The Experts below are selected from a list of 60024 Experts worldwide ranked by ideXlab platform
Monisha Gupta - One of the best experts on this subject based on the ideXlab platform.
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live zoster vaccination in an Immunocompromised Patient leading to death secondary to disseminated varicella zoster virus infection
Vaccine, 2018Co-Authors: Kate Alexander, Philip L Tong, Kristine Macartney, Rohan Beresford, Vicky Sheppeard, Monisha GuptaAbstract:In 2016, the live attenuated zoster vaccine (Zostavax, Merck and Co, USA) was introduced into the Australian National Immunisation Program for people aged 70 years who are not significantly Immunocompromised. We report the administration of Zostavax in an Immunocompromised Patient with chronic lymphocytic leukaemia and no evidence of primary varicella zoster virus (VZV) infection. The Patient presented with a bilateral vesicular facial rash 22 days after receiving Zostavax and was initially managed as an outPatient with oral acyclovir. He re-presented three days later and was diagnosed with disseminated VZV infection complicated by meningoencephalitis. The Patient died following cardiac arrest on day 10 of hospitalisation. This unfortunate case highlights the challenge of safely implementing a high titre live vaccine in a population where contraindications are prevalent. The non-live recombinant herpes zoster subunit vaccine (Shingrix, GSK) may provide a safe and effective option to protect Immunocompromised Patients from shingles and post-herpetic neuralgia.
Kate Alexander - One of the best experts on this subject based on the ideXlab platform.
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live zoster vaccination in an Immunocompromised Patient leading to death secondary to disseminated varicella zoster virus infection
Vaccine, 2018Co-Authors: Kate Alexander, Philip L Tong, Kristine Macartney, Rohan Beresford, Vicky Sheppeard, Monisha GuptaAbstract:In 2016, the live attenuated zoster vaccine (Zostavax, Merck and Co, USA) was introduced into the Australian National Immunisation Program for people aged 70 years who are not significantly Immunocompromised. We report the administration of Zostavax in an Immunocompromised Patient with chronic lymphocytic leukaemia and no evidence of primary varicella zoster virus (VZV) infection. The Patient presented with a bilateral vesicular facial rash 22 days after receiving Zostavax and was initially managed as an outPatient with oral acyclovir. He re-presented three days later and was diagnosed with disseminated VZV infection complicated by meningoencephalitis. The Patient died following cardiac arrest on day 10 of hospitalisation. This unfortunate case highlights the challenge of safely implementing a high titre live vaccine in a population where contraindications are prevalent. The non-live recombinant herpes zoster subunit vaccine (Shingrix, GSK) may provide a safe and effective option to protect Immunocompromised Patients from shingles and post-herpetic neuralgia.
Donald W. Northfelt - One of the best experts on this subject based on the ideXlab platform.
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Live, Attenuated Varicella Zoster Vaccination of an Immunocompromised Patient
Journal of General Internal Medicine, 2008Co-Authors: Kelly K. Curtis, Megan K. Connolly, Donald W. NorthfeltAbstract:A vaccine for the prevention of herpes zoster outbreaks in adults over the age of 60 years has recently been approved. A 76-year-old white female with a history of recurrent left axillary breast cancer undergoing chemotherapy was given a Zostavax® injection by her primary care physician. Eight days later, the Patient developed a rash. Given the recent administration of live, attenuated varicella zoster virus (VZV), a diagnosis of disseminated cutaneous herpes zoster was made. The Patient was treated successfully with a course of famciclovir for 10 days and cephalexin for 7 days for a secondary bacterial infection. A review of the medical literature disclosed no reports of Zostavax® given to adult cancer Patients Immunocompromised by systemic chemotherapy. Therefore, we believe this report is the first to describe the consequences of Zostavax® administration to such a host. Clinicians should take care to review contraindications and precautions prior to administering the Zostavax® vaccine.
Guy Boivin - One of the best experts on this subject based on the ideXlab platform.
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molecular pathway of influenza pan neuraminidase inhibitor resistance in an Immunocompromised Patient
Antiviral Therapy, 2020Co-Authors: Yacine Abed, Manuel Schibler, Liva Checkmahomed, Julie Carbonneau, Mariechristine Venable, Federica Giannotti, Ana Rita Goncalves, Laurent Kaiser, Clement Fage, Guy BoivinAbstract:BACKGROUND Neuraminidase (NA) inhibitors (NAIs), including oseltamivir and zanamivir, play an important therapeutic role against influenza infections in Immunocompromised Patients. In such settings, however, NAI therapy may lead to the emergence of resistance involving mutations within the influenza surface genes. The aim of this study was to investigate the evolution of NA and haemagglutinin (HA) genes of influenza A(H1N1)pdm09 virus in an Immunocompromised Patient receiving oseltamivir then zanamivir therapies. METHODS Nasopharyngeal swab (NPS) samples were collected between 27 January 2018 and 11 April 2018 from a haematopoietic stem cell transplant recipient. These include 10 samples collected either pre-therapy, during oseltamivir and zanamivir treatment as well as after therapy. The A(H1N1)pdm09 HA/NA genes were sequenced. The H275Y NA substitution was quantified by droplet digital RT-PCR assay. A(H1N1)pdm09 recombinant viruses containing HA mutations were tested by HA elution experiments to investigate in vitro binding properties. RESULTS Oseltamivir rapidly induced the H275Y NA mutation which constituted 98.33% of the viral population after 15 days of oseltamivir treatment. The related HA gene contained S135A and P183S substitutions within the receptor-binding site. After a switch to zanamivir, 275H/Y and 119E/G/D mixed populations were detected. In the last samples, the double H275Y-E119G NA variant dominated with S135A and P183S HA substitutions. CONCLUSIONS This report confirms that oseltamivir can rapidly induce the emergence of the H275Y substitution in A(H1N1)pdm09 viruses and subsequent switch to zanamivir can lead to additional substitutions at codon E119 resulting in multi-drug resistance. Such data additionally suggest a potential compensatory role for HA substitutions near the receptor binding site.
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molecular pathway of influenza pan neuraminidase inhibitors resistance in an Immunocompromised Patient
bioRxiv, 2019Co-Authors: Yacine Abed, Manuel Schibler, Liva Checkmahomed, Julie Carbonneau, Mariechristine Venable, Federica Giannotti, Ana Rita Goncalves, Laurent Kaiser, Guy BoivinAbstract:Abstract Neuraminidase (NA) inhibitors (NAIs), including oseltamivir and zanamivir, play an important therapeutic role against influenza infections in Immunocompromised Patients. In such settings, however, NAI therapy may lead to the emergence of resistance involving mutations within the influenza surface genes. The aim of this study was to investigate the evolution of hemagglutinin (HA) and NA genes of influenza A(H1N1)pdm09 virus in an Immunocompromised Patient receiving oseltamivir then zanamivir therapies. Nasopharyngeal swabs (NPS) samples were collected between 01-27-2018 and 04-20-2018 from a hematopoietic stem cell transplant recipient. These included 11 samples collected either pre-therapy, during oseltamivir and zanamivir as well as after therapy. The A(H1N1)pdm09 HA/NA genes were sequenced. The H275Y NA substitution was quantified by droplet digital RT-PCR assay. A(H1N1)pdm09 recombinant viruses containing HA mutations were tested by HA elution experiments to investigate in vitro binding properties. Oseltamivir rapidly induced the H275Y NA mutation which constituted 98.33% of the viral population after 15 days of oseltamivir treatment. The related HA gene contained S135A and P183S substitutions within the receptor-binding site. After a switch to zanamivir, 275H/Y and 119E/G/D mixed populations were detected. In the last samples, the double H275Y-E119G NA variant dominated with S135A and P183S HA substitutions. This report confirms that oseltamivir can rapidly induce the emergence of the H275Y substitution in A(H1N1)pdm09 viruses and subsequent switch to zanamivir can lead to additional substitutions at codon E119 resulting in multi-drug resistance. Such data highlight the need for novel antiviral agents.
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prolonged excretion of amantadine resistant influenza a virus quasi species after cessation of antiviral therapy in an Immunocompromised Patient
Clinical Infectious Diseases, 2002Co-Authors: Guy Boivin, Nathalie Goyette, Harold BernatchezAbstract:: Phenotypic and molecular studies were conducted to characterize multiple influenza A isolates recovered from an Immunocompromised Patient who died of viral and fungal pneumonitis. The recovery of amantadine-resistant isolates was correlated with the detection of 2 drug-resistant M2 variants (codons 27 and 31) in combination with a wild-type virus. The mutant viruses persisted within the viral population in variable proportions >1 month after cessation of antiviral therapy. These results confirm animal studies reported elsewhere regarding the genetic stability of influenza M2 mutants and their potential for transmission in humans.
Hironobu Ihn - One of the best experts on this subject based on the ideXlab platform.
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Cutaneous hyalohyphomycosis by Scedosporium apiospermum in an Immunocompromised Patient.
Mycoses, 2011Co-Authors: Koji Makino, Satoshi Fukushima, Keishi Maruo, Kiyofumi Egawa, Katsutaro Nishimoto, Hironobu IhnAbstract:Scedosporium apiospermum is a ubiquitous filamentous fungus that may infect immunocompetent Patients after trauma and may cause severe and often fatal infections in Immunocompromised hosts. Here, we present the case of a 28-year-old female with S. apiospermum infection on the left forearm that had developed while she was on long-term immunosuppressant therapy. Analysis of a skin biopsy specimen showed a mixed cell granuloma with hyaline septate hyphae. Culture of the abscess revealed S. apiospermum which was identified as S. apiospermum sensu stricto by sequencing of the internal transcribed spacer-1 region of ribosomal DNA genes. Resection of the eruption and oral itraconazole (100 mg day(-1)) therapy for 4 months was effective in curing the infection.
