn L. Ralston said at a meeting on pediatric hospital medicine.

Hospitalization for RSV-related bronchiolitis is so pervasive that up to one in five hospital admissions of infants is due to the diagnosis. However, severity and death rates have not changed since the 1970s, suggesting some children may be hospitalized unnecessarily, aid Dr. Ralston, a pediatric hospitalist at the University of Texas Health Science Center at San Antonio. She presented the results at a meeting sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.

Dr. Ralston reviewed the literature to determine apnea rates in children with RSV and bronchiolitis. From eight retrospective studies, she identified 3,623 patients as having bronchiolitis. Of those, 310 (8.5%) were deemed to have apnea either observed or indicated by a parent or health care worker report. In 1,402 cases in which gestational age at birth was clearly documented, just 4.7% of full term babies (defined as 38 weeks or greater) with bronchiolitis had associated apnea, she reported.

These rates are far lower than those reported in a series of studies, beginning with one published in 1977 by Denver physician Frederic W. Bruhn (J. Pediatr. 1977;90:382–6) that identified apnea in 56 of 274 infants less than 6 months old who were diagnosed with RSV, a rate of 20.4%.

Other studies during the 1980s had heterogeneous apnea rates ranging from 10% to 20% and left an overall impression that apnea was very common in children with RSV and bronchiolitis.

A closer look at pertinent studies found wide disparities in design, inclusion criteria, and stratification of data. The most striking methodological problem was that studies with high apnea rates failed to exclude children with underlying illnesses and conditions.

The studies also tended to deemphasize the role of patient age and gestational age at birth, which appear to be important risk factors, with the youngest babies being at the highest risk.

DENVER — Apnea risk may be lower than previously believed in otherwise normal infants with bronchiolitis. Early studies included many children with serious comorbid conditions that may have compounded their apnea risk, a systematic review of studies concluded.

Hospitalization rates for children with bronchiolitis have risen 250% in the more than 30 years since publication of a noteworthy article that cited an apnea rate of 20% in children with respiratory syncytial virus (RSV), Dr. Shawn L. Ralston said at a meeting on pediatric hospital medicine.

Hospitalization for RSV-related bronchiolitis is so pervasive that up to one in five hospital admissions of infants is due to the diagnosis. However, severity and death rates have not changed since the 1970s, suggesting some children may be hospitalized unnecessarily, aid Dr. Ralston, a pediatric hospitalist at the University of Texas Health Science Center at San Antonio. She presented the results at a meeting sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the Academic Pediatric Association.

Dr. Ralston reviewed the literature to determine apnea rates in children with RSV and bronchiolitis. From eight retrospective studies, she identified 3,623 patients as having bronchiolitis. Of those, 310 (8.5%) were deemed to have apnea either observed or indicated by a parent or health care worker report. In 1,402 cases in which gestational age at birth was clearly documented, just 4.7% of full term babies (defined as 38 weeks or greater) with bronchiolitis had associated apnea, she reported.

These rates are far lower than those reported in a series of studies, beginning with one published in 1977 by Denver physician Frederic W. Bruhn (J. Pediatr. 1977;90:382–6) that identified apnea in 56 of 274 infants less than 6 months old who were diagnosed with RSV, a rate of 20.4%.

Other studies during the 1980s had heterogeneous apnea rates ranging from 10% to 20% and left an overall impression that apnea was very common in children with RSV and bronchiolitis.

A closer look at pertinent studies found wide disparities in design, inclusion criteria, and stratification of data. The most striking methodological problem was that studies with high apnea rates failed to exclude children with underlying illnesses and conditions.

The studies also tended to deemphasize the role of patient age and gestational age at birth, which appear to be important risk factors, with the youngest babies being at the highest risk.

HONOLULU — A few simple, inexpensive laboratory tests conducted in the outpatient setting could have identified which febrile infants were likely to have serious bacterial infections and should have been considered for hospital admission, according to the results of a retrospective study of febrile infants.

Dr. Eric W. Glissmeyer and his associates examined the records of 10,316 febrile infant visits to hospitals and emergency clinics and found that in about half of cases (5,221), the infants were evaluated and sent home.

Of those, 63 (1%) were admitted within 3 days of discharge, 23 of them for serious, culture-confirmed bacterial infections, Dr. Glissmeyer said at the annual meeting of the Pediatric Academic Societies.

Bacteremia (10 cases), urinary tract infection (7 cases), bacterial meningitis (5 cases), and salmonella gastroenteritis (1 case) were among the missed cases. Most of the cases were life threatening, he said.

Among the 23 cases, just 1 infant had received a complete blood count and a urinalysis with results within normal limits at the initial presentation, conferring a low risk of a serious bacterial infection, reported Dr. Glissmeyer, who was at the University of Utah, Salt Lake City, at the time of the study.

Another 12 (52%) of these 23 infants were discharged home despite being at high risk for a serious bacterial infection. Risk was based on laboratory results and was considered high if an infant had a white blood cell count of fewer than 5,000 cells/mcL or more than 15,000 cells/mcL; an absolute band count of greater than 1,500/mm

Infants with laboratory results meeting these high-risk criteria had more than a twofold increased likelihood of being readmitted within 3 days for any reason, and for a serious bacterial infection specifically.

No laboratory tests were performed in 10 febrile infants who went on to be hospitalized with a serious bacterial infection within 3 days, said Dr. Glissmeyer, now at Children's Hospital in Boston.

Consensus guidelines issued in 1993 for the management of febrile infants (Ann. Emerg. Med. 22:1198–210) and criteria developed by several institutions on the basis of prospective studies routinely recommend a CBC and a urinalysis to detect high-risk infants aged between 1 and 90 days.

Many institutions routinely admit all febrile infants younger than 28 days because clinical appearance alone is a poor determinant of risk for serious bacterial infection for febrile infants, said Dr. Glissmeyer.

“Febrile infants with a missed serious bacterial infection are at risk for serious morbidity and mortality,” he added. “Simple laboratory testing, including a CBC and a urinalysis, should be obtained before the decision is made to manage [a febrile infant] as an outpatient.”

HONOLULU — A few simple, inexpensive laboratory tests conducted in the outpatient setting could have identified which febrile infants were likely to have serious bacterial infections and should have been considered for hospital admission, according to the results of a retrospective study of febrile infants.

Dr. Eric W. Glissmeyer and his associates examined the records of 10,316 febrile infant visits to hospitals and emergency clinics and found that in about half of cases (5,221), the infants were evaluated and sent home.

Of those, 63 (1%) were admitted within 3 days of discharge, 23 of them for serious, culture-confirmed bacterial infections, Dr. Glissmeyer said at the annual meeting of the Pediatric Academic Societies.

Bacteremia (10 cases), urinary tract infection (7 cases), bacterial meningitis (5 cases), and salmonella gastroenteritis (1 case) were among the missed cases. Most of the cases were life threatening, he said.

Among the 23 cases, just 1 infant had received a complete blood count and a urinalysis with results within normal limits at the initial presentation, conferring a low risk of a serious bacterial infection, reported Dr. Glissmeyer, who was at the University of Utah, Salt Lake City, at the time of the study.

Another 12 (52%) of these 23 infants were discharged home despite being at high risk for a serious bacterial infection. Risk was based on laboratory results and was considered high if an infant had a white blood cell count of fewer than 5,000 cells/mcL or more than 15,000 cells/mcL; an absolute band count of greater than 1,500/mm

Infants with laboratory results meeting these high-risk criteria had more than a twofold increased likelihood of being readmitted within 3 days for any reason, and for a serious bacterial infection specifically.

No laboratory tests were performed in 10 febrile infants who went on to be hospitalized with a serious bacterial infection within 3 days, said Dr. Glissmeyer, now at Children's Hospital in Boston.

Consensus guidelines issued in 1993 for the management of febrile infants (Ann. Emerg. Med. 22:1198–210) and criteria developed by several institutions on the basis of prospective studies routinely recommend a CBC and a urinalysis to detect high-risk infants aged between 1 and 90 days.

Many institutions routinely admit all febrile infants younger than 28 days because clinical appearance alone is a poor determinant of risk for serious bacterial infection for febrile infants, said Dr. Glissmeyer.

“Febrile infants with a missed serious bacterial infection are at risk for serious morbidity and mortality,” he added. “Simple laboratory testing, including a CBC and a urinalysis, should be obtained before the decision is made to manage [a febrile infant] as an outpatient.”

HONOLULU — A few simple, inexpensive laboratory tests conducted in the outpatient setting could have identified which febrile infants were likely to have serious bacterial infections and should have been considered for hospital admission, according to the results of a retrospective study of febrile infants.

Dr. Eric W. Glissmeyer and his associates examined the records of 10,316 febrile infant visits to hospitals and emergency clinics and found that in about half of cases (5,221), the infants were evaluated and sent home.

Of those, 63 (1%) were admitted within 3 days of discharge, 23 of them for serious, culture-confirmed bacterial infections, Dr. Glissmeyer said at the annual meeting of the Pediatric Academic Societies.

Bacteremia (10 cases), urinary tract infection (7 cases), bacterial meningitis (5 cases), and salmonella gastroenteritis (1 case) were among the missed cases. Most of the cases were life threatening, he said.

Among the 23 cases, just 1 infant had received a complete blood count and a urinalysis with results within normal limits at the initial presentation, conferring a low risk of a serious bacterial infection, reported Dr. Glissmeyer, who was at the University of Utah, Salt Lake City, at the time of the study.

Another 12 (52%) of these 23 infants were discharged home despite being at high risk for a serious bacterial infection. Risk was based on laboratory results and was considered high if an infant had a white blood cell count of fewer than 5,000 cells/mcL or more than 15,000 cells/mcL; an absolute band count of greater than 1,500/mm

Infants with laboratory results meeting these high-risk criteria had more than a twofold increased likelihood of being readmitted within 3 days for any reason, and for a serious bacterial infection specifically.

No laboratory tests were performed in 10 febrile infants who went on to be hospitalized with a serious bacterial infection within 3 days, said Dr. Glissmeyer, now at Children's Hospital in Boston.

Consensus guidelines issued in 1993 for the management of febrile infants (Ann. Emerg. Med. 22:1198–210) and criteria developed by several institutions on the basis of prospective studies routinely recommend a CBC and a urinalysis to detect high-risk infants aged between 1 and 90 days.

Many institutions routinely admit all febrile infants younger than 28 days because clinical appearance alone is a poor determinant of risk for serious bacterial infection for febrile infants, said Dr. Glissmeyer.

“Febrile infants with a missed serious bacterial infection are at risk for serious morbidity and mortality,” he added. “Simple laboratory testing, including a CBC and a urinalysis, should be obtained before the decision is made to manage [a febrile infant] as an outpatient.”

DENVER — Any child with atopic dermatitis who has increasing pain, erythema, edema, heat, and purulent exudate is superinfected and requires antibiotics and emollients, according to an expert in pediatric dermatology.

A culture is necessary only for prescribing the correct antibiotic.

"I'm here to plead with you that infection is a clinical diagnosis, not a microbiological diagnosis," said Dr. H. Alan Arbuckle, a dermatologist and pediatrician at the University of Colorado, Denver, and Children's Hospital in Aurora, Colo.

"Doing a culture in a superinfected AD kid is worthless if your goal is to make the diagnosis of infection.

"All of these kids are going to be colonized. All are going to be positive. If you tell me the age of the wound, I'll tell you what organisms are in there, because if you look at acute and chronic wounds, they march through a sequential order of which organisms are present," he said. The increasingly relevant purpose of doing a culture on such a child is to direct antibiotic therapy by determining sensitivities of the involved organisms.

"All children with AD are colonized with staph [Staphylococcus] and strep [Streptococcus], predominantly Staph aureus and Strep pyogenes," he said at a meeting on pediatric hospital medicine.

Recent research findings provide perspective on the course of severe atopic dermatitis, according to Dr. Arbuckle.

Most pivotally, the evidence is mounting that "the problem in atopic dermatitis is … an abnormal barrier function," he said at the meeting, which was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the American Pediatric Association.

In years past, pediatric dermatologists argued with pediatric allergists over the primary etiology of atopic dermatitis, with allergists arguing that immune dysfunction was to blame.

The issue was put to rest when Japanese researchers discovered that the vast majority of children with atopic dermatitis have a genetic defect in filaggrin, a protein that bundles keratin and provides the "mortar" in the brick-and-mortar type construction of the stratum corneum.

"We kind of had a big kumbaya, kissed, and made up. Dermatologists [had always said], well, there is an immune component, but how did the antigen get there? It got there because [the skin] had an improper barrier," Dr. Arbuckle commented.

Microcracks and microfissures, exacerbated by itching prompted by exposed nerve fibers in the epidermis, open the door to allergens, bacteria, and viruses. Compounding the problem is transepidermal water loss 600 times normal in the skin of children and adults with atopic dermatitis.

"We always knew that atopic kids have higher colony counts even when they aren't superinfected," said Dr. Arbuckle. "[It turns out], S. aureus is very adaptable, and upregulates certain adhesion proteins in a very dry environment."

Treatment is imperative in the face of superinfection, because children can harbor a profound bacterial load and develop sepsis, Dr. Arbuckle emphasized.

First-generation cephalosporins are "probably fine" as a first-line choice, but it depends on one's community and culture results, he said.

Once a proper antibiotic is selected, "You've got to restore barrier function. If you don't do this, they're not going to get better," Dr. Arbuckle emphasized.

In Denver's dry climate, he said he prefers petrolatum-based products, the simpler the better to avoid allergic responses. Plain petroleum jelly contains no lanolin or other additives that might cause a reaction. Choose topical steroids in ointment form, because creams often contain propylene glycol, which "stings like Hades," he suggested.

The "biggest failure" of most physicians is undertreatment of pruritus, which is often so severe it can preclude rapid eye movement sleep. Sedating antihistamines should be prescribed for night time and nonsedating antihistamines in the morning.

"Children with atopic dermatitis are perennially, horrifically itchy," he said, noting that he tells residents that if they prescribe an antihistamine as needed, "I will slap you upside the head."

Dr. Arbuckle disclosed no relevant conflicts of interest regarding any product used to treat atopic dermatitis.

DENVER — Any child with atopic dermatitis who has increasing pain, erythema, edema, heat, and purulent exudate is superinfected and requires antibiotics and emollients, according to an expert in pediatric dermatology.

A culture is necessary only for prescribing the correct antibiotic.

"I'm here to plead with you that infection is a clinical diagnosis, not a microbiological diagnosis," said Dr. H. Alan Arbuckle, a dermatologist and pediatrician at the University of Colorado, Denver, and Children's Hospital in Aurora, Colo.

"Doing a culture in a superinfected AD kid is worthless if your goal is to make the diagnosis of infection.

"All of these kids are going to be colonized. All are going to be positive. If you tell me the age of the wound, I'll tell you what organisms are in there, because if you look at acute and chronic wounds, they march through a sequential order of which organisms are present," he said. The increasingly relevant purpose of doing a culture on such a child is to direct antibiotic therapy by determining sensitivities of the involved organisms.

"All children with AD are colonized with staph [Staphylococcus] and strep [Streptococcus], predominantly Staph aureus and Strep pyogenes," he said at a meeting on pediatric hospital medicine.

Recent research findings provide perspective on the course of severe atopic dermatitis, according to Dr. Arbuckle.

Most pivotally, the evidence is mounting that "the problem in atopic dermatitis is … an abnormal barrier function," he said at the meeting, which was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the American Pediatric Association.

In years past, pediatric dermatologists argued with pediatric allergists over the primary etiology of atopic dermatitis, with allergists arguing that immune dysfunction was to blame.

The issue was put to rest when Japanese researchers discovered that the vast majority of children with atopic dermatitis have a genetic defect in filaggrin, a protein that bundles keratin and provides the "mortar" in the brick-and-mortar type construction of the stratum corneum.

"We kind of had a big kumbaya, kissed, and made up. Dermatologists [had always said], well, there is an immune component, but how did the antigen get there? It got there because [the skin] had an improper barrier," Dr. Arbuckle commented.

Microcracks and microfissures, exacerbated by itching prompted by exposed nerve fibers in the epidermis, open the door to allergens, bacteria, and viruses. Compounding the problem is transepidermal water loss 600 times normal in the skin of children and adults with atopic dermatitis.

"We always knew that atopic kids have higher colony counts even when they aren't superinfected," said Dr. Arbuckle. "[It turns out], S. aureus is very adaptable, and upregulates certain adhesion proteins in a very dry environment."

Treatment is imperative in the face of superinfection, because children can harbor a profound bacterial load and develop sepsis, Dr. Arbuckle emphasized.

First-generation cephalosporins are "probably fine" as a first-line choice, but it depends on one's community and culture results, he said.

Once a proper antibiotic is selected, "You've got to restore barrier function. If you don't do this, they're not going to get better," Dr. Arbuckle emphasized.

In Denver's dry climate, he said he prefers petrolatum-based products, the simpler the better to avoid allergic responses. Plain petroleum jelly contains no lanolin or other additives that might cause a reaction. Choose topical steroids in ointment form, because creams often contain propylene glycol, which "stings like Hades," he suggested.

The "biggest failure" of most physicians is undertreatment of pruritus, which is often so severe it can preclude rapid eye movement sleep. Sedating antihistamines should be prescribed for night time and nonsedating antihistamines in the morning.

"Children with atopic dermatitis are perennially, horrifically itchy," he said, noting that he tells residents that if they prescribe an antihistamine as needed, "I will slap you upside the head."

Dr. Arbuckle disclosed no relevant conflicts of interest regarding any product used to treat atopic dermatitis.

DENVER — Any child with atopic dermatitis who has increasing pain, erythema, edema, heat, and purulent exudate is superinfected and requires antibiotics and emollients, according to an expert in pediatric dermatology.

A culture is necessary only for prescribing the correct antibiotic.

"I'm here to plead with you that infection is a clinical diagnosis, not a microbiological diagnosis," said Dr. H. Alan Arbuckle, a dermatologist and pediatrician at the University of Colorado, Denver, and Children's Hospital in Aurora, Colo.

"Doing a culture in a superinfected AD kid is worthless if your goal is to make the diagnosis of infection.

"All of these kids are going to be colonized. All are going to be positive. If you tell me the age of the wound, I'll tell you what organisms are in there, because if you look at acute and chronic wounds, they march through a sequential order of which organisms are present," he said. The increasingly relevant purpose of doing a culture on such a child is to direct antibiotic therapy by determining sensitivities of the involved organisms.

"All children with AD are colonized with staph [Staphylococcus] and strep [Streptococcus], predominantly Staph aureus and Strep pyogenes," he said at a meeting on pediatric hospital medicine.

Recent research findings provide perspective on the course of severe atopic dermatitis, according to Dr. Arbuckle.

Most pivotally, the evidence is mounting that "the problem in atopic dermatitis is … an abnormal barrier function," he said at the meeting, which was sponsored by the Society of Hospital Medicine, the American Academy of Pediatrics, and the American Pediatric Association.

In years past, pediatric dermatologists argued with pediatric allergists over the primary etiology of atopic dermatitis, with allergists arguing that immune dysfunction was to blame.

The issue was put to rest when Japanese researchers discovered that the vast majority of children with atopic dermatitis have a genetic defect in filaggrin, a protein that bundles keratin and provides the "mortar" in the brick-and-mortar type construction of the stratum corneum.

"We kind of had a big kumbaya, kissed, and made up. Dermatologists [had always said], well, there is an immune component, but how did the antigen get there? It got there because [the skin] had an improper barrier," Dr. Arbuckle commented.

Microcracks and microfissures, exacerbated by itching prompted by exposed nerve fibers in the epidermis, open the door to allergens, bacteria, and viruses. Compounding the problem is transepidermal water loss 600 times normal in the skin of children and adults with atopic dermatitis.

"We always knew that atopic kids have higher colony counts even when they aren't superinfected," said Dr. Arbuckle. "[It turns out], S. aureus is very adaptable, and upregulates certain adhesion proteins in a very dry environment."

Treatment is imperative in the face of superinfection, because children can harbor a profound bacterial load and develop sepsis, Dr. Arbuckle emphasized.

First-generation cephalosporins are "probably fine" as a first-line choice, but it depends on one's community and culture results, he said.

Once a proper antibiotic is selected, "You've got to restore barrier function. If you don't do this, they're not going to get better," Dr. Arbuckle emphasized.

In Denver's dry climate, he said he prefers petrolatum-based products, the simpler the better to avoid allergic responses. Plain petroleum jelly contains no lanolin or other additives that might cause a reaction. Choose topical steroids in ointment form, because creams often contain propylene glycol, which "stings like Hades," he suggested.

The "biggest failure" of most physicians is undertreatment of pruritus, which is often so severe it can preclude rapid eye movement sleep. Sedating antihistamines should be prescribed for night time and nonsedating antihistamines in the morning.

"Children with atopic dermatitis are perennially, horrifically itchy," he said, noting that he tells residents that if they prescribe an antihistamine as needed, "I will slap you upside the head."

Dr. Arbuckle disclosed no relevant conflicts of interest regarding any product used to treat atopic dermatitis.

SANTA MONICA, CALIF. — Dermatologists have a bountiful bag of tricks when it comes to making patients look great eventually, but not so many options that make them look great instantly—especially after procedures that have left them temporarily red, bruised, or hypopigmented.

"They want appearance improvement and they want it immediately," said Dr. Howard Steinman, a dermatologist in private practice in Chula Vista, Calif.

"They're extremely unhappy when they've had a—quote—'no down time' procedure that results in discoloration."

There was a time when the only options were to call in sick to work, brave stares at the brightly lit Nordstrom cosmetic counter, or locate a highly trained professional paramedical camouflage therapist trained to cover scars and disfigurement.

However, that has all changed with the advent of highly effective, easy to apply mineral makeups, Dr. Steinman said at a cosmetic dermatology seminar sponsored by Skin Disease Education Foundation.

"These have revolutionized the use of medical makeup," he said.

A variety of products is now available that can be applied by a minimally trained individual with a brush or a sponge, with profound results for expected or unanticipated discoloration from procedures.

Patients with melasma and vitiligo also are surprised and grateful for the instantaneous improvement in appearance they can achieve with carefully applied mineral makeup, said Dr. Steinman.

"Anyone in your office can be trained to do this—your manager, receptionist, nurse, or spouse," he added.

Dr. Steinman's wife, Diedre, is a professional makeup artist who is skilled in masking difficult-to-cover abnormalities such as keloid scars, acne scars, and traumatic defects.

However, she saw the need for products that were more easily applied by office personnel and evaluated a variety of mineral makeup for use on routine patients.

Her choice, Youngblood, offers a variety of concealers, foundations, and powders that can used on men or women, said Dr. Steinman, who has no financial connections with the company.

The amount required to cover a patient's face for a few days or weeks of healing costs so little—$10–$12—that Dr. Steinman makes the service complimentary, rather than charging a fee.

It is well worth the cost, he said, not only in terms of patient satisfaction. "When you do something untoward to a patient [like cause a bruise with a Botox injection], you don't have to worry about it as much. You're going to fix it immediately in your office," he said.

Male patients are quietly appreciative, he said. Female patients are thrilled that they can safely use make-up right away.

Mineral makeups, which are crushed inert minerals in powder form, are non-comedogenic, hypoallergenic, and water resistant. As soon as sutures are removed and the skin is completely epithelialized and dry to the touch, they can be applied.

For some women, "not wearing makeup is like not being completely dressed," he said—like going to "a formal event in a bathing suit and a T-shirt."

Even postprocedure trips to a dermatology office can be traumatic, Dr. Steinman explained.

After an ablative procedure, for example, a physician will say, "You look great! This is great healing. I'll see you in 2 weeks," he said.

"But she doesn't feel great. She doesn't feel like she can go out in public," he said.

A woman's normal makeup will fail to cover bruises or dyspigmentation, but mineral makeup will, and give her confidence to return to her regular routine while she waits to enjoy the final results of her procedure, he concluded.

Dr. Steinman and his wife disclosed having no conflicts of interest.

SDEF and this news organization are wholly owned subsidiaries of Elsevier.

Since the amount of makeup required costs so little, consider making the service complimentary. DR. STEINMAN

SANTA MONICA, CALIF. — Dermatologists have a bountiful bag of tricks when it comes to making patients look great eventually, but not so many options that make them look great instantly—especially after procedures that have left them temporarily red, bruised, or hypopigmented.

"They want appearance improvement and they want it immediately," said Dr. Howard Steinman, a dermatologist in private practice in Chula Vista, Calif.

"They're extremely unhappy when they've had a—quote—'no down time' procedure that results in discoloration."

There was a time when the only options were to call in sick to work, brave stares at the brightly lit Nordstrom cosmetic counter, or locate a highly trained professional paramedical camouflage therapist trained to cover scars and disfigurement.

However, that has all changed with the advent of highly effective, easy to apply mineral makeups, Dr. Steinman said at a cosmetic dermatology seminar sponsored by Skin Disease Education Foundation.

"These have revolutionized the use of medical makeup," he said.

A variety of products is now available that can be applied by a minimally trained individual with a brush or a sponge, with profound results for expected or unanticipated discoloration from procedures.

Patients with melasma and vitiligo also are surprised and grateful for the instantaneous improvement in appearance they can achieve with carefully applied mineral makeup, said Dr. Steinman.

"Anyone in your office can be trained to do this—your manager, receptionist, nurse, or spouse," he added.

Dr. Steinman's wife, Diedre, is a professional makeup artist who is skilled in masking difficult-to-cover abnormalities such as keloid scars, acne scars, and traumatic defects.

However, she saw the need for products that were more easily applied by office personnel and evaluated a variety of mineral makeup for use on routine patients.

Her choice, Youngblood, offers a variety of concealers, foundations, and powders that can used on men or women, said Dr. Steinman, who has no financial connections with the company.

The amount required to cover a patient's face for a few days or weeks of healing costs so little—$10–$12—that Dr. Steinman makes the service complimentary, rather than charging a fee.

It is well worth the cost, he said, not only in terms of patient satisfaction. "When you do something untoward to a patient [like cause a bruise with a Botox injection], you don't have to worry about it as much. You're going to fix it immediately in your office," he said.

Male patients are quietly appreciative, he said. Female patients are thrilled that they can safely use make-up right away.

Mineral makeups, which are crushed inert minerals in powder form, are non-comedogenic, hypoallergenic, and water resistant. As soon as sutures are removed and the skin is completely epithelialized and dry to the touch, they can be applied.

For some women, "not wearing makeup is like not being completely dressed," he said—like going to "a formal event in a bathing suit and a T-shirt."

Even postprocedure trips to a dermatology office can be traumatic, Dr. Steinman explained.

After an ablative procedure, for example, a physician will say, "You look great! This is great healing. I'll see you in 2 weeks," he said.

"But she doesn't feel great. She doesn't feel like she can go out in public," he said.

A woman's normal makeup will fail to cover bruises or dyspigmentation, but mineral makeup will, and give her confidence to return to her regular routine while she waits to enjoy the final results of her procedure, he concluded.

Dr. Steinman and his wife disclosed having no conflicts of interest.

SDEF and this news organization are wholly owned subsidiaries of Elsevier.

Since the amount of makeup required costs so little, consider making the service complimentary. DR. STEINMAN

SANTA MONICA, CALIF. — Dermatologists have a bountiful bag of tricks when it comes to making patients look great eventually, but not so many options that make them look great instantly—especially after procedures that have left them temporarily red, bruised, or hypopigmented.

"They want appearance improvement and they want it immediately," said Dr. Howard Steinman, a dermatologist in private practice in Chula Vista, Calif.

"They're extremely unhappy when they've had a—quote—'no down time' procedure that results in discoloration."

There was a time when the only options were to call in sick to work, brave stares at the brightly lit Nordstrom cosmetic counter, or locate a highly trained professional paramedical camouflage therapist trained to cover scars and disfigurement.

However, that has all changed with the advent of highly effective, easy to apply mineral makeups, Dr. Steinman said at a cosmetic dermatology seminar sponsored by Skin Disease Education Foundation.

"These have revolutionized the use of medical makeup," he said.

A variety of products is now available that can be applied by a minimally trained individual with a brush or a sponge, with profound results for expected or unanticipated discoloration from procedures.

Patients with melasma and vitiligo also are surprised and grateful for the instantaneous improvement in appearance they can achieve with carefully applied mineral makeup, said Dr. Steinman.

"Anyone in your office can be trained to do this—your manager, receptionist, nurse, or spouse," he added.

Dr. Steinman's wife, Diedre, is a professional makeup artist who is skilled in masking difficult-to-cover abnormalities such as keloid scars, acne scars, and traumatic defects.

However, she saw the need for products that were more easily applied by office personnel and evaluated a variety of mineral makeup for use on routine patients.

Her choice, Youngblood, offers a variety of concealers, foundations, and powders that can used on men or women, said Dr. Steinman, who has no financial connections with the company.

The amount required to cover a patient's face for a few days or weeks of healing costs so little—$10–$12—that Dr. Steinman makes the service complimentary, rather than charging a fee.

It is well worth the cost, he said, not only in terms of patient satisfaction. "When you do something untoward to a patient [like cause a bruise with a Botox injection], you don't have to worry about it as much. You're going to fix it immediately in your office," he said.

Male patients are quietly appreciative, he said. Female patients are thrilled that they can safely use make-up right away.

Mineral makeups, which are crushed inert minerals in powder form, are non-comedogenic, hypoallergenic, and water resistant. As soon as sutures are removed and the skin is completely epithelialized and dry to the touch, they can be applied.

For some women, "not wearing makeup is like not being completely dressed," he said—like going to "a formal event in a bathing suit and a T-shirt."

Even postprocedure trips to a dermatology office can be traumatic, Dr. Steinman explained.

After an ablative procedure, for example, a physician will say, "You look great! This is great healing. I'll see you in 2 weeks," he said.

"But she doesn't feel great. She doesn't feel like she can go out in public," he said.

A woman's normal makeup will fail to cover bruises or dyspigmentation, but mineral makeup will, and give her confidence to return to her regular routine while she waits to enjoy the final results of her procedure, he concluded.

Dr. Steinman and his wife disclosed having no conflicts of interest.

SDEF and this news organization are wholly owned subsidiaries of Elsevier.

Since the amount of makeup required costs so little, consider making the service complimentary. DR. STEINMAN