Displaying all 8 publications

  1. Keynan Y, Card CM, Ball BT, Li Y, Plummer FA, Fowke KR
    Clin Microbiol Infect, 2010 Aug;16(8):1179-86.
    PMID: 20670292 DOI: 10.1111/j.1469-0691.2010.03142.x
    Influenza vaccine provides protection against infection with matched strains, and this protection correlates with serum antibody titres. In addition to antibodies, influenza-specific CD8+ T-lymphocyte responses are important in decreasing disease severity and facilitating viral clearance. Because this response is directed at internal, relatively conserved antigens, it affords some cross-protection within a given subtype of influenza virus. With the possibility of a broader A(H1N1) Mexico outbreak in the fall of 2009, it appeared worthwhile studying the degree of cellular immune response-mediated cross-reactivity among influenza virus isolates. The composition of the 2006-2007 influenza vaccine included the A/New Caledonia/20/1999 strain (comprising a virus that has been circulating, and was included in vaccine preparations, for 6-7 years) and two strains not previously included (Wisconsin and Malaysia). This combination afforded us the opportunity to determine the degree of cross-reactive cellular immunity after exposure to new viral strains. We analysed the antibody responses and the phenotype and function of the T cell response to vaccine components. The results obtained show that antibody responses to A/New-Caledonia were already high and vaccination did not increase antibody or cytotoxic T lymphocyte responses. These data suggest that repeated exposure to the same influenza stain results in limited boosting of humoral and cellular immune responses.
  2. Ghasemzadeh-Moghaddam H, Neela V, van Wamel W, Hamat RA, Shamsudin MN, Hussin NS, et al.
    Clin Microbiol Infect, 2015 Nov;21(11):998.e1-7.
    PMID: 26183299 DOI: 10.1016/j.cmi.2015.07.006
    We performed a prospective observational study in a clinical setting to test the hypothesis that prior colonization by a Staphylococcus aureus strain would protect, by colonization interference or other processes, against de novo colonization and, hence, possible endo-infections by newly acquired S. aureus strains. Three hundred and six patients hospitalized for >7 days were enrolled. For every patient, four nasal swabs (days 1, 3, 5, and 7) were taken, and patients were identified as carriers when a positive nasal culture for S. aureus was obtained on day 1 of hospitalization. For all patients who acquired methicillin-resistant S. aureus (MRSA) or methicillin-susceptible S. aureus via colonization and/or infection during hospitalization, strains were collected. We note that our study may suffer from false-negative cultures, local problems with infection control and hospital hygiene, or staphylococcal carriage at alternative anatomical sites. Among all patients, 22% were prior carriers of S. aureus, including 1.9% whom carried MRSA upon admission. The overall nasal staphylococcal carriage rate among dermatology patients was significantly higher than that among neurosurgery patients (n = 25 (55.5%) vs. n = 42 (16.1%), p 0.005). This conclusion held when the carriage definition included individuals who were nasal culture positive on day 1 and day 3 of hospitalization (p 0.0001). All MRSA carriers were dermatology patients. There was significantly less S. aureus acquisition among non-carriers than among carriers during hospitalization (p 0.005). The mean number of days spent in the hospital before experiencing MRSA acquisition in nasal carriers was 5.1, which was significantly lower than the score among non-carriers (22 days, p 0.012). In conclusion, we found that nasal carriage of S. aureus predisposes to rather than protects against staphylococcal acquisition in the nose, thereby refuting our null hypothesis.
  3. Altay A, Yahiro T, Bozdayi G, Matsumoto T, Sahin F, Ozkan S, et al.
    Clin Microbiol Infect, 2015 Oct;21(10):965.e1-4.
    PMID: 26086570 DOI: 10.1016/j.cmi.2015.06.006
    Recently a parvovirus called bufavirus (BuV) has been implicated as a causative agent of diarrhoea. To further reveal the epidemiology and genetic characteristics of BuV, this study was performed in Turkish children with diarrhoea. BuV was detected in 1.4% (8/583) of stool samples. All stool samples from healthy children (n = 148) were negative for BuV. Diarrhoea in BuV-positive patients was severe and occurred mainly during the colder months of the year. Complete genome sequences were generated from four BuVs. Only BuV3 was found, which was genetically and phylogenetically similar to Bhutanese BuV3, indicating that BuV3 is prevalent in Asian countries.
  4. Millar SB, Cox-Singh J
    Clin Microbiol Infect, 2015 Jul;21(7):640-8.
    PMID: 25843504 DOI: 10.1016/j.cmi.2015.03.017
    In 2004 a large focus of Plasmodium knowlesi malaria was reported in the human population in Sarawak, Malaysian Borneo. Plasmodium knowlesi, a parasite of the South-East Asian macaques (Macaca fascicularis and Macaca nemestrina), had entered the human population. Plasmodium knowlesi is transmitted by the leucosphyrus group of Anopheline mosquitoes and transmission is largely zoonotic and restricted to the jungle setting. Humans entering jungle transmission sites are at risk. Since 2004, human cases of P. knowlesi have been continuously reported in local communities and in travellers returning from South East Asia. Plasmodium knowlesi is the most common type of indigenous malaria reported in Malaysia. Infections are most often uncomplicated but at least 10% of patients report with severe malaria and 1-2% of cases have a fatal outcome. Parasitaemia is positively associated with the clinical and laboratory markers of severe malaria. The current literature on P. knowlesi, including epidemiology, natural hosts and vectors, pathogenesis, clinical descriptions, treatment and diagnosis, is reviewed. There are many gaps in our understanding of this disease that are highlighted here with suggestions for further research to inform pre-emptive control measures that would be required to prevent a full emergence of this parasite into the human population.
  5. Asplund M, Kjartansdóttir KR, Mollerup S, Vinner L, Fridholm H, Herrera JAR, et al.
    Clin Microbiol Infect, 2019 Oct;25(10):1277-1285.
    PMID: 31059795 DOI: 10.1016/j.cmi.2019.04.028
    OBJECTIVES: Sample preparation for high-throughput sequencing (HTS) includes treatment with various laboratory components, potentially carrying viral nucleic acids, the extent of which has not been thoroughly investigated. Our aim was to systematically examine a diverse repertoire of laboratory components used to prepare samples for HTS in order to identify contaminating viral sequences.

    METHODS: A total of 322 samples of mainly human origin were analysed using eight protocols, applying a wide variety of laboratory components. Several samples (60% of human specimens) were processed using different protocols. In total, 712 sequencing libraries were investigated for viral sequence contamination.

    RESULTS: Among sequences showing similarity to viruses, 493 were significantly associated with the use of laboratory components. Each of these viral sequences had sporadic appearance, only being identified in a subset of the samples treated with the linked laboratory component, and some were not identified in the non-template control samples. Remarkably, more than 65% of all viral sequences identified were within viral clusters linked to the use of laboratory components.

    CONCLUSIONS: We show that high prevalence of contaminating viral sequences can be expected in HTS-based virome data and provide an extensive list of novel contaminating viral sequences that can be used for evaluation of viral findings in future virome and metagenome studies. Moreover, we show that detection can be problematic due to stochastic appearance and limited non-template controls. Although the exact origin of these viral sequences requires further research, our results support laboratory-component-linked viral sequence contamination of both biological and synthetic origin.

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