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  Table of Contents  
RESEARCH SNIPPETS
Year : 2014  |  Volume : 32  |  Issue : 1  |  Page : 102-104
 

Snippets


Department of Microbiology, Bhopal Memorial Hospital andResearch Center, Raisen Bypass Road, Karnod, Bhopal, Madhya Pradesh, India

Date of Web Publication4-Jan-2014

Correspondence Address:
Prabha Desikan
Department of Microbiology, Bhopal Memorial Hospital andResearch Center, Raisen Bypass Road, Karnod, Bhopal, Madhya Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0255-0857.124362

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How to cite this article:
Desikan P. Snippets. Indian J Med Microbiol 2014;32:102-4

How to cite this URL:
Desikan P. Snippets. Indian J Med Microbiol [serial online] 2014 [cited 2019 Aug 23];32:102-4. Available from: http://www.ijmm.org/text.asp?2014/32/1/102/124362


An avian influenza strain, H6N1, is thought to have recently made the jump from birds to human beings in Taiwan (http://healthland.time.com/2013/11/13/first-case-of-new-bird-flu-identified-in-human-patient/). The patient, a 20-year-old female, worked as a clerk in a deli and did not have direct contact with raw meats or poultry. Scientists at the Centers for Disease Control (CDC) in Taiwan identified and tested 36 of her close contacts but none showed signs of persistent infection with the virus. The unsubtyped influenza A virus was identified as the H6N1 subtype, based on sequences of the genes encoding haemagglutinin and neuraminidase. The source of infection was not established. Sequence analyses showed that this human isolate was highly homologous to chicken H6N1 viruses in Taiwan and had been generated through inter-clade re-assortment. Notably, the virus had a G228S substitution in the haemagglutinin protein that might increase its affinity for the human alpha 2-6 linked sialic acid receptor. This is the first report of human infection with a wild avian influenza A H6N1 virus. These viruses continue to evolve and accumulate changes, increasing the potential risk of human-to-human transmission. This highlights the continuous need for preparedness for a pandemic of unpredictable and complex avian influenza ( http://www.thelancet.com/journals/lanres/article/PIIS2213-2600(13)70221-2/fulltext ).

The availability of anti-malarial therapies using the drug artemisinin has helped cut global malaria deaths by a quarter in the past decade. But resistance to it emerged on the Thai-Cambodia border in 2003, and has since been confirmed in Vietnam and Myanmar too. It has also been detected in southwest China and suspected as far away as Guyana and Suriname, according to a new report by the Center for Strategic and International Studies think tank (http://www.firstpost.com/world/rise-of-drug-resistant-malaria-in-southeast-asia-alarming-doctors-1224043.html). This could be a health catastrophe in the making, as no alternative anti-malarial drug is on the horizon. The World Health Organisation (WHO) warns that what seems to be a localised threat could easily get out of control and have serious implications for global health. Resistance to artemisinin can be driven by various factors: delays in giving treatment, use of counterfeit or substandard drugs, and prescribing artemisinin on its own rather than in combination with another longer-acting drug.

Despite widespread coverage of the emergence of artemisinin resistance, relatively little is known about the parasite populations responsible. A study examined 143 adult patients presenting with uncomplicated falciparum malaria during a clinical trial of artesunate (AS) monotherapy in western Cambodia (Malar J. 2013 Nov 9;12(1):403. [Epub ahead of print]). Nested allelic type-specific amplification of the genes encoding the merozoite surface proteins 1 and 2 (msp1 and msp2) and the glutamate-rich protein (glurp) was performed at baseline, daily during 7 days of treatment, and again at failure. Allelic variants were analysed with respect to the size of polymorphisms using Quantity One software to enable identification of polyclonal infections. The primary objective was to assess the emergence of minority parasite clones during 7 days of AS treatment in a location with established artemisinin resistance. An additional objective was to investigate whether the classification of clinical outcomes remained valid when additional genotyping was performed. Considerable variation of msp2 alleles but well-conserved msp1 and glurp were identified. At baseline, 31% of infections were polyclonal for one or more genes. Patients with recurrent malaria were significantly more likely to have polyclonal infections than patients without recurrence (7 of 9 versus 36 of 127, P =0.004). Emergence of minority alleles during treatment was detected in only 1 of 23 cases defined as being artemisinin resistant. Moreover, daily genotyping did not alter the final outcome classification in any recurrent cases. Disproportionately high rates of polyclonal infections in cases of recurrence suggest that complex infections lead to poor treatment outcomes.

An ongoing outbreak of fever, rash and joint pain in Yap, Micronesia, transmitted through mosquito bites has been identified as being caused by chikungunya virus (CHIKV). The US Centers for Disease Control and Prevention's Epi-Aid team has been in Yap assisting with control measures. A travel situation awareness advisory is in place, which states that the same species of mosquito lives on Guam as well ( http://www.guampdn.com/article/20131114/NEWS01/311140013/Virus-Mosquito-borne-outbreak-identified-Yap ). Chikungunya was, from the European perspective, considered to be a travel-related tropical mosquito-borne disease prior to the first European outbreak in Northern Italy in 2007. This was followed by cases of autochthonous transmission reported in south-eastern France in 2010. Both events occurred after the introduction, establishment and expansion of the Chikungunya-competent and highly invasive disease vector Aedesalbopictus (Asian tiger mosquito) in Europe. In order to assess whether these outbreaks are indicative of the beginning of a trend or one-off events, there is a need to further examine the factors driving the potential transmission of Chikungunya in Europe. The climatic suitability, both now and in the future, is an essential starting point for such an analysis. The climatic suitability for Chikungunya outbreaks was, therefore, determined by using bioclimatic factors that influence both vector and pathogen (Int J Health Geogr. 2013 Nov 12;12(1):51. [Epub ahead of print]). European areas with current and future climatic suitability of Chikungunya transmission were identified. An increase in risk was projected for Western Europe (e.g. France and Benelux-States) in the first half of the 21 st century and from mid-century onwards for central parts of Europe (e.g. Germany). Many Mediterranean regions would persist to be climatically suitable for transmission. Overall, the highest risk of transmission by the end of the 21 st century was projected for France, Northern Italy and the Pannonian Basin (East-central Europe).

The re-emergence of CHIKV has resulted in numerous outbreaks in the eastern hemisphere, and threatens to expand in the foreseeable future. Unfortunately, no effective treatment is currently available. A study reports the use of resazurin in a cell-based high-throughput assay, and an image-based high-content assay to identify and characterise inhibitors of CHIKV-infection in vitro. CHIKV is a highly cytopathic virus that rapidly kills infected cells. Thus, cell viability of HuH-7 cells infected with CHIKV in the presence of compounds was determined by measuring metabolic reduction of resazurin to identify inhibitors of CHIKV-associated cell death. A kinase inhibitor library of 4000 compounds was screened against CHIKV infection of HuH-7 cells using the resazurin reduction assay, and the cell toxicity was also measured in non-infected cells. CHIKV-infected cells manifested less prominent apoptotic blebs typical of CHIKV cytopathic effect compared with the control infection. Treatment with these compounds reduced viral titres in the medium of CHIKV-infected cells by up to 100-fold (PLoSNegl Trop Dis 2013;7:e2471. doi: 10.1371/journal.pntd.0002471).

Gabon, in Central Africa, was affected for the first time in 2007 and then in 2010 by simultaneous outbreaks of chikungunya and Dengue serotype 2 (DENV-2) viruses. Through the national surveillance of dengue-like syndromes between 2007 and 2010, continuous circulation of DENV-2 was observed in a southward movement. This rapid spread of DENV-2 was associated with the emergence of DENV-1 in 2007 and DENV-3 in 2010. Interestingly, six DENV-2 infected patients with hemorrhagic signs were detected during the second outbreak in 2010. Although these cases did not meet all standard WHO criteria for severe Dengue with haemorrhage (formerly DHF), this was the first finding of several dengue fever cases associated with hemorrhagic signs during a simultaneous circulation of different DENV serotypes in Africa. Together, these findings suggest that DENV is becoming more widely established on this continent and that DHF is likely to become a serious public-health problem in the near future (PLoS One 2013;8:e78030. doi: 10.1371/journal.pone.0078030).

Clinical manifestations of dengue include fever, headache, retro-orbital pain, myalgia and arthralgia; and a severe form of the disease denominated dengue haemorrhagic fever/dengue shock syndrome, characterised by haemoconcentration, thrombocytopenia and bleeding tendency. However, atypical manifestations, such as liver, central nervous system and cardiac involvement, have been increasingly reported. A report describes an atypical and rare presentation of dengue disease marked by a dramatic and fatal cardiogenic shock due to acute myocarditis. Histopathological analysis of heart tissue showed several multi-focal areas of muscle necrosis and intense interstitial oedema associated with clusters of virus particles inside the cardiomyocytes and in the interstitial space, providing evidence of a possible direct action of dengue virus on myocardium (Eur Heart J Acute Cardiovasc Care 2013;2:127-30. doi: 10.1177/2048872613475889).

The dual epidemics of HIV and tuberculosis (TB) (including MDR-TB) are major contributors to high morbidity and mortality rates in South Africa. Rifampicin (RIF) resistance is regarded as a proxy for MDR-TB. Currently available molecular assays have the advantage of rapidly detecting resistant strains of MTB, but the GeneXpert does not detect isoniazid (INH) resistance and the GenoType MTBDRplus (LPA) assay may underestimate resistance to INH. Increasing proportions of rifampicin mono-resistance (RMR) have recently been reported from South Africa and other countries. A study retrospectively determined, for the period 2007 to 2009, the proportion of RMR among Mycobacterium tuberculosis (MTB) isolates, that were tested for both RIF and INH, using the gold standard of culture-based phenotypic drug susceptibility testing (DST). RMR was observed throughout the study period. The proportion of RMR varied from a low of 7.3% to a high of 10.0% [overall 8.8%]. Overall, males had a 42% increased odds of being RMR as compared with females. In comparison to the 50 plus age group, RMR was 37% more likely to occur in the 25-29 year age category (PLoS One 2013;8:e77712. doi: 10.1371/journal.pone.0077712).

On the basis of data from two Phase IIb trials (i.e. well-controlled trials to evaluate the efficacy and safety of drugs in patients with a disease or condition to be treated, diagnosed or prevented), the Food and Drug Administration (FDA) approved use of bedaquiline under the provisions of the accelerated approval regulations for "serious or life-threatening illnesses" (21CFR314.500) (Cox EM. FDA accelerated approval letter to Janssen Research and Development. Available at http://www.accessdata.fda.gov/drugsatfda_docs/appletter/2012/204384Orig1s000ltr.pdf). This report provides provisional CDC guidelines for FDA-approved and unapproved, or off-label, uses of bedaquiline in certain populations, such as children, pregnant women or persons with extrapulmonary MDR-TB who were not included in the clinical trials for the drug. CDC's Division of TB Elimination developed these guidelines on the basis of expert opinion informed by data from systematic reviews and literature searches. This approach is different from the statutory standards that FDA uses when approving drugs and drug labelling. These guidelines are intended for healthcare professionals who might use bedaquiline for the treatment of MDR-TB for indicated and off-label uses. Aspects of these guidelines are not identical to current FDA-approved labelling for bedaquiline.

Mucosal boosting of BCG-immunised individuals with a subunit TB vaccine would be highly desirable, considering that the lungs are the principal port of entry for MTB and the site of the primary infection and reactivation. However, the main roadblock for subunit TB vaccine development is the lack of suitable adjuvants that could induce robust local and systemic immune responses. To overcome this, a novel vaccine delivery system was designed to mimic, in part, the MTB pathogen itself (Eur J Immunol 2013. doi: 10.1002/eji.201343887. [Epub ahead of print]). The surface of yellow carnauba wax nanoparticles was coated with the highly immunogenic Ag85B antigen of MTB and they were directed to the alveolar epithelial surfaces by the incorporation of the heparin-binding haemagglutinin adhesion (HBHA) protein. Results showed that the intra-nasal immunisation of BCG-primed BALB/c mice with nanoparticles adsorbed with Ag85B-HBHA (NanoAH vaccine) induced robust humoral and cellular immune responses and IFN-γ production, and multi-functional CD4+ T cells expressing IFN-γ, IL-2 and TNF-α. Mice challenged with H37Rv MTB had a significantly reduced bacterial load in their lungs when compared with controls immunised with BCG alone. It was, therefore, concluded, that this immunisation approach is an effective means of boosting the BCG-induced anti-TB immunity.




 

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