In 2002, the coagulase-negative staphylococci species Staphylococcus pettenkoferi was first described. In addition to an overview of the laboratory detection of uncommon coagulase-negative staphylococci, this report describes, to the author’s knowledge, the first case of S pettenkoferi bacteremia in Canada.
{"title":"Staphylococcus pettenkoferi bacteremia: A case report and review of the literature","authors":"A. Hashi, J. Delport, S. Elsayed, M. Silverman","doi":"10.1155/2015/748154","DOIUrl":"https://doi.org/10.1155/2015/748154","url":null,"abstract":"In 2002, the coagulase-negative staphylococci species Staphylococcus pettenkoferi was first described. In addition to an overview of the laboratory detection of uncommon coagulase-negative staphylococci, this report describes, to the author’s knowledge, the first case of S pettenkoferi bacteremia in Canada.","PeriodicalId":22481,"journal":{"name":"The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Médicale","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82750739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Due to poor penetration of systemic or topical antibiotics into the vitreous chamber, treating endophthalmitis is challenging, especially in rare cases in which vancomycin-resistant enterococci are present. Caused by the unique mechanism of high-velocity water stream trauma, a case of exogenous endophthalmitis in a four-year-old-boy is discussed.
{"title":"Exogenous endophthalmitis caused by Enterococcus casseliflavus: A case report and discussion regarding treatment of intraocular infection with vancomycin-resistant enterococci","authors":"B. Berenger, Shobhana Kulkarni, B. Hinz, S. E. Md","doi":"10.1155/2015/784910","DOIUrl":"https://doi.org/10.1155/2015/784910","url":null,"abstract":"Due to poor penetration of systemic or topical antibiotics into the vitreous chamber, treating endophthalmitis is challenging, especially in rare cases in which vancomycin-resistant enterococci are present. Caused by the unique mechanism of high-velocity water stream trauma, a case of exogenous endophthalmitis in a four-year-old-boy is discussed.","PeriodicalId":22481,"journal":{"name":"The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Médicale","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82259386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The magnitude of the increasing problem of resistance really takes all its meaning when appraised side-by-side with the paucity of new antimicrobials reaching the market (1). Several factors have contributed to making antimicrobial discovery less fashionable nowadays. The gigantic costs of bringing a new compound to market, from the identification of a promising target at the preclinical stages, to the final clinical trials and approval, are clearly a strong deterrent. This emphasizes the difficulty in realizing an interesting financial return, given that antimicrobials are used for diseases occurring on a very short timespan (compared with the treatment of chronic conditions) and that regulatory requirements are strict (2). In the United States, in an attempt to stimulate the discovery of new antimicrobials, the Generating Antibiotic Incentives Now (GAIN) Act has been passed by the Obama administration. Among the provisions of the Act, sponsors developing new antibiotics may benefit from the following incentives: five additional years of market exclusivity, priority review, fast-track approval and updated guidance (3). The impact of the GAIN Act is difficult to evaluate such a short time after its implementation, but considering the high costs of development and evaluation, five additional years of market exclusivity appears to be a small upgrade to really provide incentive to pharmaceutical companies to invest in this field.
{"title":"Digging for new solutions","authors":"L. Valiquette, K. Laupland","doi":"10.1155/2015/971858","DOIUrl":"https://doi.org/10.1155/2015/971858","url":null,"abstract":"The magnitude of the increasing problem of resistance really takes all its meaning when appraised side-by-side with the paucity of new antimicrobials reaching the market (1). Several factors have contributed to making antimicrobial discovery less fashionable nowadays. The gigantic costs of bringing a new compound to market, from the identification of a promising target at the preclinical stages, to the final clinical trials and approval, are clearly a strong deterrent. This emphasizes the difficulty in realizing an interesting financial return, given that antimicrobials are used for diseases occurring on a very short timespan (compared with the treatment of chronic conditions) and that regulatory requirements are strict (2). In the United States, in an attempt to stimulate the discovery of new antimicrobials, the Generating Antibiotic Incentives Now (GAIN) Act has been passed by the Obama administration. Among the provisions of the Act, sponsors developing new antibiotics may benefit from the following incentives: five additional years of market exclusivity, priority review, fast-track approval and updated guidance (3). The impact of the GAIN Act is difficult to evaluate such a short time after its implementation, but considering the high costs of development and evaluation, five additional years of market exclusivity appears to be a small upgrade to really provide incentive to pharmaceutical companies to invest in this field.","PeriodicalId":22481,"journal":{"name":"The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Médicale","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83598106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
C. O’Neil, J. Pang, Samuel S. Lee, M. Swain, K. Burak, P. Klein, R. Myers, Jeff Kapler, M. Gill, Martin Labrie, C. Coffin
To the Editor: Hepatitis C virus (HCV) infection is an important cause of morbidity and mortality among individuals living with HIV (1). Before the introduction of direct-acting antivirals (DAAs), pegylated interferon (peg-IFN) and ribavirin (RBV) were standard of care for coinfected patients with dismal sustained virological response (SVR) rates of <30% (2,3). Telaprevir (TVR), an NS3/4A protease inhibitor, was a first-generation DAA approved for HCV treatment in Canada, in November 2012. In randomized trials, the rate of SVR to TVR/peg-IFN/RBV was 65% to 75% in monoinfected patients and similar in coinfected patients (4-8). Few studies have reported treatment outcomes of TVR-based therapy outside of clinical trials. Our objective was to compare clinical outcomes of HCV-monoinfected and HIV-HCV coinfected patients treated with TVR-based triple therapy at a regional referral centre in Alberta. Patients who initiated TVR/pegIFN/RBV combination therapy from June 2011 to December 2013, were included in the study. Patients were treated according to Canadian guidelines for HCV treatment (9,10). All patients with HCV genotype 1 were eligible for therapy and were treated at the discretion of their HCV care provider. Demographic, clinical and laboratory data were collected at baseline and during therapy. Parameters of interest included HIV-coinfection, body mass index (BMI), Child-Pugh classification, previous injection drug use, haemophilia, liver transplantation, hepatitis B coinfection and previous HCV treatment. Fibrosis was determined using transient elastography by FibroScan (Echosens, France) with the following parameters: F0 to F1 ≤7.0, F2 7.1 to 9.4, F3 9.5 to 12.4, F4 (cirrhosis) ≥12.5 (11). Where applicable, HIV viral load and CD4+ T cell count were collected. Severe treatment-related anemia and thrombocytopenia were defined as nadir of hemoglobin ≤80 g/L and platelet count ≤50×109, respectively. Treatment response was determined using established definitions according to Canadian guidelines (9). Patients lost to follow-up were considered to have virological failure. In total, 103 patients received TVR at our clinics (Table 1). This included 13 (12.6%) HIV-HCV coinfected patients and seven (6.7%) patients who experienced recurrent HCV after liver transplantation. The median age at treatment onset was 56 years (interquartile range [IQR]: 51 to 59 years); 72% of patients were male and 86% were Caucasian. One-third (37%) of patients reported a history of injection drug use, nine (10%) had hemophilia and three (3%) were HCVhepatitis B virus coinfected. The median BMI was 26.8 kg/m2 (IQR 24.0 kg/m2 to 30.5 kg/m2). Forty-seven percent (n=45) of patients had been previously treated with pegIFN-RBV and 13% (n=12) were previous null responders. Most patients were HCV genotype 1a and IL28B non-CC genotype (71% and 70%, respectively). The majority (60%) of patients had advanced fibrosis or cirrhosis (F3 or F4). One patient had decompensated Child-Pugh B
致编辑:丙型肝炎病毒(HCV)感染是HIV感染者发病和死亡的重要原因(1)。在引入直接作用抗病毒药物(DAAs)之前，聚乙二醇化干扰素(peg-IFN)和利巴韦林(RBV)是治疗持续病毒学反应(SVR)率<30%的合并感染患者的标准治疗方法(2,3)。Telaprevir (TVR)是一种NS3/4A蛋白酶抑制剂，是加拿大于2012年11月批准用于HCV治疗的第一代DAA。在随机试验中，单感染患者对TVR/peg-IFN/RBV的SVR率为65%至75%，合并感染患者的SVR率相似(4-8)。在临床试验之外，很少有研究报道基于tvr的治疗结果。我们的目的是比较在阿尔伯塔省的一个区域转诊中心接受基于tvr的三联疗法治疗的单hcv感染和HIV-HCV合并感染患者的临床结果。研究纳入2011年6月至2013年12月期间接受TVR/pegIFN/RBV联合治疗的患者。患者按照加拿大HCV治疗指南进行治疗(9,10)。所有HCV基因型为1的患者均符合治疗条件，并由其HCV医护人员自行决定治疗。在基线和治疗期间收集人口统计学、临床和实验室数据。感兴趣的参数包括hiv合并感染、体重指数(BMI)、Child-Pugh分类、既往注射药物使用、血友病、肝移植、乙型肝炎合并感染和既往HCV治疗。纤维化采用FibroScan (Echosens, France)瞬时弹性成像测定，参数为F0 ~ F1≤7.0,F2 7.1 ~ 9.4, F3 9.5 ~ 12.4, F4(肝硬化)≥12.5(11)。在适用的情况下，收集HIV病毒载量和CD4+ T细胞计数。重度治疗相关性贫血和血小板减少的定义分别为血红蛋白≤80 g/L和血小板计数≤50×109的最低点。根据加拿大指南的既定定义确定治疗效果(9)。未能随访的患者被认为是病毒学失败。共有103例患者在我们的诊所接受了TVR(表1)。其中包括13例(12.6%)HIV-HCV合并感染患者和7例(6.7%)肝移植后复发的HCV患者。治疗开始时的中位年龄为56岁(四分位数间距[IQR]: 51至59岁);72%的患者为男性，86%为白种人。三分之一(37%)的患者报告有注射吸毒史，9例(10%)有血友病，3例(3%)合并感染hcvhbv病毒。中位BMI为26.8 kg/m2 (IQR为24.0 kg/m2至30.5 kg/m2)。47% (n=45)的患者以前曾接受过pegIFN-RBV治疗，13% (n=12)的患者以前是无效应答者。大多数患者为HCV基因型1a和IL28B非cc基因型(分别为71%和70%)。大多数(60%)患者有晚期纤维化或肝硬化(F3或F4)。1例失代偿Child-Pugh B肝硬化。HCV- hiv共感染患者在既往抗HCV治疗、HCV基因型亚型、白细胞介素(IL)28B基因型或纤维化程度方面无显著差异。合并感染患者报告注射用药(P=0.05)和血友病(P=0.03)的可能性更大。大多数(92%)HIV合并感染患者在接受抗逆转录病毒治疗时无法检测到HIV RNA，基线CD4细胞计数中位数为490细胞/mm3 (IQR为250细胞/mm3至639细胞/mm3)。大多数(85%)患者在TVR开始前需要调整抗逆转录病毒治疗方案。以整合酶为基础的抗逆转录病毒治疗是最常用的方案(77%)。在我们的队列中，SVR的总比率为66%(表2)。在HIV-HCV合并感染的患者中，SVR的比率为62%(13人中有8人)。肝硬化和既往无应答者的SVR率较低(分别为54%和42%)。57%(七分之四)的肝移植后受者达到了SVR。肝移植后患者的预后既往有报道(12)。在治疗失败中，因不良事件而停药最为常见(20%)，其次是病毒学复发(15%)。5例(5%)患者因肝功能失代偿而停止治疗。2例(2%)患者失访。2例(2%)患者死亡;一名患者在治疗期间因药物和酒精中毒死亡。另一位患者基线时为Child-Pugh B肝硬化，死于失代偿肝硬化并发症。最常见的副作用是疲劳(65%)、皮疹(68%)、情绪症状(42%)、肛肠症状(43%)和感染(17%)。15%的参与者出现严重贫血，11%和2%的参与者需要输血或使用促红细胞生成素。24%的参与者出现了严重的血小板减少症。大多数(57%)患者需要减少RBV剂量。 比较HCV单感染者和HIV合并感染者，SVR无显著差异(67% vs 62%， P=0.76)。单感染和合并感染患者因不良事件而停止治疗的比例无差异(20% vs 15%;P=1.00)或病毒学复发(13% vs 23%;P = 0.40)。一名合并HIV感染的患者因肝功能失代偿而停止治疗，但仍然达到了SVR。合并感染艾滋病毒的患者中没有死亡病例。合并HIV感染的患者更容易发生感染(12%对48%;P≤0.01)，重度贫血(11%对38%;P=0.02)，需要调整peg-IFN剂量(6% vs 46%;P≤0.01)。在hiv感染患者中，感染性并发症包括蜂窝织炎(n=2)、败血症(n=1)、胃肠炎(n=1)和尿路感染(n=1)。所有HIV合并感染的患者在接受治疗时都维持着检测不到的HIV RNA。在双变量分析中，与SVR增加率相关的变量包括较低的BMI (26.0 kg/m2 [IQR 24.0 kg/m2至29.1 kg/m2] vs . 29.1 kg/m2 [IQR 26.6 kg/m2至32.0 kg/m2];P=0.05)， IL28B基因型CC (37% vs 12%;P=0.02)和肝硬化(37% vs 60%;P = 0.03)。在多变量分析中，只有纤维化级别(F0至F2 vs F3至F4;调整OR 0.34 [95% CI 0.12 ~ 0.99];P=0.05)仍与SVR显著相关。HIV状态、注射药物使用史和既往对peg-IFN治疗的反应不能预测SVR。在临床试验之外，关于基于tvr的治疗在hiv合并感染患者中的有效性的报道很少。在我们的研究中，hcv单感染患者的总SVR为67%，合并感染患者的SVR为62%。这与临床试验相当，尽管在我们的队列中肝硬化患者的比例更高(45%)(4-6)。较低的BMI、IL28B CC基因型和纤维化程度与SVR的概率增加相关，尽管在多变量分析中，只有纤维化程度仍然是SVR的重要预测因子。基于tvr治疗的SVR的其他负面预测因素包括非裔美国人种族和既往治疗反应(13)。我们还证明HIV合并感染不是SVR的负向预测因子。这与涉及第二代daa(如ledipasvir和sofosbuvir)的试验一致。数据来自接受治疗的HCV单感染患者
{"title":"Treatment outcomes with telaprevir-based therapy for HIV/hepatitis C coinfected patients are comparable with hepatitis C monoinfected patients","authors":"C. O’Neil, J. Pang, Samuel S. Lee, M. Swain, K. Burak, P. Klein, R. Myers, Jeff Kapler, M. Gill, Martin Labrie, C. Coffin","doi":"10.1155/2015/974871","DOIUrl":"https://doi.org/10.1155/2015/974871","url":null,"abstract":"To the Editor: Hepatitis C virus (HCV) infection is an important cause of morbidity and mortality among individuals living with HIV (1). Before the introduction of direct-acting antivirals (DAAs), pegylated interferon (peg-IFN) and ribavirin (RBV) were standard of care for coinfected patients with dismal sustained virological response (SVR) rates of <30% (2,3). Telaprevir (TVR), an NS3/4A protease inhibitor, was a first-generation DAA approved for HCV treatment in Canada, in November 2012. In randomized trials, the rate of SVR to TVR/peg-IFN/RBV was 65% to 75% in monoinfected patients and similar in coinfected patients (4-8). Few studies have reported treatment outcomes of TVR-based therapy outside of clinical trials. Our objective was to compare clinical outcomes of HCV-monoinfected and HIV-HCV coinfected patients treated with TVR-based triple therapy at a regional referral centre in Alberta. Patients who initiated TVR/pegIFN/RBV combination therapy from June 2011 to December 2013, were included in the study. Patients were treated according to Canadian guidelines for HCV treatment (9,10). All patients with HCV genotype 1 were eligible for therapy and were treated at the discretion of their HCV care provider. Demographic, clinical and laboratory data were collected at baseline and during therapy. Parameters of interest included HIV-coinfection, body mass index (BMI), Child-Pugh classification, previous injection drug use, haemophilia, liver transplantation, hepatitis B coinfection and previous HCV treatment. Fibrosis was determined using transient elastography by FibroScan (Echosens, France) with the following parameters: F0 to F1 ≤7.0, F2 7.1 to 9.4, F3 9.5 to 12.4, F4 (cirrhosis) ≥12.5 (11). Where applicable, HIV viral load and CD4+ T cell count were collected. Severe treatment-related anemia and thrombocytopenia were defined as nadir of hemoglobin ≤80 g/L and platelet count ≤50×109, respectively. Treatment response was determined using established definitions according to Canadian guidelines (9). Patients lost to follow-up were considered to have virological failure. In total, 103 patients received TVR at our clinics (Table 1). This included 13 (12.6%) HIV-HCV coinfected patients and seven (6.7%) patients who experienced recurrent HCV after liver transplantation. The median age at treatment onset was 56 years (interquartile range [IQR]: 51 to 59 years); 72% of patients were male and 86% were Caucasian. One-third (37%) of patients reported a history of injection drug use, nine (10%) had hemophilia and three (3%) were HCVhepatitis B virus coinfected. The median BMI was 26.8 kg/m2 (IQR 24.0 kg/m2 to 30.5 kg/m2). Forty-seven percent (n=45) of patients had been previously treated with pegIFN-RBV and 13% (n=12) were previous null responders. Most patients were HCV genotype 1a and IL28B non-CC genotype (71% and 70%, respectively). The majority (60%) of patients had advanced fibrosis or cirrhosis (F3 or F4). One patient had decompensated Child-Pugh B ","PeriodicalId":22481,"journal":{"name":"The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Médicale","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78917692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Raymond Sw Tsang, Dennis Ks Law, Rita R Gad, Tim Mailman, Gregory German, Robert Needle
Background: Serogroup B Neisseria meningitidis (MenB) has always been a major cause of invasive meningococcal disease (IMD) in Canada. With the successful implementation of a meningitis C conjugate vaccine, the majority of IMD in Canada is now caused by MenB.
Objective: To investigate IMD case isolates in Atlantic Canada from 2009 to 2013. Data were analyzed to determine the potential coverage of the newly licensed MenB vaccine.
Methods: Serogroup, serotype and serosubtype antigens were determined from IMD case isolates. Clonal analysis was performed using multilocus sequence typing. The protein-based vaccine antigen genes were sequenced and the predicted peptides were investigated.
Results: The majority of the IMD isolates were MenB (82.5%, 33 of 40) and, in particular, sequence type (ST)-154 B:4:P1.4 was responsible for 47.5% (19 of 40) of all IMD case isolates in Atlantic Canada. Isolates of this clone expressed the PorA antigen P1.4 and possessed the nhba genes encoding for Neisseria heparin-binding antigen peptide 2, which together matched exactly with two of the four components of the new four-component meningococcal B vaccine. Nineteen MenB isolates had two antigenic matches, another five MenB and one meningitis Y isolate had one antigenic match. This provided 75.8% (25 of 33) potential coverage for MenB, or a 62.5% (25 of 40) overall potential coverage for IMD.
Conclusion: From 2009 to 2013, IMD in Atlantic Canada was mainly caused by MenB and, in particular, the B:4:P1.4 ST-154 clone, which accounted for 47.5% of all IMD case isolates. The new four-component meningococcal B vaccine appeared to offer adequate coverage against MenB in Atlantic Canada.
{"title":"Characterization of invasive Neisseria meningitidis from Atlantic Canada, 2009 to 2013: With special reference to the nonpolysaccharide vaccine targets (PorA, factor H binding protein, Neisseria heparin-binding antigen and Neisseria adhesin A).","authors":"Raymond Sw Tsang, Dennis Ks Law, Rita R Gad, Tim Mailman, Gregory German, Robert Needle","doi":"10.1155/2015/393659","DOIUrl":"10.1155/2015/393659","url":null,"abstract":"<p><strong>Background: </strong>Serogroup B Neisseria meningitidis (MenB) has always been a major cause of invasive meningococcal disease (IMD) in Canada. With the successful implementation of a meningitis C conjugate vaccine, the majority of IMD in Canada is now caused by MenB.</p><p><strong>Objective: </strong>To investigate IMD case isolates in Atlantic Canada from 2009 to 2013. Data were analyzed to determine the potential coverage of the newly licensed MenB vaccine.</p><p><strong>Methods: </strong>Serogroup, serotype and serosubtype antigens were determined from IMD case isolates. Clonal analysis was performed using multilocus sequence typing. The protein-based vaccine antigen genes were sequenced and the predicted peptides were investigated.</p><p><strong>Results: </strong>The majority of the IMD isolates were MenB (82.5%, 33 of 40) and, in particular, sequence type (ST)-154 B:4:P1.4 was responsible for 47.5% (19 of 40) of all IMD case isolates in Atlantic Canada. Isolates of this clone expressed the PorA antigen P1.4 and possessed the nhba genes encoding for Neisseria heparin-binding antigen peptide 2, which together matched exactly with two of the four components of the new four-component meningococcal B vaccine. Nineteen MenB isolates had two antigenic matches, another five MenB and one meningitis Y isolate had one antigenic match. This provided 75.8% (25 of 33) potential coverage for MenB, or a 62.5% (25 of 40) overall potential coverage for IMD.</p><p><strong>Conclusion: </strong>From 2009 to 2013, IMD in Atlantic Canada was mainly caused by MenB and, in particular, the B:4:P1.4 ST-154 clone, which accounted for 47.5% of all IMD case isolates. The new four-component meningococcal B vaccine appeared to offer adequate coverage against MenB in Atlantic Canada.</p>","PeriodicalId":22481,"journal":{"name":"The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Médicale","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4692298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74755033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eleonora Vaisben, Ronen Brand, Anas Kadakh, F. Nassar
Hypereosinophilia can lead to life-threatening organ damage when associated with eosinophilic infiltration of tissues. Although it is associated with a broad variety of diseases, sometimes no other abnormalities are detected. The authors present a novel approach to the treatment of hypereosinophilia, especially when an underlying cause fails to be detected.
{"title":"The role of empirical albendazole treatment in idiopathic hypereosinophilia – a case series","authors":"Eleonora Vaisben, Ronen Brand, Anas Kadakh, F. Nassar","doi":"10.1155/2015/531675","DOIUrl":"https://doi.org/10.1155/2015/531675","url":null,"abstract":"Hypereosinophilia can lead to life-threatening organ damage when associated with eosinophilic infiltration of tissues. Although it is associated with a broad variety of diseases, sometimes no other abnormalities are detected. The authors present a novel approach to the treatment of hypereosinophilia, especially when an underlying cause fails to be detected.","PeriodicalId":22481,"journal":{"name":"The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Médicale","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85609789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Vaughan, M. Sadler, S. Jayakumar, B. Missaghi, W. Chan, D. Church
CASE PRESENTATION A 50-year-old man presented to the emergency department (ED) with vomitting and epigastric pain 1 h after eating raw, wild salmon, which he had purchased from a major chain grocery store. He experienced immediate onset of profuse emesis and upper abdominal pain with no diarrhea. The epigastric pain was severe (described as 8 of 10) and persisted for 2 h. On presentation to the ED 6 h after eating the fish, he had a fever of 39°C and continued to experience severe abdominal pain, which localized to the left upper quadrant. On examination, the patient had abdominal tenderness, which was worse over the left upper quadrant and epigastrium. Hematological tests revealed a hemoglobin level of 167 g/L, a platelet count of 96×109/L and an elevated white blood cell count of 11.4×109/L, with predominant neutrophilia but no eosinophilia. His chest x-ray was unremarkable, and stool culture for ova and parasites was negative. An abdominal x-ray revealed an abnormal contour of air surrounding the gastric mucosa, suggesting extensive lobular thickening. A subsequent computed tomography scan revealed uniform thickening of the ruggae in the fundus and body of the stomach, suggestive of acute gastritis or neoplasia. He underwent esophagogastroduodenoscopy (EGD), at which time a diagnosis was made.
{"title":"An unusual case of abdominal pain","authors":"S. Vaughan, M. Sadler, S. Jayakumar, B. Missaghi, W. Chan, D. Church","doi":"10.1155/2015/578715","DOIUrl":"https://doi.org/10.1155/2015/578715","url":null,"abstract":"CASE PRESENTATION A 50-year-old man presented to the emergency department (ED) with vomitting and epigastric pain 1 h after eating raw, wild salmon, which he had purchased from a major chain grocery store. He experienced immediate onset of profuse emesis and upper abdominal pain with no diarrhea. The epigastric pain was severe (described as 8 of 10) and persisted for 2 h. On presentation to the ED 6 h after eating the fish, he had a fever of 39°C and continued to experience severe abdominal pain, which localized to the left upper quadrant. On examination, the patient had abdominal tenderness, which was worse over the left upper quadrant and epigastrium. Hematological tests revealed a hemoglobin level of 167 g/L, a platelet count of 96×109/L and an elevated white blood cell count of 11.4×109/L, with predominant neutrophilia but no eosinophilia. His chest x-ray was unremarkable, and stool culture for ova and parasites was negative. An abdominal x-ray revealed an abnormal contour of air surrounding the gastric mucosa, suggesting extensive lobular thickening. A subsequent computed tomography scan revealed uniform thickening of the ruggae in the fundus and body of the stomach, suggestive of acute gastritis or neoplasia. He underwent esophagogastroduodenoscopy (EGD), at which time a diagnosis was made.","PeriodicalId":22481,"journal":{"name":"The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Médicale","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82272628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To the Editor: A recent article argues for inclusion of meningococcal serogroup B vaccine in the routine Ontario immunization schedule (1). Unfortunately, titres to some vaccine components wane significantly over a period as short as 12 months after a primary series, indicating that frequent boosters may be required (2,3). There was only a 16.5% (95% CI 1.5% to 29.2%) decline in carriage rates when university students were immunized (4), potentially yielding less herd effect than with conjugated meningococcal vaccines (5,6). The authors of the article state “... even while the vaccine is not yet included in routine vaccination programs, it remains the responsibility of pediatricians, general practitioners and public health officials to educate and advise parents about the vaccine, enabling them to make informed decisions regarding immunization of their children” (1). The advice from the Canadian Medical Protective Association on this dilemma is:
致编辑:最近的一篇文章主张将脑膜炎球菌血清B组疫苗纳入安大略省常规免疫计划(1)。不幸的是，一些疫苗成分的滴度在初次接种后短短12个月内显著下降，这表明可能需要频繁加强接种(2,3)。当大学生接种疫苗时，携带率仅下降16.5% (95% CI 1.5%至29.2%)(4)，可能比接种脑膜炎球菌结合疫苗产生更少的群体效应(5,6)。这篇文章的作者指出“……即使这种疫苗尚未纳入常规疫苗接种计划，儿科医生、全科医生和公共卫生官员仍有责任对父母进行疫苗教育和建议，使他们能够在知情的情况下决定是否给孩子接种疫苗”(1)。加拿大医疗保护协会对这一困境的建议是:
{"title":"Are physicians obligated to tell parents about the meningococcal serogroup B vaccine?","authors":"Dr Joan L Robinson","doi":"10.1155/2015/506367","DOIUrl":"https://doi.org/10.1155/2015/506367","url":null,"abstract":"To the Editor: A recent article argues for inclusion of meningococcal serogroup B vaccine in the routine Ontario immunization schedule (1). Unfortunately, titres to some vaccine components wane significantly over a period as short as 12 months after a primary series, indicating that frequent boosters may be required (2,3). There was only a 16.5% (95% CI 1.5% to 29.2%) decline in carriage rates when university students were immunized (4), potentially yielding less herd effect than with conjugated meningococcal vaccines (5,6). The authors of the article state “... even while the vaccine is not yet included in routine vaccination programs, it remains the responsibility of pediatricians, general practitioners and public health officials to educate and advise parents about the vaccine, enabling them to make informed decisions regarding immunization of their children” (1). The advice from the Canadian Medical Protective Association on this dilemma is:","PeriodicalId":22481,"journal":{"name":"The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Médicale","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85717076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Michael T Hawkes, Sarah Forgie, Jason Brophy, Maryanne Crockett
{"title":"Artesunate treatment of severe pediatric malaria: A review of parasite clearance kinetics and clinical implications.","authors":"Michael T Hawkes, Sarah Forgie, Jason Brophy, Maryanne Crockett","doi":"10.1155/2015/736159","DOIUrl":"10.1155/2015/736159","url":null,"abstract":"","PeriodicalId":22481,"journal":{"name":"The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Médicale","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4644001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73239526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Lefebvre, B. Malette, I. Brukner, C. Saint-Martin, J. Papenburg
CASE PRESENTATION A nine-week-old girl presented to the emergency department with a 12 h history of fever and a 1 min generalized tonic-clonic seizure. Review of systems was otherwise negative. Her two-year-old sister experienced a fever and oropharyngeal ulcers two weeks before. On physical examination, she was febrile to 39.2°C rectal, but with otherwise normal vital signs. She was well-appearing and her examination was normal, including the neurological examination. Blood, urine and cerebrospinal fluid (CSF) specimens were obtained, and intravenous ceftriaxone, vancomycin and acyclovir were started. Laboratory investigations showed a normal complete blood cell count and transaminase levels. CSF examination revealed 55 white blood cells/μL (51% monocytes, 37% lymphocytes, 12% neutrophils), 7 red blood cells/μL, normal protein (0.35 g/L) and normal glucose (2.9 mmol/L). An electroencephalogram revealed active epileptiform activity over the right centroparietal regions. She was admitted to the pediatric ward and underwent magnetic resonance imaging of her head, which revealed multifocal nonenhancing lesions in the subcortical white matter of the right precentral gyrus, right cingular gyrus, right corticospinal tract, as well as the right internal capsule and thalamus (Figure 1). Bacterial cultures were without growth and antibiotics were discontinued after 48 h. CSF herpes simplex virus (HSV) 1 and HSV 2 polymerase chain reaction (PCR) (LightCycler 2.0 HSV 1/2 qualitative kit [Roche Diagnostics, Canada]) and enterovirus PCR were also negative. Repeat lumbar puncture and blood testing were performed on hospital day 3. DIAGNOSIS Both the CSF and blood samples obtained on hospital day 3 returned positive results for HSV-1 using PCR, confirming a diagnosis of HSV encephalitis. Extracted DNA from the initial CSF was re-tested using a different laboratory-developed HSV 1 and HSV 2 quantitative realtime PCR assay at another reference laboratory. In retrospect, the initial CSF specimen was positive for HSV 1 (2,675 copies/mL) using this assay, as were the second CSF specimen (21,905 copies/mL) and the blood sample (12,089 copies/mL).
{"title":"A nine-week-old girl with fever and seizures","authors":"M. Lefebvre, B. Malette, I. Brukner, C. Saint-Martin, J. Papenburg","doi":"10.1155/2015/397285","DOIUrl":"https://doi.org/10.1155/2015/397285","url":null,"abstract":"CASE PRESENTATION A nine-week-old girl presented to the emergency department with a 12 h history of fever and a 1 min generalized tonic-clonic seizure. Review of systems was otherwise negative. Her two-year-old sister experienced a fever and oropharyngeal ulcers two weeks before. On physical examination, she was febrile to 39.2°C rectal, but with otherwise normal vital signs. She was well-appearing and her examination was normal, including the neurological examination. Blood, urine and cerebrospinal fluid (CSF) specimens were obtained, and intravenous ceftriaxone, vancomycin and acyclovir were started. Laboratory investigations showed a normal complete blood cell count and transaminase levels. CSF examination revealed 55 white blood cells/μL (51% monocytes, 37% lymphocytes, 12% neutrophils), 7 red blood cells/μL, normal protein (0.35 g/L) and normal glucose (2.9 mmol/L). An electroencephalogram revealed active epileptiform activity over the right centroparietal regions. She was admitted to the pediatric ward and underwent magnetic resonance imaging of her head, which revealed multifocal nonenhancing lesions in the subcortical white matter of the right precentral gyrus, right cingular gyrus, right corticospinal tract, as well as the right internal capsule and thalamus (Figure 1). Bacterial cultures were without growth and antibiotics were discontinued after 48 h. CSF herpes simplex virus (HSV) 1 and HSV 2 polymerase chain reaction (PCR) (LightCycler 2.0 HSV 1/2 qualitative kit [Roche Diagnostics, Canada]) and enterovirus PCR were also negative. Repeat lumbar puncture and blood testing were performed on hospital day 3. DIAGNOSIS Both the CSF and blood samples obtained on hospital day 3 returned positive results for HSV-1 using PCR, confirming a diagnosis of HSV encephalitis. Extracted DNA from the initial CSF was re-tested using a different laboratory-developed HSV 1 and HSV 2 quantitative realtime PCR assay at another reference laboratory. In retrospect, the initial CSF specimen was positive for HSV 1 (2,675 copies/mL) using this assay, as were the second CSF specimen (21,905 copies/mL) and the blood sample (12,089 copies/mL).","PeriodicalId":22481,"journal":{"name":"The Canadian Journal of Infectious Diseases & Medical Microbiology = Journal Canadien des Maladies Infectieuses et de la Microbiologie Médicale","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77920397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：