Mobile phones became commonplace in just a few years and are now used everywhere, included remote areas of the world. These communication tools are used for personal and professional purposes, frequently by health care workers (HCWs) during care.

We and others believe that mobile phones improve the quality, rapidity, and efficiency of communication in health care settings and, therefore, improve the management of patients. In fact, professional mobile phones allow communication between HCWs anywhere in the hospital. In addition, personal mobile phones, frequently smartphones, allow the use of medical apps for evidence-based management of patients.

Mobile phones, both professional and personal, are used in close proximity to patients, as reported in behavioral studies. In a recent study we performed in a hospital setting (Clin Microbiol Infect. 2016 May;22[5]:456.e1-e6. doi: 10.1016/j.cmi.2015.12.008), more than 60% of HCWs who participated declared using phones during care, and also declared that they had halted care to patients while answering a call.

Several studies have shown that mobile phones used at hospitals are contaminated by bacteria, including highly pathogenic ones, such as methicillin-resistant Staphylococcus aureus (MRSA), Acinetobacter species, vancomycin-resistant enterococci, Pseudomonas species, and coliforms. Research suggests that these devices may serve as a reservoir of bacteria known to cause nosocomial infections and may play a role in transmission of them to patients through the hands of HCWs.

For the first time, we demonstrated the presence of RNA of epidemic viruses such as rotavirus, influenza virus, syncytial respiratory virus, and metapneumovirus on mobile phones (professional and personal) held by HCWs. In our study, 38.5% of sampled mobile phones were contaminated with RNA from viruses. RNA of rotavirus was the most frequently-detected virus, mainly on phones sampled in the pediatric emergency ward. Interestingly, we found that HCWs in pediatric wards admitted disinfecting their mobile phones less frequently than did other HCWs we interviewed.

Epidemic viruses have already been discovered on other electronic device surfaces, such as keyboards, computers, and telephone handsets. However, in contrast to these other devices, mobile phones are mobile and could be shared and transported anywhere, including in close proximity to patients. Rotaviruses are frequently found on hospital surfaces several months after an epidemic period, after surfaces were cleaned. The high prevalence of rotavirus in pediatric ward patients during our study, and its capacity to persist in the environment, are probably the main factors that explain the high frequency of rotavirus RNA detection on mobile phones in our study.

This finding highlights the possible role of mobile phones in cross-transmission of epidemic viruses, with the transfer from nonporous fomites to fingers, and from fingers to fomites – including mobile phones. Due to the difficulty and fastidiousness of viral culture, the viruses were detected only by molecular biology; the viability of the viruses could not be demonstrated. However, we believe that cross-transmission of viruses may occur, notably in health care settings. The recently reported case of a 40-year-old Ugandan man who stole a phone from a patient with Ebola and contracted the disease, also supports this hypothesis.

We also demonstrated in our study that hand hygiene after the use of mobile phones does not seem to be systematic, even for HCWs continuing care that was in process before picking up their phones. Around 30% of HCWs declared that they never perform hand hygiene before or after handling mobile phones. In addition, more than 30% of HCWs admitted that they never disinfect their phones, even their professional ones; this lack of hygiene could contribute to the persistence of RNA of epidemic viruses.

Our study does not support banning the use of mobile phones in hospitals. We just want to make HCWs aware that mobile phones, which are part of our daily practice, can be contaminated by pathogens, notably viruses. The use of disinfection wipes to clean phones, together with adherence to hand hygiene, is crucial to prevent cross-transmission.

Frequent disinfection of personal and professional mobile phones needs to be promoted to reduce contamination of phones by viruses, especially during epidemics.

In practice, each clinician needs to remember that hand hygiene should be the last thing done before patient contact, as recommended by the World Health Organization. Touching a mobile phone could transfer bacteria or viruses onto hands, and we hypothesize that it could be a factor in cross-transmission of pathogens.

Elisabeth Botelho-Nevers, MD, PhD, is an infectious diseases specialist at the University Hospital of Saint-Étienne (France) and Sylvie Pillet, PharmD, PhD, is a virologist in the Laboratory of Infectious Agents and Hygiene, University Hospital of Saint-Étienne.

Mobile phones became commonplace in just a few years and are now used everywhere, included remote areas of the world. These communication tools are used for personal and professional purposes, frequently by health care workers (HCWs) during care.

We and others believe that mobile phones improve the quality, rapidity, and efficiency of communication in health care settings and, therefore, improve the management of patients. In fact, professional mobile phones allow communication between HCWs anywhere in the hospital. In addition, personal mobile phones, frequently smartphones, allow the use of medical apps for evidence-based management of patients.

Mobile phones, both professional and personal, are used in close proximity to patients, as reported in behavioral studies. In a recent study we performed in a hospital setting (Clin Microbiol Infect. 2016 May;22[5]:456.e1-e6. doi: 10.1016/j.cmi.2015.12.008), more than 60% of HCWs who participated declared using phones during care, and also declared that they had halted care to patients while answering a call.

Several studies have shown that mobile phones used at hospitals are contaminated by bacteria, including highly pathogenic ones, such as methicillin-resistant Staphylococcus aureus (MRSA), Acinetobacter species, vancomycin-resistant enterococci, Pseudomonas species, and coliforms. Research suggests that these devices may serve as a reservoir of bacteria known to cause nosocomial infections and may play a role in transmission of them to patients through the hands of HCWs.

For the first time, we demonstrated the presence of RNA of epidemic viruses such as rotavirus, influenza virus, syncytial respiratory virus, and metapneumovirus on mobile phones (professional and personal) held by HCWs. In our study, 38.5% of sampled mobile phones were contaminated with RNA from viruses. RNA of rotavirus was the most frequently-detected virus, mainly on phones sampled in the pediatric emergency ward. Interestingly, we found that HCWs in pediatric wards admitted disinfecting their mobile phones less frequently than did other HCWs we interviewed.

Epidemic viruses have already been discovered on other electronic device surfaces, such as keyboards, computers, and telephone handsets. However, in contrast to these other devices, mobile phones are mobile and could be shared and transported anywhere, including in close proximity to patients. Rotaviruses are frequently found on hospital surfaces several months after an epidemic period, after surfaces were cleaned. The high prevalence of rotavirus in pediatric ward patients during our study, and its capacity to persist in the environment, are probably the main factors that explain the high frequency of rotavirus RNA detection on mobile phones in our study.

This finding highlights the possible role of mobile phones in cross-transmission of epidemic viruses, with the transfer from nonporous fomites to fingers, and from fingers to fomites – including mobile phones. Due to the difficulty and fastidiousness of viral culture, the viruses were detected only by molecular biology; the viability of the viruses could not be demonstrated. However, we believe that cross-transmission of viruses may occur, notably in health care settings. The recently reported case of a 40-year-old Ugandan man who stole a phone from a patient with Ebola and contracted the disease, also supports this hypothesis.

We also demonstrated in our study that hand hygiene after the use of mobile phones does not seem to be systematic, even for HCWs continuing care that was in process before picking up their phones. Around 30% of HCWs declared that they never perform hand hygiene before or after handling mobile phones. In addition, more than 30% of HCWs admitted that they never disinfect their phones, even their professional ones; this lack of hygiene could contribute to the persistence of RNA of epidemic viruses.

Our study does not support banning the use of mobile phones in hospitals. We just want to make HCWs aware that mobile phones, which are part of our daily practice, can be contaminated by pathogens, notably viruses. The use of disinfection wipes to clean phones, together with adherence to hand hygiene, is crucial to prevent cross-transmission.

Frequent disinfection of personal and professional mobile phones needs to be promoted to reduce contamination of phones by viruses, especially during epidemics.

In practice, each clinician needs to remember that hand hygiene should be the last thing done before patient contact, as recommended by the World Health Organization. Touching a mobile phone could transfer bacteria or viruses onto hands, and we hypothesize that it could be a factor in cross-transmission of pathogens.

Elisabeth Botelho-Nevers, MD, PhD, is an infectious diseases specialist at the University Hospital of Saint-Étienne (France) and Sylvie Pillet, PharmD, PhD, is a virologist in the Laboratory of Infectious Agents and Hygiene, University Hospital of Saint-Étienne.

Mobile phones became commonplace in just a few years and are now used everywhere, included remote areas of the world. These communication tools are used for personal and professional purposes, frequently by health care workers (HCWs) during care.

We and others believe that mobile phones improve the quality, rapidity, and efficiency of communication in health care settings and, therefore, improve the management of patients. In fact, professional mobile phones allow communication between HCWs anywhere in the hospital. In addition, personal mobile phones, frequently smartphones, allow the use of medical apps for evidence-based management of patients.

Mobile phones, both professional and personal, are used in close proximity to patients, as reported in behavioral studies. In a recent study we performed in a hospital setting (Clin Microbiol Infect. 2016 May;22[5]:456.e1-e6. doi: 10.1016/j.cmi.2015.12.008), more than 60% of HCWs who participated declared using phones during care, and also declared that they had halted care to patients while answering a call.

Several studies have shown that mobile phones used at hospitals are contaminated by bacteria, including highly pathogenic ones, such as methicillin-resistant Staphylococcus aureus (MRSA), Acinetobacter species, vancomycin-resistant enterococci, Pseudomonas species, and coliforms. Research suggests that these devices may serve as a reservoir of bacteria known to cause nosocomial infections and may play a role in transmission of them to patients through the hands of HCWs.

For the first time, we demonstrated the presence of RNA of epidemic viruses such as rotavirus, influenza virus, syncytial respiratory virus, and metapneumovirus on mobile phones (professional and personal) held by HCWs. In our study, 38.5% of sampled mobile phones were contaminated with RNA from viruses. RNA of rotavirus was the most frequently-detected virus, mainly on phones sampled in the pediatric emergency ward. Interestingly, we found that HCWs in pediatric wards admitted disinfecting their mobile phones less frequently than did other HCWs we interviewed.

Epidemic viruses have already been discovered on other electronic device surfaces, such as keyboards, computers, and telephone handsets. However, in contrast to these other devices, mobile phones are mobile and could be shared and transported anywhere, including in close proximity to patients. Rotaviruses are frequently found on hospital surfaces several months after an epidemic period, after surfaces were cleaned. The high prevalence of rotavirus in pediatric ward patients during our study, and its capacity to persist in the environment, are probably the main factors that explain the high frequency of rotavirus RNA detection on mobile phones in our study.

This finding highlights the possible role of mobile phones in cross-transmission of epidemic viruses, with the transfer from nonporous fomites to fingers, and from fingers to fomites – including mobile phones. Due to the difficulty and fastidiousness of viral culture, the viruses were detected only by molecular biology; the viability of the viruses could not be demonstrated. However, we believe that cross-transmission of viruses may occur, notably in health care settings. The recently reported case of a 40-year-old Ugandan man who stole a phone from a patient with Ebola and contracted the disease, also supports this hypothesis.

We also demonstrated in our study that hand hygiene after the use of mobile phones does not seem to be systematic, even for HCWs continuing care that was in process before picking up their phones. Around 30% of HCWs declared that they never perform hand hygiene before or after handling mobile phones. In addition, more than 30% of HCWs admitted that they never disinfect their phones, even their professional ones; this lack of hygiene could contribute to the persistence of RNA of epidemic viruses.

Our study does not support banning the use of mobile phones in hospitals. We just want to make HCWs aware that mobile phones, which are part of our daily practice, can be contaminated by pathogens, notably viruses. The use of disinfection wipes to clean phones, together with adherence to hand hygiene, is crucial to prevent cross-transmission.

Frequent disinfection of personal and professional mobile phones needs to be promoted to reduce contamination of phones by viruses, especially during epidemics.

In practice, each clinician needs to remember that hand hygiene should be the last thing done before patient contact, as recommended by the World Health Organization. Touching a mobile phone could transfer bacteria or viruses onto hands, and we hypothesize that it could be a factor in cross-transmission of pathogens.

Elisabeth Botelho-Nevers, MD, PhD, is an infectious diseases specialist at the University Hospital of Saint-Étienne (France) and Sylvie Pillet, PharmD, PhD, is a virologist in the Laboratory of Infectious Agents and Hygiene, University Hospital of Saint-Étienne.

Estrogen receptor mutations in estrogen receptor–positive metastatic breast cancer are more prevalent than previous studies and methodologies suggest, investigators found during a secondary analysis of patients enrolled in the BOLERO-2 trial.

Furthermore, two specific estrogen receptor 1 (ESR1) mutations, D538G and Y537S, were associated with reduced overall survival.

Of the 724 patients enrolled in the BOLERO-2, a phase III trial of women with postmenopausal ER-positive, HER2-nonamplified advanced breast cancer refractory to nonsteroidal aromatase inhibitors, 541 had evaluable cell-free DNA from baseline plasma samples and consented to genomic testing. Cell-free DNA (cfDNA) was extracted from patient’s plasma samples and assayed (via BioRad’s QX200 Droplet Digital PCR [polymerase chain reaction] System) for two specific ESR1 mutations, D538G and Y537S.

ESR1 mutations were detected in 156 of the 541 patients (28.8%), with D538G mutations occurring in 114 patients (21.1%), Y537S mutations occurring in 72 patients (13.3%), and both mutations occurring in 30 patients (5.55%), according to Sarat Chandarlapaty, MD, PhD, of Memorial Sloan Kettering Cancer Center, New York, and his associates.

Frequency of ESR1 mutation did not differ by age, race, or site of metastatic disease. However, mutation prevalence was significantly associated with ECOG status (P = .04). Also, “there was a threefold increase in mutation prevalence in patients who had failed first-line therapy for metastatic disease (33% were mutant) compared with those who were initiating first-line treatment for MBC (11% were mutant), in whom exposure to AI therapy occurred only in the adjuvant setting,” the researchers wrote (JAMA Oncol. 2016 Aug 11. doi: 10.1001/jamaoncol.2016.1279).

Overall, patients with ESR1 mutations had shorter median overall survival times. Among patients with only D538G mutations, median overall survival was 25.99 months (95% CI, 19.19-32.36 months). Patients with only Y537S mutations had a median overall survival of 19.98 months (95% CI,13.01-29.31 months) whereas patients with neither mutation had an overall survival of 32.1 months (95% CI, 28.09-36.4 months). Patients carrying both mutations had an even further reduced median overall survival of 15.15 months (95% CI, 10.87-27.43).

Patients in BOLERO-2 had been randomized in a 2:1 ratio to receive either exemestane plus everolimus or exemestane plus placebo. For this secondary analysis, researchers found that patients who had received exemestane therapy and had the D538G mutation experienced a shorter median progression-free survival time (2.69 months; hazard ratio, 1.71; 95% CI, 1.09-2.68) compared with patients with no mutations who received exemestane therapy (3.94 months). Patients with no mutations who received everolimus had a median progression-free survival of 8.48 months, and patients with D538G mutations who received everolimus had a median progression-free survival of 5.78 months.

“One of the key findings of this work is the high prevalence of ER mutations in this patient population,” the investigators said.

The investigators also noted the ease, feasibility, and affordability with which cfDNA can be analyzed for these genetic mutations, and they believe the digital drop polymerase chain reaction assay used in this study could easily be implemented into regular clinical practice.

This study was funded by Novartis and supported by the Integrated Genomics Operation Core. Four of the investigators reported being employed by Novartis, and Dr. Chandarlapaty reported receiving financial compensation from AstraZeneca.

[email protected]

On Twitter @jessnicolecraig

Estrogen receptor mutations in estrogen receptor–positive metastatic breast cancer are more prevalent than previous studies and methodologies suggest, investigators found during a secondary analysis of patients enrolled in the BOLERO-2 trial.

Furthermore, two specific estrogen receptor 1 (ESR1) mutations, D538G and Y537S, were associated with reduced overall survival.

Of the 724 patients enrolled in the BOLERO-2, a phase III trial of women with postmenopausal ER-positive, HER2-nonamplified advanced breast cancer refractory to nonsteroidal aromatase inhibitors, 541 had evaluable cell-free DNA from baseline plasma samples and consented to genomic testing. Cell-free DNA (cfDNA) was extracted from patient’s plasma samples and assayed (via BioRad’s QX200 Droplet Digital PCR [polymerase chain reaction] System) for two specific ESR1 mutations, D538G and Y537S.

ESR1 mutations were detected in 156 of the 541 patients (28.8%), with D538G mutations occurring in 114 patients (21.1%), Y537S mutations occurring in 72 patients (13.3%), and both mutations occurring in 30 patients (5.55%), according to Sarat Chandarlapaty, MD, PhD, of Memorial Sloan Kettering Cancer Center, New York, and his associates.

Frequency of ESR1 mutation did not differ by age, race, or site of metastatic disease. However, mutation prevalence was significantly associated with ECOG status (P = .04). Also, “there was a threefold increase in mutation prevalence in patients who had failed first-line therapy for metastatic disease (33% were mutant) compared with those who were initiating first-line treatment for MBC (11% were mutant), in whom exposure to AI therapy occurred only in the adjuvant setting,” the researchers wrote (JAMA Oncol. 2016 Aug 11. doi: 10.1001/jamaoncol.2016.1279).

Overall, patients with ESR1 mutations had shorter median overall survival times. Among patients with only D538G mutations, median overall survival was 25.99 months (95% CI, 19.19-32.36 months). Patients with only Y537S mutations had a median overall survival of 19.98 months (95% CI,13.01-29.31 months) whereas patients with neither mutation had an overall survival of 32.1 months (95% CI, 28.09-36.4 months). Patients carrying both mutations had an even further reduced median overall survival of 15.15 months (95% CI, 10.87-27.43).

Patients in BOLERO-2 had been randomized in a 2:1 ratio to receive either exemestane plus everolimus or exemestane plus placebo. For this secondary analysis, researchers found that patients who had received exemestane therapy and had the D538G mutation experienced a shorter median progression-free survival time (2.69 months; hazard ratio, 1.71; 95% CI, 1.09-2.68) compared with patients with no mutations who received exemestane therapy (3.94 months). Patients with no mutations who received everolimus had a median progression-free survival of 8.48 months, and patients with D538G mutations who received everolimus had a median progression-free survival of 5.78 months.

“One of the key findings of this work is the high prevalence of ER mutations in this patient population,” the investigators said.

The investigators also noted the ease, feasibility, and affordability with which cfDNA can be analyzed for these genetic mutations, and they believe the digital drop polymerase chain reaction assay used in this study could easily be implemented into regular clinical practice.

This study was funded by Novartis and supported by the Integrated Genomics Operation Core. Four of the investigators reported being employed by Novartis, and Dr. Chandarlapaty reported receiving financial compensation from AstraZeneca.

[email protected]

On Twitter @jessnicolecraig

Estrogen receptor mutations in estrogen receptor–positive metastatic breast cancer are more prevalent than previous studies and methodologies suggest, investigators found during a secondary analysis of patients enrolled in the BOLERO-2 trial.

Furthermore, two specific estrogen receptor 1 (ESR1) mutations, D538G and Y537S, were associated with reduced overall survival.

Of the 724 patients enrolled in the BOLERO-2, a phase III trial of women with postmenopausal ER-positive, HER2-nonamplified advanced breast cancer refractory to nonsteroidal aromatase inhibitors, 541 had evaluable cell-free DNA from baseline plasma samples and consented to genomic testing. Cell-free DNA (cfDNA) was extracted from patient’s plasma samples and assayed (via BioRad’s QX200 Droplet Digital PCR [polymerase chain reaction] System) for two specific ESR1 mutations, D538G and Y537S.

ESR1 mutations were detected in 156 of the 541 patients (28.8%), with D538G mutations occurring in 114 patients (21.1%), Y537S mutations occurring in 72 patients (13.3%), and both mutations occurring in 30 patients (5.55%), according to Sarat Chandarlapaty, MD, PhD, of Memorial Sloan Kettering Cancer Center, New York, and his associates.

Frequency of ESR1 mutation did not differ by age, race, or site of metastatic disease. However, mutation prevalence was significantly associated with ECOG status (P = .04). Also, “there was a threefold increase in mutation prevalence in patients who had failed first-line therapy for metastatic disease (33% were mutant) compared with those who were initiating first-line treatment for MBC (11% were mutant), in whom exposure to AI therapy occurred only in the adjuvant setting,” the researchers wrote (JAMA Oncol. 2016 Aug 11. doi: 10.1001/jamaoncol.2016.1279).

Overall, patients with ESR1 mutations had shorter median overall survival times. Among patients with only D538G mutations, median overall survival was 25.99 months (95% CI, 19.19-32.36 months). Patients with only Y537S mutations had a median overall survival of 19.98 months (95% CI,13.01-29.31 months) whereas patients with neither mutation had an overall survival of 32.1 months (95% CI, 28.09-36.4 months). Patients carrying both mutations had an even further reduced median overall survival of 15.15 months (95% CI, 10.87-27.43).

Patients in BOLERO-2 had been randomized in a 2:1 ratio to receive either exemestane plus everolimus or exemestane plus placebo. For this secondary analysis, researchers found that patients who had received exemestane therapy and had the D538G mutation experienced a shorter median progression-free survival time (2.69 months; hazard ratio, 1.71; 95% CI, 1.09-2.68) compared with patients with no mutations who received exemestane therapy (3.94 months). Patients with no mutations who received everolimus had a median progression-free survival of 8.48 months, and patients with D538G mutations who received everolimus had a median progression-free survival of 5.78 months.

“One of the key findings of this work is the high prevalence of ER mutations in this patient population,” the investigators said.

The investigators also noted the ease, feasibility, and affordability with which cfDNA can be analyzed for these genetic mutations, and they believe the digital drop polymerase chain reaction assay used in this study could easily be implemented into regular clinical practice.

This study was funded by Novartis and supported by the Integrated Genomics Operation Core. Four of the investigators reported being employed by Novartis, and Dr. Chandarlapaty reported receiving financial compensation from AstraZeneca.

[email protected]

On Twitter @jessnicolecraig

Incidence of circulating vaccine-derived poliovirus (cVDPV ) decreased during the period from January 2015 to May 2016, but cases were reported in a larger number of countries, according to a report from the Centers for Disease Control and Prevention.

Seven countries reported cases of cVDPV, up from four during the previous reporting period. Seven cases were reported in Guinea, 11 in Laos, 10 in Madagascar, 2 in Myanmar, 1 in Nigeria, 2 in Pakistan, and 2 cases were reported in the Ukraine. Case incidence in Nigeria and Pakistan was significantly less than in the previous reporting period.

Immunodeficiency-associated VDPVs were reported in 21 countries during the study period, up from 8 countries in 2014; however, this was due to a newly implemented intensive surveillance program. Ambiguous VDPVs were reported in 19 countries.

“The expansion of environmental surveillance in countries at high risk has increased the sensitivity of poliovirus detection. However, detection of polioviruses from sewage presents logistical and technical challenges, including determination of VDPV genetic signatures. Determination of epidemiologic linkages from sequence data in environmental isolates represents an additional challenge,” the CDC investigators said.

Find the full report in Morbidity and Mortality Weekly Report (doi: 10.15585/mmwr.mm6530a3).

[email protected]

Incidence of circulating vaccine-derived poliovirus (cVDPV ) decreased during the period from January 2015 to May 2016, but cases were reported in a larger number of countries, according to a report from the Centers for Disease Control and Prevention.

Seven countries reported cases of cVDPV, up from four during the previous reporting period. Seven cases were reported in Guinea, 11 in Laos, 10 in Madagascar, 2 in Myanmar, 1 in Nigeria, 2 in Pakistan, and 2 cases were reported in the Ukraine. Case incidence in Nigeria and Pakistan was significantly less than in the previous reporting period.

Immunodeficiency-associated VDPVs were reported in 21 countries during the study period, up from 8 countries in 2014; however, this was due to a newly implemented intensive surveillance program. Ambiguous VDPVs were reported in 19 countries.

“The expansion of environmental surveillance in countries at high risk has increased the sensitivity of poliovirus detection. However, detection of polioviruses from sewage presents logistical and technical challenges, including determination of VDPV genetic signatures. Determination of epidemiologic linkages from sequence data in environmental isolates represents an additional challenge,” the CDC investigators said.

Find the full report in Morbidity and Mortality Weekly Report (doi: 10.15585/mmwr.mm6530a3).

[email protected]

Incidence of circulating vaccine-derived poliovirus (cVDPV ) decreased during the period from January 2015 to May 2016, but cases were reported in a larger number of countries, according to a report from the Centers for Disease Control and Prevention.

Seven countries reported cases of cVDPV, up from four during the previous reporting period. Seven cases were reported in Guinea, 11 in Laos, 10 in Madagascar, 2 in Myanmar, 1 in Nigeria, 2 in Pakistan, and 2 cases were reported in the Ukraine. Case incidence in Nigeria and Pakistan was significantly less than in the previous reporting period.

Immunodeficiency-associated VDPVs were reported in 21 countries during the study period, up from 8 countries in 2014; however, this was due to a newly implemented intensive surveillance program. Ambiguous VDPVs were reported in 19 countries.

“The expansion of environmental surveillance in countries at high risk has increased the sensitivity of poliovirus detection. However, detection of polioviruses from sewage presents logistical and technical challenges, including determination of VDPV genetic signatures. Determination of epidemiologic linkages from sequence data in environmental isolates represents an additional challenge,” the CDC investigators said.

Find the full report in Morbidity and Mortality Weekly Report (doi: 10.15585/mmwr.mm6530a3).

[email protected]

The Diagnosis: Subcutaneous Phaeohyphomycosis

Subcutaneous phaeohyphomycosis (SP), also called mycotic cyst, is characterized by a painless, nodular lesion that develops in response to traumatic implantation of dematiaceous, pigment-forming fungi.¹ Similar to other fungal infections, SP can arise opportunistically in immunocompromised patients.^2,3 More than 60 genera (and more than 100 species) are known etiologic agents of phaeohyphomycosis; the 2 main causes of infection are Bipolaris spicifera and Exophiala jeanselmei.^4,5 Given this variety, phaeohyphomycosis can present superficially as black piedra or tinea nigra, cutaneously as scytalidiosis, subcutaneously as SP, or disseminated as sinusitis or systemic phaeohyphomycosis.

Coined in 1974 by Ajello et al,⁶ the term phaeohyphomycosis translates to “condition of dark hyphal fungus,” a term used to designate mycoses caused by fungi with melanized hyphae. Histologically, SP demonstrates a circumscribed chronic cyst or abscess with a dense fibrous wall (quiz image A). At high power, the wall is composed of chronic granulomatous inflammation with foamy macrophages, and the cystic cavity contains necrotic debris admixed with neutrophils. Pigmented filamentous hyphae and yeastlike entities can be seen in the cyst wall, in multinucleated giant cells, in the necrotic debris, or directly attached to the implanted foreign material (quiz image B).⁷ The first-line treatment of SP is wide local excision and oral itraconazole. It often requires adjustments to dosage or change to antifungal due to recurrence and etiologic variation.⁸ Furthermore, if SP is not definitively treated, immunocompromised patients are at an increased risk for developing potentially fatal systemic phaeohyphomycosis.³

Chromoblastomycosis (CBM), also caused by dematiaceous fungi, is characterized by an initially indolent clinical presentation. Typically found on the legs and lower thighs of agricultural workers, the lesion begins as a slow-growing, nodular papule with subsequent transformation into an edematous verrucous plaque with peripheral erythema.⁹ Lesions can be annular with central clearing, and lymphedema with elephantiasis may be present.¹⁰ Histologically, CBM shows pseudoepitheliomatous hyperplasia and intraepidermal pustules as the host rids the infection via transepithelial elimination. Dematiaceous fungi often are seen in the dermis, either freestanding or attached to foreign plant material. Medlar bodies, also called copper penny spores or sclerotic bodies, are the most defining histologic finding and are characterized by groups of brown, thick-walled cells found in giant cells or neutrophil abscesses (Figure 1). Hyphae are not typically found in this type of infection.¹¹

Granulomatous foreign body reactions occur in response to the inoculation of nonhuman material and are characterized by dermal or subcutaneous nodules. Tissue macrophages phagocytize material not removed shortly after implantation, which initiates an inflammatory response that attempts to isolate the material from the uninvolved surrounding tissue. Vegetative foreign bodies will cause the most severe inflammatory reactions.¹² Histologically, foreign body granulomas are noncaseating with epithelioid histiocytes surrounding a central foreign body (Figure 2). Occasionally, foreign bodies may be difficult to detect; some are birefringent to polarized light.¹³ Additionally, inoculation injuries can predispose patients to SP, CBM, and other fungal infections.

Tattoos are characterized by exogenous pigment deposition into the dermis.¹⁴ Histologically, tattoos display exogenous pigment deposited throughout the reticular dermis, attached to collagen bundles, within macrophages, or adjacent to adnexal structures (eg, pilosebaceous units or eccrine glands). Although all tattoo pigments can cause adverse reactions, hypersensitivity reactions occur most commonly in response to red pigment, resulting in discrete areas of spongiosis and granulomatous or lichenoid inflammation. Occasionally, hypersensitivity reactions can induce necrobiotic granulomatous reactions characterized by collagen alteration surrounded by palisaded histiocytes and lymphocytes (Figure 3).^15,16 There also may be focally dense areas of superficial and deep perivascular lymphohistiocytic infiltrate. Clinical context is important, as brown tattoo pigment (Figure 3) can be easily confused with the pigmented hyphae of phaeohyphomycosis, melanin, or hemosiderin.

Subcutaneous hyalohyphomycosis is a nondemat-iaceous (nonpigmented) infection that is caused by hyaline septate hyphal cells.¹⁷ Hyalohyphomycosis skin lesions can present as painful erythematous nodules that evolve into excoriated pustules.¹⁸ Hyalohyphomycosis most often arises in immunocompromised patients. Causative organisms are ubiquitous soil saprophytes and plant pathogens, most often Aspergillus and Fusarium species, with a predilection for affecting severely immunocompromised hosts, particularly children.¹⁹ These species tend to be vasculotropic, which can result in tissue necrosis and systemic dissemination. Histologically, fungi are dispersed within tissue. They have a bright, bubbly, mildly basophilic cytoplasm and are nonpigmented, branching, and septate (Figure 4).¹¹

The Diagnosis: Subcutaneous Phaeohyphomycosis

Subcutaneous phaeohyphomycosis (SP), also called mycotic cyst, is characterized by a painless, nodular lesion that develops in response to traumatic implantation of dematiaceous, pigment-forming fungi.¹ Similar to other fungal infections, SP can arise opportunistically in immunocompromised patients.^2,3 More than 60 genera (and more than 100 species) are known etiologic agents of phaeohyphomycosis; the 2 main causes of infection are Bipolaris spicifera and Exophiala jeanselmei.^4,5 Given this variety, phaeohyphomycosis can present superficially as black piedra or tinea nigra, cutaneously as scytalidiosis, subcutaneously as SP, or disseminated as sinusitis or systemic phaeohyphomycosis.

Coined in 1974 by Ajello et al,⁶ the term phaeohyphomycosis translates to “condition of dark hyphal fungus,” a term used to designate mycoses caused by fungi with melanized hyphae. Histologically, SP demonstrates a circumscribed chronic cyst or abscess with a dense fibrous wall (quiz image A). At high power, the wall is composed of chronic granulomatous inflammation with foamy macrophages, and the cystic cavity contains necrotic debris admixed with neutrophils. Pigmented filamentous hyphae and yeastlike entities can be seen in the cyst wall, in multinucleated giant cells, in the necrotic debris, or directly attached to the implanted foreign material (quiz image B).⁷ The first-line treatment of SP is wide local excision and oral itraconazole. It often requires adjustments to dosage or change to antifungal due to recurrence and etiologic variation.⁸ Furthermore, if SP is not definitively treated, immunocompromised patients are at an increased risk for developing potentially fatal systemic phaeohyphomycosis.³

Chromoblastomycosis (CBM), also caused by dematiaceous fungi, is characterized by an initially indolent clinical presentation. Typically found on the legs and lower thighs of agricultural workers, the lesion begins as a slow-growing, nodular papule with subsequent transformation into an edematous verrucous plaque with peripheral erythema.⁹ Lesions can be annular with central clearing, and lymphedema with elephantiasis may be present.¹⁰ Histologically, CBM shows pseudoepitheliomatous hyperplasia and intraepidermal pustules as the host rids the infection via transepithelial elimination. Dematiaceous fungi often are seen in the dermis, either freestanding or attached to foreign plant material. Medlar bodies, also called copper penny spores or sclerotic bodies, are the most defining histologic finding and are characterized by groups of brown, thick-walled cells found in giant cells or neutrophil abscesses (Figure 1). Hyphae are not typically found in this type of infection.¹¹

Granulomatous foreign body reactions occur in response to the inoculation of nonhuman material and are characterized by dermal or subcutaneous nodules. Tissue macrophages phagocytize material not removed shortly after implantation, which initiates an inflammatory response that attempts to isolate the material from the uninvolved surrounding tissue. Vegetative foreign bodies will cause the most severe inflammatory reactions.¹² Histologically, foreign body granulomas are noncaseating with epithelioid histiocytes surrounding a central foreign body (Figure 2). Occasionally, foreign bodies may be difficult to detect; some are birefringent to polarized light.¹³ Additionally, inoculation injuries can predispose patients to SP, CBM, and other fungal infections.

Tattoos are characterized by exogenous pigment deposition into the dermis.¹⁴ Histologically, tattoos display exogenous pigment deposited throughout the reticular dermis, attached to collagen bundles, within macrophages, or adjacent to adnexal structures (eg, pilosebaceous units or eccrine glands). Although all tattoo pigments can cause adverse reactions, hypersensitivity reactions occur most commonly in response to red pigment, resulting in discrete areas of spongiosis and granulomatous or lichenoid inflammation. Occasionally, hypersensitivity reactions can induce necrobiotic granulomatous reactions characterized by collagen alteration surrounded by palisaded histiocytes and lymphocytes (Figure 3).^15,16 There also may be focally dense areas of superficial and deep perivascular lymphohistiocytic infiltrate. Clinical context is important, as brown tattoo pigment (Figure 3) can be easily confused with the pigmented hyphae of phaeohyphomycosis, melanin, or hemosiderin.

Subcutaneous hyalohyphomycosis is a nondemat-iaceous (nonpigmented) infection that is caused by hyaline septate hyphal cells.¹⁷ Hyalohyphomycosis skin lesions can present as painful erythematous nodules that evolve into excoriated pustules.¹⁸ Hyalohyphomycosis most often arises in immunocompromised patients. Causative organisms are ubiquitous soil saprophytes and plant pathogens, most often Aspergillus and Fusarium species, with a predilection for affecting severely immunocompromised hosts, particularly children.¹⁹ These species tend to be vasculotropic, which can result in tissue necrosis and systemic dissemination. Histologically, fungi are dispersed within tissue. They have a bright, bubbly, mildly basophilic cytoplasm and are nonpigmented, branching, and septate (Figure 4).¹¹

The Diagnosis: Subcutaneous Phaeohyphomycosis

Subcutaneous phaeohyphomycosis (SP), also called mycotic cyst, is characterized by a painless, nodular lesion that develops in response to traumatic implantation of dematiaceous, pigment-forming fungi.¹ Similar to other fungal infections, SP can arise opportunistically in immunocompromised patients.^2,3 More than 60 genera (and more than 100 species) are known etiologic agents of phaeohyphomycosis; the 2 main causes of infection are Bipolaris spicifera and Exophiala jeanselmei.^4,5 Given this variety, phaeohyphomycosis can present superficially as black piedra or tinea nigra, cutaneously as scytalidiosis, subcutaneously as SP, or disseminated as sinusitis or systemic phaeohyphomycosis.

Coined in 1974 by Ajello et al,⁶ the term phaeohyphomycosis translates to “condition of dark hyphal fungus,” a term used to designate mycoses caused by fungi with melanized hyphae. Histologically, SP demonstrates a circumscribed chronic cyst or abscess with a dense fibrous wall (quiz image A). At high power, the wall is composed of chronic granulomatous inflammation with foamy macrophages, and the cystic cavity contains necrotic debris admixed with neutrophils. Pigmented filamentous hyphae and yeastlike entities can be seen in the cyst wall, in multinucleated giant cells, in the necrotic debris, or directly attached to the implanted foreign material (quiz image B).⁷ The first-line treatment of SP is wide local excision and oral itraconazole. It often requires adjustments to dosage or change to antifungal due to recurrence and etiologic variation.⁸ Furthermore, if SP is not definitively treated, immunocompromised patients are at an increased risk for developing potentially fatal systemic phaeohyphomycosis.³

Chromoblastomycosis (CBM), also caused by dematiaceous fungi, is characterized by an initially indolent clinical presentation. Typically found on the legs and lower thighs of agricultural workers, the lesion begins as a slow-growing, nodular papule with subsequent transformation into an edematous verrucous plaque with peripheral erythema.⁹ Lesions can be annular with central clearing, and lymphedema with elephantiasis may be present.¹⁰ Histologically, CBM shows pseudoepitheliomatous hyperplasia and intraepidermal pustules as the host rids the infection via transepithelial elimination. Dematiaceous fungi often are seen in the dermis, either freestanding or attached to foreign plant material. Medlar bodies, also called copper penny spores or sclerotic bodies, are the most defining histologic finding and are characterized by groups of brown, thick-walled cells found in giant cells or neutrophil abscesses (Figure 1). Hyphae are not typically found in this type of infection.¹¹

Granulomatous foreign body reactions occur in response to the inoculation of nonhuman material and are characterized by dermal or subcutaneous nodules. Tissue macrophages phagocytize material not removed shortly after implantation, which initiates an inflammatory response that attempts to isolate the material from the uninvolved surrounding tissue. Vegetative foreign bodies will cause the most severe inflammatory reactions.¹² Histologically, foreign body granulomas are noncaseating with epithelioid histiocytes surrounding a central foreign body (Figure 2). Occasionally, foreign bodies may be difficult to detect; some are birefringent to polarized light.¹³ Additionally, inoculation injuries can predispose patients to SP, CBM, and other fungal infections.

Tattoos are characterized by exogenous pigment deposition into the dermis.¹⁴ Histologically, tattoos display exogenous pigment deposited throughout the reticular dermis, attached to collagen bundles, within macrophages, or adjacent to adnexal structures (eg, pilosebaceous units or eccrine glands). Although all tattoo pigments can cause adverse reactions, hypersensitivity reactions occur most commonly in response to red pigment, resulting in discrete areas of spongiosis and granulomatous or lichenoid inflammation. Occasionally, hypersensitivity reactions can induce necrobiotic granulomatous reactions characterized by collagen alteration surrounded by palisaded histiocytes and lymphocytes (Figure 3).^15,16 There also may be focally dense areas of superficial and deep perivascular lymphohistiocytic infiltrate. Clinical context is important, as brown tattoo pigment (Figure 3) can be easily confused with the pigmented hyphae of phaeohyphomycosis, melanin, or hemosiderin.

Subcutaneous hyalohyphomycosis is a nondemat-iaceous (nonpigmented) infection that is caused by hyaline septate hyphal cells.¹⁷ Hyalohyphomycosis skin lesions can present as painful erythematous nodules that evolve into excoriated pustules.¹⁸ Hyalohyphomycosis most often arises in immunocompromised patients. Causative organisms are ubiquitous soil saprophytes and plant pathogens, most often Aspergillus and Fusarium species, with a predilection for affecting severely immunocompromised hosts, particularly children.¹⁹ These species tend to be vasculotropic, which can result in tissue necrosis and systemic dissemination. Histologically, fungi are dispersed within tissue. They have a bright, bubbly, mildly basophilic cytoplasm and are nonpigmented, branching, and septate (Figure 4).¹¹

Case Report

A 44-year-old woman presented with a localized patch of hair loss on the frontal scalp of several month’s duration. She had been bitten by a tick at this site during the summer. Two months later a primary care provider prescribed triamcinolone cream because of intense itching at the bite site. The patient returned to her primary care provider 2 weeks later due to persistent itching, hyperpigmentation, and hair loss. At that time, the clinician probed the central portion of the lesion because of a concern for retained tick parts. A few weeks later, a dermatologist evaluated the patient and found a roughly circular zone of alopecia measuring approximately 5 cm in diameter that was just posterior to the left frontal hairline (Figure 1). In the center of the plaque there was a small eschar surrounded by a zone of hyperpigmentation, mild induration, and almost complete loss of terminal hairs. At the periphery of the lesion, hair density gradually increased and skin pigmentation normalized.

A punch biopsy was obtained from an indurated area of hyperpigmentation adjacent to the eschar. Both vertical and horizontal sections were obtained, revealing a relatively normal epidermis, a marked decrease in follicular structures with loss of sebaceous glands, and dense perifollicular lymphocytic inflammation with a few scattered eosinophils (Figures 2 and 3).

Historical Perspective

Tick bite alopecia was first described in the French literature in 1921¹ and in the English-language literature in 1955.² A few additional cases were subsequently reported.^3-5 In 2008, Castelli et al⁶ described the histologic and immunohistochemical features of 25 tick bite cases, a few of which resulted in alopecia. Other than these reports, little original information has been written about tick bite alopecia.

Clinical and Histologic Presentation

Tick bite alopecia is well described in the veterinary literature.^7-9 It is possible that the condition is underreported in humans because the cause is often obvious or the alopecia is never discovered. The typical presentation is a roughly oval zone of alopecia that develops 1 to 2 weeks after the removal of a tick from the scalp. Often there is a small central eschar representing the site of tick attachment and the surrounding scalp may appear scaly. In one report of 2 siblings, multiple oval zones of alopecia resembling the moth-eaten alopecia of syphilis were noted in both patients, but only a single attached tick was found.² In some reported cases, hair loss was only temporary, and at least partial if not complete regrowth of hair occurred.^3,4 Follow-up on most cases is not provided, but to our knowledge permanent alopecia has not been described.

Information about the histologic findings of tick bite alopecia is particularly limited. In a report by Heyl,³ biopsies were conducted in 2 patients, but the areas selected for biopsy were the sites of tick attachment. Centrally dense, acute, and chronic inflammation was seen, as well as marked tissue necrosis of the connective tissue and hair follicles. Peripheral to the attachment zone, tissue necrosis was not found, but telogen hairs with “crumpled up hair shafts” were present.³ The histologic findings presented by Castelli et al⁶ were based on a single case of tick bite alopecia; however, the specimen was a generous excisional biopsy, allowing for a panoramic histologic view of the lesion. In the center of the specimen, hair follicles were absent, but residual follicular streamers and follicular remnants were surrounded by lymphocytic inflammation. Sebaceous glands were conspicuously absent, but foci with naked hairs, fibrosis, and granulomatous inflammation were seen. Peripherally, the hair follicles were thinned and miniaturized with an increased number of catagen/telogen hairs. Some follicles showed lamellar fibroplasia and perifollicular chronic inflammation. The inflammatory infiltrate consisted predominantly of helper T cells with a smaller population of B lymphocytes and a few plasma cells.⁶ In 2016, Lynch et al⁵ described a single case of tick bite alopecia and noted pseudolymphomatous inflammation with germinal center formation associated with hair miniaturization and an elevated catagen/telogen count; focal follicular mucinosis also was noted.Our histologic findings are similar to those of Castelli et al,⁶ except that the inflammatory infiltrate was clearly B-cell dominant, with a suggestion of germinal center formation, as noted by Lynch et al.⁵ This inflammatory pattern often can be encountered in a chronic tick bite lesion. Destruction of follicles and associated sebaceous glands and their replacement by follicular scars indicate that at least in the central portion of the lesion some permanent hair loss occurs. The presence of catagen/telogen hairs and miniaturized follicles indicates the potential for at least partial regrowth.

Similar to other investigators who have described tick bite alopecia, we can only speculate as to the mechanism by which clinical alopecia occurs. Given the density of the inflammatory infiltrate and perifollicular inflammation, it seems reasonable to assume that inflammation either destroys hair follicles or precipitates the catagen/telogen phase, resulting in temporary hair loss. The inflammation itself may be due to the presence of tick parts or the antigens in their saliva (or both). The delay between tick attachment and the onset of alopecia can be attributed to the time it takes follicles to cycle into the catagen/telogen phase and shed the hair shaft.

Case Report

A 44-year-old woman presented with a localized patch of hair loss on the frontal scalp of several month’s duration. She had been bitten by a tick at this site during the summer. Two months later a primary care provider prescribed triamcinolone cream because of intense itching at the bite site. The patient returned to her primary care provider 2 weeks later due to persistent itching, hyperpigmentation, and hair loss. At that time, the clinician probed the central portion of the lesion because of a concern for retained tick parts. A few weeks later, a dermatologist evaluated the patient and found a roughly circular zone of alopecia measuring approximately 5 cm in diameter that was just posterior to the left frontal hairline (Figure 1). In the center of the plaque there was a small eschar surrounded by a zone of hyperpigmentation, mild induration, and almost complete loss of terminal hairs. At the periphery of the lesion, hair density gradually increased and skin pigmentation normalized.

A punch biopsy was obtained from an indurated area of hyperpigmentation adjacent to the eschar. Both vertical and horizontal sections were obtained, revealing a relatively normal epidermis, a marked decrease in follicular structures with loss of sebaceous glands, and dense perifollicular lymphocytic inflammation with a few scattered eosinophils (Figures 2 and 3).

Historical Perspective

Tick bite alopecia was first described in the French literature in 1921¹ and in the English-language literature in 1955.² A few additional cases were subsequently reported.^3-5 In 2008, Castelli et al⁶ described the histologic and immunohistochemical features of 25 tick bite cases, a few of which resulted in alopecia. Other than these reports, little original information has been written about tick bite alopecia.

Clinical and Histologic Presentation

Tick bite alopecia is well described in the veterinary literature.^7-9 It is possible that the condition is underreported in humans because the cause is often obvious or the alopecia is never discovered. The typical presentation is a roughly oval zone of alopecia that develops 1 to 2 weeks after the removal of a tick from the scalp. Often there is a small central eschar representing the site of tick attachment and the surrounding scalp may appear scaly. In one report of 2 siblings, multiple oval zones of alopecia resembling the moth-eaten alopecia of syphilis were noted in both patients, but only a single attached tick was found.² In some reported cases, hair loss was only temporary, and at least partial if not complete regrowth of hair occurred.^3,4 Follow-up on most cases is not provided, but to our knowledge permanent alopecia has not been described.

Information about the histologic findings of tick bite alopecia is particularly limited. In a report by Heyl,³ biopsies were conducted in 2 patients, but the areas selected for biopsy were the sites of tick attachment. Centrally dense, acute, and chronic inflammation was seen, as well as marked tissue necrosis of the connective tissue and hair follicles. Peripheral to the attachment zone, tissue necrosis was not found, but telogen hairs with “crumpled up hair shafts” were present.³ The histologic findings presented by Castelli et al⁶ were based on a single case of tick bite alopecia; however, the specimen was a generous excisional biopsy, allowing for a panoramic histologic view of the lesion. In the center of the specimen, hair follicles were absent, but residual follicular streamers and follicular remnants were surrounded by lymphocytic inflammation. Sebaceous glands were conspicuously absent, but foci with naked hairs, fibrosis, and granulomatous inflammation were seen. Peripherally, the hair follicles were thinned and miniaturized with an increased number of catagen/telogen hairs. Some follicles showed lamellar fibroplasia and perifollicular chronic inflammation. The inflammatory infiltrate consisted predominantly of helper T cells with a smaller population of B lymphocytes and a few plasma cells.⁶ In 2016, Lynch et al⁵ described a single case of tick bite alopecia and noted pseudolymphomatous inflammation with germinal center formation associated with hair miniaturization and an elevated catagen/telogen count; focal follicular mucinosis also was noted.Our histologic findings are similar to those of Castelli et al,⁶ except that the inflammatory infiltrate was clearly B-cell dominant, with a suggestion of germinal center formation, as noted by Lynch et al.⁵ This inflammatory pattern often can be encountered in a chronic tick bite lesion. Destruction of follicles and associated sebaceous glands and their replacement by follicular scars indicate that at least in the central portion of the lesion some permanent hair loss occurs. The presence of catagen/telogen hairs and miniaturized follicles indicates the potential for at least partial regrowth.

Similar to other investigators who have described tick bite alopecia, we can only speculate as to the mechanism by which clinical alopecia occurs. Given the density of the inflammatory infiltrate and perifollicular inflammation, it seems reasonable to assume that inflammation either destroys hair follicles or precipitates the catagen/telogen phase, resulting in temporary hair loss. The inflammation itself may be due to the presence of tick parts or the antigens in their saliva (or both). The delay between tick attachment and the onset of alopecia can be attributed to the time it takes follicles to cycle into the catagen/telogen phase and shed the hair shaft.

Case Report

A 44-year-old woman presented with a localized patch of hair loss on the frontal scalp of several month’s duration. She had been bitten by a tick at this site during the summer. Two months later a primary care provider prescribed triamcinolone cream because of intense itching at the bite site. The patient returned to her primary care provider 2 weeks later due to persistent itching, hyperpigmentation, and hair loss. At that time, the clinician probed the central portion of the lesion because of a concern for retained tick parts. A few weeks later, a dermatologist evaluated the patient and found a roughly circular zone of alopecia measuring approximately 5 cm in diameter that was just posterior to the left frontal hairline (Figure 1). In the center of the plaque there was a small eschar surrounded by a zone of hyperpigmentation, mild induration, and almost complete loss of terminal hairs. At the periphery of the lesion, hair density gradually increased and skin pigmentation normalized.

A punch biopsy was obtained from an indurated area of hyperpigmentation adjacent to the eschar. Both vertical and horizontal sections were obtained, revealing a relatively normal epidermis, a marked decrease in follicular structures with loss of sebaceous glands, and dense perifollicular lymphocytic inflammation with a few scattered eosinophils (Figures 2 and 3).

Historical Perspective

Tick bite alopecia was first described in the French literature in 1921¹ and in the English-language literature in 1955.² A few additional cases were subsequently reported.^3-5 In 2008, Castelli et al⁶ described the histologic and immunohistochemical features of 25 tick bite cases, a few of which resulted in alopecia. Other than these reports, little original information has been written about tick bite alopecia.

Clinical and Histologic Presentation

Tick bite alopecia is well described in the veterinary literature.^7-9 It is possible that the condition is underreported in humans because the cause is often obvious or the alopecia is never discovered. The typical presentation is a roughly oval zone of alopecia that develops 1 to 2 weeks after the removal of a tick from the scalp. Often there is a small central eschar representing the site of tick attachment and the surrounding scalp may appear scaly. In one report of 2 siblings, multiple oval zones of alopecia resembling the moth-eaten alopecia of syphilis were noted in both patients, but only a single attached tick was found.² In some reported cases, hair loss was only temporary, and at least partial if not complete regrowth of hair occurred.^3,4 Follow-up on most cases is not provided, but to our knowledge permanent alopecia has not been described.

Information about the histologic findings of tick bite alopecia is particularly limited. In a report by Heyl,³ biopsies were conducted in 2 patients, but the areas selected for biopsy were the sites of tick attachment. Centrally dense, acute, and chronic inflammation was seen, as well as marked tissue necrosis of the connective tissue and hair follicles. Peripheral to the attachment zone, tissue necrosis was not found, but telogen hairs with “crumpled up hair shafts” were present.³ The histologic findings presented by Castelli et al⁶ were based on a single case of tick bite alopecia; however, the specimen was a generous excisional biopsy, allowing for a panoramic histologic view of the lesion. In the center of the specimen, hair follicles were absent, but residual follicular streamers and follicular remnants were surrounded by lymphocytic inflammation. Sebaceous glands were conspicuously absent, but foci with naked hairs, fibrosis, and granulomatous inflammation were seen. Peripherally, the hair follicles were thinned and miniaturized with an increased number of catagen/telogen hairs. Some follicles showed lamellar fibroplasia and perifollicular chronic inflammation. The inflammatory infiltrate consisted predominantly of helper T cells with a smaller population of B lymphocytes and a few plasma cells.⁶ In 2016, Lynch et al⁵ described a single case of tick bite alopecia and noted pseudolymphomatous inflammation with germinal center formation associated with hair miniaturization and an elevated catagen/telogen count; focal follicular mucinosis also was noted.Our histologic findings are similar to those of Castelli et al,⁶ except that the inflammatory infiltrate was clearly B-cell dominant, with a suggestion of germinal center formation, as noted by Lynch et al.⁵ This inflammatory pattern often can be encountered in a chronic tick bite lesion. Destruction of follicles and associated sebaceous glands and their replacement by follicular scars indicate that at least in the central portion of the lesion some permanent hair loss occurs. The presence of catagen/telogen hairs and miniaturized follicles indicates the potential for at least partial regrowth.

Similar to other investigators who have described tick bite alopecia, we can only speculate as to the mechanism by which clinical alopecia occurs. Given the density of the inflammatory infiltrate and perifollicular inflammation, it seems reasonable to assume that inflammation either destroys hair follicles or precipitates the catagen/telogen phase, resulting in temporary hair loss. The inflammation itself may be due to the presence of tick parts or the antigens in their saliva (or both). The delay between tick attachment and the onset of alopecia can be attributed to the time it takes follicles to cycle into the catagen/telogen phase and shed the hair shaft.

SHM Fellows designation is a prestigious way to differentiate yourself in the rapidly growing profession of hospital medicine. There are currently 2,000 hospitalists who have earned the FHM/SFHM designation by demonstrating core values of leadership, teamwork, and quality improvement.

Apply by Sept. 15 to receive an early decision on or before Oct. 28. The regular decision application will remain open through Nov. 30. Apply now at www.hospitalmedicine.org/fellows.

SHM Fellows designation is a prestigious way to differentiate yourself in the rapidly growing profession of hospital medicine. There are currently 2,000 hospitalists who have earned the FHM/SFHM designation by demonstrating core values of leadership, teamwork, and quality improvement.

Apply by Sept. 15 to receive an early decision on or before Oct. 28. The regular decision application will remain open through Nov. 30. Apply now at www.hospitalmedicine.org/fellows.

SHM Fellows designation is a prestigious way to differentiate yourself in the rapidly growing profession of hospital medicine. There are currently 2,000 hospitalists who have earned the FHM/SFHM designation by demonstrating core values of leadership, teamwork, and quality improvement.

Apply by Sept. 15 to receive an early decision on or before Oct. 28. The regular decision application will remain open through Nov. 30. Apply now at www.hospitalmedicine.org/fellows.

Nominations for SHM Awards of Excellence, committees, Board of Director seats, and Masters of Hospital Medicine designations are now open. The deadline for award, committee, and board election nominations is Oct. 14. The deadline for MHM submission is Dec. 9. Make your nominations now at www.hospitalmedicine.org:

• Awards of Excellence: www.hospitalmedicine.org/awards

• Board of Directors: www.hospitalmedicine.org/boardelection

• Committee nominations: www.hospitalmedicine.org/committee

• Masters of Hospital Medicine: www.hospitalmedicine.org/masters

Nominations for SHM Awards of Excellence, committees, Board of Director seats, and Masters of Hospital Medicine designations are now open. The deadline for award, committee, and board election nominations is Oct. 14. The deadline for MHM submission is Dec. 9. Make your nominations now at www.hospitalmedicine.org:

• Awards of Excellence: www.hospitalmedicine.org/awards

• Board of Directors: www.hospitalmedicine.org/boardelection

• Committee nominations: www.hospitalmedicine.org/committee

• Masters of Hospital Medicine: www.hospitalmedicine.org/masters

Nominations for SHM Awards of Excellence, committees, Board of Director seats, and Masters of Hospital Medicine designations are now open. The deadline for award, committee, and board election nominations is Oct. 14. The deadline for MHM submission is Dec. 9. Make your nominations now at www.hospitalmedicine.org:

• Awards of Excellence: www.hospitalmedicine.org/awards

• Board of Directors: www.hospitalmedicine.org/boardelection

• Committee nominations: www.hospitalmedicine.org/committee

• Masters of Hospital Medicine: www.hospitalmedicine.org/masters

Lab mice

Photo by Aaron Logan

Research in mice suggests it’s feasible to use an immunotherapy conditioning regimen rather than radiation or chemotherapy prior to hematopoietic stem cell transplant (HSCT).

Investigators found that combining an antibody against the HSC receptor c-Kit with a CD47-blocking therapy could eliminate host HSCs and allow for successful engraftment of donor HSCs in immunocompetent recipient mice.

Adding T-cell-depleting antibodies to the mix allowed for robust HSC engraftment in a clinically relevant model of allogeneic HSCT.

Irving Weissman, MD, of Stanford University School of Medicine in California, and his colleagues conducted this research and reported the results in Science Translational Medicine.

The researchers first found that ACK2, an antibody against c-Kit, successfully depleted HSCs in immune-deficient mice.

“However, this antibody alone would not be effective in immune-competent recipients, who represent a majority of potential bone marrow transplant recipients,” said study author Akanksha Chhabra, PhD, of Stanford University School of Medicine.

So the researchers sought to enhance the effectiveness of ACK2 by combining it with antibodies or biologic agents that block CD47. They found that blocking CD47—particularly with an antagonist known as CV1mb—liberated macrophages to engulf target cells.

In this way, the immune system effectively depleted host HSCs in the immunocompetent mice, clearing the way for donor HSCs to take up residence in the bone marrow.

Finally, the researchers set out to determine whether conditioning with an anti-c-Kit antibody and CD47-blocking therapy could be extended to a clinically relevant model of allogeneic HSCT, in which the donor and recipient are matched through human leukocyte antigen alleles but mismatched at minor histocompatibility complex (mHC) antigens.

So the team conditioned mice with either ACK2 and CV1mb or ACK2 and the anti-CD47 antibody MIAP410. And they achieved immune ablation with T-cell-depleting antibodies—GK1.5 (anti-CD4) and YTS169.4 (anti-CD8). The mice then received mHC-mismatched HSCs.

The researchers found that either conditioning regimen, when combined with a T-cell-depleting regimen, resulted in substantial granulocyte, B-cell, T-cell, and NK-cell chimerism, as well as HSC engraftment in the bone marrow.

The success of these techniques in mice raises the researchers’ hopes that similar techniques will succeed in humans.

“If it works in humans like it did in mice, we would expect that the risk of death from blood stem cell transplant would drop from 20% to effectively 0,” said study author Judith Shizuru, MD, PhD, of Stanford University School of Medicine.

“If and when this is accomplished, it will be a whole new era in disease treatment and regenerative medicine,” Dr Weissman said.

Lab mice

Photo by Aaron Logan

Research in mice suggests it’s feasible to use an immunotherapy conditioning regimen rather than radiation or chemotherapy prior to hematopoietic stem cell transplant (HSCT).

Investigators found that combining an antibody against the HSC receptor c-Kit with a CD47-blocking therapy could eliminate host HSCs and allow for successful engraftment of donor HSCs in immunocompetent recipient mice.

Adding T-cell-depleting antibodies to the mix allowed for robust HSC engraftment in a clinically relevant model of allogeneic HSCT.

Irving Weissman, MD, of Stanford University School of Medicine in California, and his colleagues conducted this research and reported the results in Science Translational Medicine.

The researchers first found that ACK2, an antibody against c-Kit, successfully depleted HSCs in immune-deficient mice.

“However, this antibody alone would not be effective in immune-competent recipients, who represent a majority of potential bone marrow transplant recipients,” said study author Akanksha Chhabra, PhD, of Stanford University School of Medicine.

So the researchers sought to enhance the effectiveness of ACK2 by combining it with antibodies or biologic agents that block CD47. They found that blocking CD47—particularly with an antagonist known as CV1mb—liberated macrophages to engulf target cells.

In this way, the immune system effectively depleted host HSCs in the immunocompetent mice, clearing the way for donor HSCs to take up residence in the bone marrow.

Finally, the researchers set out to determine whether conditioning with an anti-c-Kit antibody and CD47-blocking therapy could be extended to a clinically relevant model of allogeneic HSCT, in which the donor and recipient are matched through human leukocyte antigen alleles but mismatched at minor histocompatibility complex (mHC) antigens.

So the team conditioned mice with either ACK2 and CV1mb or ACK2 and the anti-CD47 antibody MIAP410. And they achieved immune ablation with T-cell-depleting antibodies—GK1.5 (anti-CD4) and YTS169.4 (anti-CD8). The mice then received mHC-mismatched HSCs.

The researchers found that either conditioning regimen, when combined with a T-cell-depleting regimen, resulted in substantial granulocyte, B-cell, T-cell, and NK-cell chimerism, as well as HSC engraftment in the bone marrow.

The success of these techniques in mice raises the researchers’ hopes that similar techniques will succeed in humans.

“If it works in humans like it did in mice, we would expect that the risk of death from blood stem cell transplant would drop from 20% to effectively 0,” said study author Judith Shizuru, MD, PhD, of Stanford University School of Medicine.

“If and when this is accomplished, it will be a whole new era in disease treatment and regenerative medicine,” Dr Weissman said.

Lab mice

Photo by Aaron Logan

Research in mice suggests it’s feasible to use an immunotherapy conditioning regimen rather than radiation or chemotherapy prior to hematopoietic stem cell transplant (HSCT).

Investigators found that combining an antibody against the HSC receptor c-Kit with a CD47-blocking therapy could eliminate host HSCs and allow for successful engraftment of donor HSCs in immunocompetent recipient mice.

Adding T-cell-depleting antibodies to the mix allowed for robust HSC engraftment in a clinically relevant model of allogeneic HSCT.

Irving Weissman, MD, of Stanford University School of Medicine in California, and his colleagues conducted this research and reported the results in Science Translational Medicine.

The researchers first found that ACK2, an antibody against c-Kit, successfully depleted HSCs in immune-deficient mice.

“However, this antibody alone would not be effective in immune-competent recipients, who represent a majority of potential bone marrow transplant recipients,” said study author Akanksha Chhabra, PhD, of Stanford University School of Medicine.

So the researchers sought to enhance the effectiveness of ACK2 by combining it with antibodies or biologic agents that block CD47. They found that blocking CD47—particularly with an antagonist known as CV1mb—liberated macrophages to engulf target cells.

In this way, the immune system effectively depleted host HSCs in the immunocompetent mice, clearing the way for donor HSCs to take up residence in the bone marrow.

Finally, the researchers set out to determine whether conditioning with an anti-c-Kit antibody and CD47-blocking therapy could be extended to a clinically relevant model of allogeneic HSCT, in which the donor and recipient are matched through human leukocyte antigen alleles but mismatched at minor histocompatibility complex (mHC) antigens.

So the team conditioned mice with either ACK2 and CV1mb or ACK2 and the anti-CD47 antibody MIAP410. And they achieved immune ablation with T-cell-depleting antibodies—GK1.5 (anti-CD4) and YTS169.4 (anti-CD8). The mice then received mHC-mismatched HSCs.

The researchers found that either conditioning regimen, when combined with a T-cell-depleting regimen, resulted in substantial granulocyte, B-cell, T-cell, and NK-cell chimerism, as well as HSC engraftment in the bone marrow.

The success of these techniques in mice raises the researchers’ hopes that similar techniques will succeed in humans.

“If it works in humans like it did in mice, we would expect that the risk of death from blood stem cell transplant would drop from 20% to effectively 0,” said study author Judith Shizuru, MD, PhD, of Stanford University School of Medicine.

“If and when this is accomplished, it will be a whole new era in disease treatment and regenerative medicine,” Dr Weissman said.

Blood sample collection

Photo by Juan D. Alfonso

The US Food and Drug Administration (FDA) has granted emergency use authorization (EUA) for the xMAP® MultiFLEX™ Zika RNA Assay.

This multiplex nucleic acid test is designed to detect Zika virus RNA in blood serum, plasma, or urine (collected alongside a patient-matched serum or plasma specimen).

The xMAP® MultiFLEX™ Zika RNA Assay is available for purchase by laboratories that are certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA) to perform high complexity tests.

The assay uses the Luminex® 100/200™ analyzer, MAGPIX® system, or other authorized instruments to simultaneously test for 6 genetic targets of the Zika virus.

The xMAP® MultiFLEX™ Zika RNA Assay was designed by GenArraytion, Inc. and is marketed by Luminex Corporation.

For more information on the test, see the fact sheet for healthcare providers on the Luminex website.

About the EUA

The EUA does not mean the xMAP® MultiFLEX™ Zika RNA Assay is FDA cleared or approved.

An EUA allows for the use of unapproved medical products or unapproved uses of approved medical products in an emergency.

The products must be used to diagnose, treat, or prevent serious or life-threatening conditions caused by chemical, biological, radiological, or nuclear threat agents, when there are no adequate alternatives.

This means the xMAP® MultiFLEX™ Zika RNA Assay is only authorized as long as circumstances exist to justify the authorization of the emergency use of in vitro diagnostics for the detection of Zika virus, unless the authorization is terminated or revoked sooner.

Blood sample collection

Photo by Juan D. Alfonso

The US Food and Drug Administration (FDA) has granted emergency use authorization (EUA) for the xMAP® MultiFLEX™ Zika RNA Assay.

This multiplex nucleic acid test is designed to detect Zika virus RNA in blood serum, plasma, or urine (collected alongside a patient-matched serum or plasma specimen).

The xMAP® MultiFLEX™ Zika RNA Assay is available for purchase by laboratories that are certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA) to perform high complexity tests.

The assay uses the Luminex® 100/200™ analyzer, MAGPIX® system, or other authorized instruments to simultaneously test for 6 genetic targets of the Zika virus.

The xMAP® MultiFLEX™ Zika RNA Assay was designed by GenArraytion, Inc. and is marketed by Luminex Corporation.

For more information on the test, see the fact sheet for healthcare providers on the Luminex website.

About the EUA

The EUA does not mean the xMAP® MultiFLEX™ Zika RNA Assay is FDA cleared or approved.

An EUA allows for the use of unapproved medical products or unapproved uses of approved medical products in an emergency.

The products must be used to diagnose, treat, or prevent serious or life-threatening conditions caused by chemical, biological, radiological, or nuclear threat agents, when there are no adequate alternatives.

This means the xMAP® MultiFLEX™ Zika RNA Assay is only authorized as long as circumstances exist to justify the authorization of the emergency use of in vitro diagnostics for the detection of Zika virus, unless the authorization is terminated or revoked sooner.

Blood sample collection

Photo by Juan D. Alfonso

The US Food and Drug Administration (FDA) has granted emergency use authorization (EUA) for the xMAP® MultiFLEX™ Zika RNA Assay.

This multiplex nucleic acid test is designed to detect Zika virus RNA in blood serum, plasma, or urine (collected alongside a patient-matched serum or plasma specimen).

The xMAP® MultiFLEX™ Zika RNA Assay is available for purchase by laboratories that are certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA) to perform high complexity tests.

The assay uses the Luminex® 100/200™ analyzer, MAGPIX® system, or other authorized instruments to simultaneously test for 6 genetic targets of the Zika virus.

The xMAP® MultiFLEX™ Zika RNA Assay was designed by GenArraytion, Inc. and is marketed by Luminex Corporation.

For more information on the test, see the fact sheet for healthcare providers on the Luminex website.

About the EUA

The EUA does not mean the xMAP® MultiFLEX™ Zika RNA Assay is FDA cleared or approved.

An EUA allows for the use of unapproved medical products or unapproved uses of approved medical products in an emergency.

The products must be used to diagnose, treat, or prevent serious or life-threatening conditions caused by chemical, biological, radiological, or nuclear threat agents, when there are no adequate alternatives.

This means the xMAP® MultiFLEX™ Zika RNA Assay is only authorized as long as circumstances exist to justify the authorization of the emergency use of in vitro diagnostics for the detection of Zika virus, unless the authorization is terminated or revoked sooner.

Patient receiving chemotherapy

Photo by Rhoda Baer

The US Food and Drug Administration (FDA) has approved granisetron extended-release injection (Sustol®) for the prevention of chemotherapy-induced nausea and vomiting (CINV) in adults.

Extended-release granisetron is a serotonin-3 (5-HT3) receptor antagonist that utilizes Biochronomer® polymer-based drug delivery technology to maintain therapeutic levels of granisetron for at least 5 days, covering both the acute and delayed phases of CINV.

The product is intended for use in combination with other anti-emetics to prevent acute and delayed nausea and vomiting associated with initial and repeat courses of moderately emetogenic chemotherapy (MEC) or anthracycline and cyclophosphamide (AC) combination chemotherapy regimens.

“Despite advances in the management of CINV, up to half of patients receiving chemotherapy can still experience CINV, with delayed CINV being particularly challenging to control,” said Ralph V. Boccia, MD, of the Center for Cancer and Blood Disorders in Bethesda, Maryland.

“In our experience, other 5-HT3 receptor antagonists, including palonosetron, are generally effective for 48 hours or less. Sustol, due to its extended-release profile, represents a novel option that can protect patients from CINV for a full 5 days.”

Extended-release granisetron (formerly known as APF530) is a product of Heron Therapeutics, Inc. The US commercial launch of the drug is planned for the fourth quarter of 2016.

Phase 3 trials

The global phase 3 development program of extended-release granisetron consisted of 2 large, guideline-based clinical trials of more than 2000 cancer patients.

In one trial, researchers compared extended-release granisetron to palonosetron for the prevention of acute and delayed CINV after MEC or highly emetogenic chemotherapy (HEC).

Results suggested extended-release granisetron was non-inferior to palonosetron. The most common adverse events observed in patients receiving granisetron were injection-site reactions and constipation.

In another trial, researchers compared extended-release granisetron to ondansetron for control of delayed CINV after HEC. Patients received extended-release granisetron, dexamethasone, and fosaprepitant or ondansetron, dexamethasone, and fosaprepitant.

A higher percentage of patients in the granisetron arm had delayed-phase complete response. The incidence of treatment-emergent adverse events was similar between the treatment arms.

“The Sustol clinical trial populations and results are highly representative of cancer patients in our real-world clinical practice,” said Jeffrey Vacirca, MD, of North Shore Hematology Oncology Associates in East Setauket, New York.

“Use of MEC regimens is widespread, and AC-based regimens are among the most commonly prescribed highly emetogenic chemotherapy regimens. The most significant challenge for my breast cancer patients receiving AC is chemotherapy-induced nausea and vomiting. Sustol represents a better option to manage this devastating side effect of therapy.”

For more details on the drug, access the full prescribing information at www.SUSTOL.com.

Patient receiving chemotherapy

Photo by Rhoda Baer

The US Food and Drug Administration (FDA) has approved granisetron extended-release injection (Sustol®) for the prevention of chemotherapy-induced nausea and vomiting (CINV) in adults.

Extended-release granisetron is a serotonin-3 (5-HT3) receptor antagonist that utilizes Biochronomer® polymer-based drug delivery technology to maintain therapeutic levels of granisetron for at least 5 days, covering both the acute and delayed phases of CINV.

The product is intended for use in combination with other anti-emetics to prevent acute and delayed nausea and vomiting associated with initial and repeat courses of moderately emetogenic chemotherapy (MEC) or anthracycline and cyclophosphamide (AC) combination chemotherapy regimens.

“Despite advances in the management of CINV, up to half of patients receiving chemotherapy can still experience CINV, with delayed CINV being particularly challenging to control,” said Ralph V. Boccia, MD, of the Center for Cancer and Blood Disorders in Bethesda, Maryland.

“In our experience, other 5-HT3 receptor antagonists, including palonosetron, are generally effective for 48 hours or less. Sustol, due to its extended-release profile, represents a novel option that can protect patients from CINV for a full 5 days.”

Extended-release granisetron (formerly known as APF530) is a product of Heron Therapeutics, Inc. The US commercial launch of the drug is planned for the fourth quarter of 2016.

Phase 3 trials

The global phase 3 development program of extended-release granisetron consisted of 2 large, guideline-based clinical trials of more than 2000 cancer patients.

In one trial, researchers compared extended-release granisetron to palonosetron for the prevention of acute and delayed CINV after MEC or highly emetogenic chemotherapy (HEC).

Results suggested extended-release granisetron was non-inferior to palonosetron. The most common adverse events observed in patients receiving granisetron were injection-site reactions and constipation.

In another trial, researchers compared extended-release granisetron to ondansetron for control of delayed CINV after HEC. Patients received extended-release granisetron, dexamethasone, and fosaprepitant or ondansetron, dexamethasone, and fosaprepitant.

A higher percentage of patients in the granisetron arm had delayed-phase complete response. The incidence of treatment-emergent adverse events was similar between the treatment arms.

“The Sustol clinical trial populations and results are highly representative of cancer patients in our real-world clinical practice,” said Jeffrey Vacirca, MD, of North Shore Hematology Oncology Associates in East Setauket, New York.

“Use of MEC regimens is widespread, and AC-based regimens are among the most commonly prescribed highly emetogenic chemotherapy regimens. The most significant challenge for my breast cancer patients receiving AC is chemotherapy-induced nausea and vomiting. Sustol represents a better option to manage this devastating side effect of therapy.”

For more details on the drug, access the full prescribing information at www.SUSTOL.com.

Patient receiving chemotherapy

Photo by Rhoda Baer

The US Food and Drug Administration (FDA) has approved granisetron extended-release injection (Sustol®) for the prevention of chemotherapy-induced nausea and vomiting (CINV) in adults.

Extended-release granisetron is a serotonin-3 (5-HT3) receptor antagonist that utilizes Biochronomer® polymer-based drug delivery technology to maintain therapeutic levels of granisetron for at least 5 days, covering both the acute and delayed phases of CINV.

The product is intended for use in combination with other anti-emetics to prevent acute and delayed nausea and vomiting associated with initial and repeat courses of moderately emetogenic chemotherapy (MEC) or anthracycline and cyclophosphamide (AC) combination chemotherapy regimens.

“Despite advances in the management of CINV, up to half of patients receiving chemotherapy can still experience CINV, with delayed CINV being particularly challenging to control,” said Ralph V. Boccia, MD, of the Center for Cancer and Blood Disorders in Bethesda, Maryland.

“In our experience, other 5-HT3 receptor antagonists, including palonosetron, are generally effective for 48 hours or less. Sustol, due to its extended-release profile, represents a novel option that can protect patients from CINV for a full 5 days.”

Extended-release granisetron (formerly known as APF530) is a product of Heron Therapeutics, Inc. The US commercial launch of the drug is planned for the fourth quarter of 2016.

Phase 3 trials

The global phase 3 development program of extended-release granisetron consisted of 2 large, guideline-based clinical trials of more than 2000 cancer patients.

In one trial, researchers compared extended-release granisetron to palonosetron for the prevention of acute and delayed CINV after MEC or highly emetogenic chemotherapy (HEC).

Results suggested extended-release granisetron was non-inferior to palonosetron. The most common adverse events observed in patients receiving granisetron were injection-site reactions and constipation.

In another trial, researchers compared extended-release granisetron to ondansetron for control of delayed CINV after HEC. Patients received extended-release granisetron, dexamethasone, and fosaprepitant or ondansetron, dexamethasone, and fosaprepitant.

A higher percentage of patients in the granisetron arm had delayed-phase complete response. The incidence of treatment-emergent adverse events was similar between the treatment arms.

“The Sustol clinical trial populations and results are highly representative of cancer patients in our real-world clinical practice,” said Jeffrey Vacirca, MD, of North Shore Hematology Oncology Associates in East Setauket, New York.

“Use of MEC regimens is widespread, and AC-based regimens are among the most commonly prescribed highly emetogenic chemotherapy regimens. The most significant challenge for my breast cancer patients receiving AC is chemotherapy-induced nausea and vomiting. Sustol represents a better option to manage this devastating side effect of therapy.”

For more details on the drug, access the full prescribing information at www.SUSTOL.com.