The relative gene transfer was calculated

by dividing the

The relative gene transfer was calculated

by dividing the % value of each treatment by the % value for the standard. Here transconjugants serve as a standard. Data were analyzed using Graph Pad InStat-3 and expressed as mean ± standard deviation (SD) of three independent experiment. The continuous variables were tested with one-way analysis of variance (ANOVA) and Dunnett’s test. Values <0.05 were considered statistically significant. Re-identification of all of the clinical isolates were done and found to be of VRSA. Among the clinical isolates, only 8 clinical isolates (1 surgical wounds, 2 bacteremia and 5 burns) were found to be positive for vanA ( Fig. 1) and one of the vanA positive isolates (from burns sample) used as a donor for conjugation study. Transconjugants were selected by using 16 μg/ml of vancomycin and 2.5 μg/ml ciprofloxacin because these were able to grow PF-06463922 mouse in the presence of both of the drugs. Further analysis of transconjugants through PCR confirmed that transconjugants carrying the same gene as donor suggesting that gene transfer had taken place from donor to recipient ( Fig. 2A and B). Conjugative transfer of resistant gene has been demonstrated in-vitro, 13, 14 and 19 suggesting that genetic

exchange of resistance http://www.selleckchem.com/products/ink128.html may occur naturally. Moreover, results of conjugation study revealed that when conjugative system was provided with disodium edetate caused a concentration dependent inhibition of conjugation. Treatment with disodium edetate showed a significant conjugation inhibition which started from 4.0 mM (77.5 ± 4.9; p > 0.05) and continued up to 10 mM of disodium edetate ( Fig. 3 & Table 1). The author hypothesized that 10 mM disodium edetate in combination of antibiotic can be a novel approach to control and spreading of antibiotic resistance. Our lab has already established that disodium edetate to be safe upto 40 mg/kg/body weight when administered intravenously to Swiss albino

mice (communicated for publication). Additionally, Casein kinase 1 disodium edetate has been using intravenously in combination with vitamins and minerals in the treatment of various diseases including atherosclerotic vascular disease and renal ischemia. 20 and 21 Similarly, when conjugation was studied with various concentration of EGTA and boric acid, EGTA was found to inhibit conjugal transfer for vanA gene from donor to recipient at very high concentration that is 120 mM whereas boric acid failed to produces conjugation inhibition upto 150 mM (data not shown). The inhibition of conjugation by disodium edetate could be due to the inhibition of relaxases enzyme. DNA conjugative relaxases and rolling-circle replicating (RCR) initiator proteins, have been known to participate in the binding and coordination of the metal cation (Mg2+ or Mn2+) needed for cleavage of the DNA substrate.

(1972) We observed the latency to seizure onset, the tonic-cloni

(1972). We observed the latency to seizure onset, the tonic-clonic seizure time, the total seizure time, the number of seizures and how many seizures reached the fifth stage CX 5461 on Racine’s scale (tonic-clonic seizures). Following the seizure tests, all animals, with or without PTZ treatment, were killed by decapitation. The hippocampus, cerebellum and cerebral cortex

were isolated and stored at −80 °C. Prior to each assay, the tissues were homogenized in phosphate buffered saline (pH 7.4) using a ground-glass-type Potter–Elvehjem homogenizer and were centrifuged for five minutes. The supernatant was used in all assays. All processes were carried out under cold conditions. To evaluate a possible neuroprotective effect of the juices, we measured the lipid and protein oxidative damage, the nitric oxide content and the enzymatic (superoxide dismutase and catalase) and non-enzymatic (sulfhydryl protein) antioxidant defenses.

We used the formation of thiobarbituric acid-reactive species (TBARS) during an acid-heating reaction as an index of lipid peroxidation, as previously described by Wills (1996). The results were expressed as nmol of malondialdehyde (MDA)/mg protein. The oxidative damage to proteins was assessed by the formation of carbonyl groups based on the reaction with dinitrophenylhydrazine, as previously described by Levine et al. (1990). The results

were expressed JQ1 as nmol/mg of protein. Nitric oxide production ADP ribosylation factor was determined based on the Griess reaction (Green et al., 1981). Nitrite concentration was determined from a standard nitrite curve generated using sodium nitroprusside. The results were expressed as mg/mL of sodium nitroprusside/mg protein. Superoxide dismutase (SOD) activity was assayed by measuring the inhibition of adrenaline auto-oxidation, as previously described (Bannister and Calabarese, 1987), and the results were expressed as U SOD (units of enzyme activity)/mg of protein. One unit was defined as the amount of enzyme that inhibits the rate of adrenochrome formation in 50%. Catalase (CAT) activity was assayed by measuring the rate of decrease in hydrogen peroxide (H2O2) absorbance at 240 nm, as previously described (Aebi, 1984), and the results were expressed as mmol H2O2/min/ mg of protein. The protein sulfhydryl content was evaluated by the 5,5′-dithiobis-(2-nitrobenzoic acid) (DTNB) method (Aksenov and Markesbery, 2001), and the results are expressed as nmol DTNB/mg of protein. Protein concentration was measured by the Bradford method Bradford (1976) using bovine serum albumin as a standard. The total phenolic content of the organic and conventional grape juices were measured using the modification of the Folin–Ciocalteau colorimetric method, as described by Singleton et al. (1999).

39; N, 12 06; O,18 26; S,9 35, [M + H]+: 350 11 Mol Wt: 431 50,

Wt: 431.50,M.P.: 209–210 °C; Yield 59% Rf 0.80; IR (cm−1): 1700(C]O ester), 3142(N–H), 1142, 1326 (>S]O); 1513 (C]N); 3479 (NH–C]O), 1H NMR

(δppm): 2.11 (s, 6H, Di-Methyl), 7.14–7.94 (m, 14H, Ar–H); Elemental analysis for C24H21N3O3S; Calculated: C, 66.74; H, 4.86; NVP-AUY922 N, 9.70; O,11.12; S,7.41 Found: C, 66.83; H, 4.83; N, 9.70; O,11.21; S,7.49, [M + H]+: 432.16. Wt: 443.60,M.P.: 207–208 °C; Yield 81% Rf 0.80; IR (cm−1): 1705(C]O ester), 3130(NH),1175, 1313 (>S]O); 1516 (C]N); 3404 (NH–C]O), 1H NMR (δppm): 2.12 (s, 6H, Di-Methyl), 1.34–1.82 (m, 20H, –(CH2)10–), 3.53(m,–NH–CH-)7.38–7.68 (m, 4H, Ar–H); Elemental analysis for C24H33N3O3S; Calculated: C, 64.92; H, 7.43; N, 9.46; O,10.82; S,7.21 Found: C, 64.98; H, 7.49; N, 9.89; O,10.73; S,7.10, [M + H]+: 444.56. The activity was determined using the disc diffusion method i.e. the zone of inhibition was measured in mm. All the compounds, (2a–j) were screened in vitro at a concentration of 100 μg/ml using DMSO as a solvent. Their antibacterial activities against Gram-positive (Staphylococcus aureus and Bacillus subtilis) and Gram-negative strains (Escherichia coli and Pseudomonas aeruginosa) were measured. Antifungal

evaluation was carried out against Candida albicans and Aspergillus niger at a concentration of 100 μg/ml. The antibacterial drug ciprofloxacin (10 μg/disc) and antifungal drug fluconazole (10 μg/disc) Staurosporine were also tested under similar conditions against these organisms. Each experiment was performed in triplicate and the average tabulated. We synthesized novel N-alkyl-2-(3,5-dimethyl-1,1-dioxido-2H-1,2,6-thiadiazin-4-yl)benzamides bearing novel substituent groups at the fourth position of the 1,2,6-thiadiazine ring. Historically acyl chloride mediated procedures for preparation of amides have been employed. In our study we found that at the temperatures typically used for these reactions there was decomposition of our starting material. In an effort to overcome this we then employed DCC at room temperature. Bay 11-7085 The byproduct DCU persisted in the workup of

the reaction and thus any products could not be purified. 18 In the end we used CDI for the coupling reaction which afforded typical yields of 80+%. The spectroscopic data for all the compounds were consistent with those observed for similar 1,2,6-thiadiazine 1,1-dioxide molecules and our compounds were fully characterized using by 1H NMR, high-resolution mass spectroscopy and elemental analysis. 19 All of the compounds demonstrated activity against the bacterial strains. In particular, this family of molecules was more active against the Gram-positive species S. aureus and B. subtilis than the Gram-negative E. coli and P. aeruginosa. The best results were achieved with molecules that had a cyclic aliphatic group i.e.2c, 2e and 2g (See Scheme 2). We were unable to synthesize the derivative with a benzyl group at the same position.

The NSP4 gene of the outbreak strains displayed a close relations

The NSP4 gene of the outbreak strains displayed a close relationship to a 2008 G9P[8] strain isolated in the USA, displaying 98.8–99.0% nucleotide and 99.4–100% amino acid identity. When compared to previously circulating Australian G9P[8] strains,

the outbreak strains exhibited 90.6–93.8% nucleotide and 94.6–97.0% amino acid identity. Four unique conserved amino acid substitutions were identified in the NSP4 gene from the 2007 outbreak strains at positions 137 (Pro-Ser), 140 (Thr/Ile-Val), learn more 144 (Thr-Ser) and 168 (Ile-Ser) when compared to previously published NSP4 sequences. The present study details the molecular characterisation of a G9P[8] rotavirus strain identified during a large gastroenteritis outbreak in 2007 in Alice Springs, Northern Territory, Australia. Based on PAGE analysis of the entire dsRNA genome and sequence analysis of gene segments encoding VP7, VP8* and NSP4 from representative strains, the Alice Springs 2007 outbreak was caused by a single G9P[8] strain. The same strain infected both vaccinated and non-vaccinated infants and remained highly conserved during the outbreak period. The 2007 outbreak strain was distinct from G9P[8] strains that have caused previous outbreaks in the same region and to Australian

isolates collected between 1997 and 2002. The presence BIBF 1120 order of G9P[8] strains in Alice Springs has fluctuated over the last decade. G9P[8] strains were first isolated in 1999 as a minor circulating genotype [26]. It re-emerged in 2001 and was responsible for a large gastroenteritis outbreak [27]. G9P[8] strains remained as the dominant type the following

two years (2002–2003) [28]. The prevalence rate declined from 2003 to 2004, with very few G9P[8] strains subsequently isolated in the years prior to the 2007 outbreak with G3 strains dominant between 2004 and 2007 [28] and [29]. Genetic analysis of several genes from the G9P[8] strains were performed to explore their origins. The VP7 however outer capsid protein is highly immunogenic and induces neutralising antibodies [4]. The VP7 gene of the 2007 outbreak strain contained three conserved amino acid changes compared to previously circulating Australian isolates. Two amino acid changes 263 (Val-Ile) and 279 (Ala-Thr) were also identified in two other G9P[8] strains, a 2005 Brazil isolate and a 2008 USA isolate. The Brazil isolate was collected during a rotavirus outbreak that caused 12,145 hospitalisations and eight deaths in the Acre State of Brazil [30]. Crystallographic models of the 3D structure of the VP7 gene revealed that the 263 (Val-Ile) amino acid substitution, present in all the Acre outbreak samples, was spatially very close to the major antigenic site B and the authors proposed that this amino acid change could have modified the antigenicity of the corresponding region [31]. The VP4 outer capsid protein is responsible for several important biological functions.

13, 14, 15 and 16 In the present study the binding interactions o

13, 14, 15 and 16 In the present study the binding interactions of some of the 3,4-heteroannelated quinolin-2-ones with DNA Gyrase as well as their antibacterial activity has been reported. These compounds are assumed to bind to inhibit the DNA Gyrase 2 of S. aureus in a similar fashion as ciprofloxacin does, since the compounds share structural similarity with Ciprofloxacin. The potential compounds are identified and their antibacterial activity is evaluated against S. aureus and Escherichia coli and

reported here. To study the click here extent of interaction of the synthesized 3,4-heteroannelated quinolin-2-ones with the DNA Gyrase of S. aureus, the compounds were docked to the protein using the GOLD 3.2 (Genetic Optimization for Ligand Docking) software. The docked poses of each ligand were analyzed and fitness Scores are calculated with Silver. Screening of antibacterial activity of title compounds was done by adopting disc diffusion method as described by Cruickshank et al (1975)17 using S. aureus

Gram +ve (Oxford strain) and E. coli Gram −ve (NCTC 10148). The synthesized compounds were constructed and prepared for docking using the Ligprep Protocol of Maestro. Ligand minimization was done using OPLS 2005 Force field. The synthesized compounds were constructed and prepared for docking using the Ligprep Protocol of Maestro. A high resolution (2.1 Å) crystal structure of S. aureus DNA Gyrase is selected and docked using GOLD 3.2. The GOLD LY2109761 clinical trial fitness function is made up of four components: protein–ligand hydrogen bond energy, protein–ligand Vander Waals energy, ligand internal vdw energy and ligand torsional strain energy and the fitness score is taken as the negative of the sum of the component energy terms. The docked poses of each ligand were visualized and the interactions were analyzed with Silver. The best Fitness

Scores for each ligand are tabulated along with the details of H-bonds and other interactions in Table 1. The binding poses of the ligands to the proteins are shown in Fig. 1. Compound 1b has the highest fitness score of 51.23. Compounds 1a, 1c, 2d and 2j also showed good fitness scores Digestive enzyme next to 1b. 11 compounds show good fitness score values as compared to Ciprofloxacin. Screening of antibacterial activity of title compounds was done by adopting disc diffusion method as described by Cruickshank et al (1975).17 The compounds were dissolved in appropriate solvents (AR grade) and Whatman No.1 filter paper discs of 6 mm diameter were prepared with various concentrations of test compounds ranging from 200 to 3.125 μg/disc. The test organisms used were S. aureus Gram +ve (Oxford strain) and E. coli Gram −ve (NCTC 10148).

Study participants over estimated the sero-prevalence of WNv in S

Study participants over estimated the sero-prevalence of WNv in Saskatchewan at 20%. Recently completed sero-prevalence studies from 2003 to 2007 estimate the sero-prevalence see more in Saskatchewan at 3.3% (range: 2:0–5.3% depending on geographic area) (unpublished data, J. Tataryn and P. Curry), with one specific geographic area of Saskatchewan as high as 8.5% [2]. Risk perceptions of the

public are likely influenced by media coverage and personal knowledge of individuals directly affected by WNv. The main concern for public health is the burden of illness to WNv patients and their families as well as the impact on the health care system. For example, in 2007, the Saskatoon Health Region reported

358 cases, including 32 neurological cases and 2 deaths; 15% of all cases were hospitalized. In that year, WNv was a leading cause of human encephalitis and aseptic meningitis in the region (Saskatoon Health Region Health Status Report, 2008; http://www.saskatoonhealthregion.ca/your_health/documents/PHO/shr_health_status_report_2008_full.pdf). Adults, seniors, and individuals who have chronic illnesses or who are immunosuppressed were perceived by study participants PF-01367338 order to be at greater risk of WNv disease and complications. Literature from across North America suggests that certain co-morbidity groups are at higher risk of prolonged recovery due to WNv, even the more mild form of West Nile fever [10]. Other factors, identified by study participants, believed to increase the risk of contracting WNv included living during in the southern part of the province, living

in a rural setting, working primarily outdoors, or participating in outdoor recreational activities. Again, these risk factors are reported in other studies from across North America [2] and [10]. Nearly all public health practitioners personally recommended preventive strategies against contracting WNv. The methods most commonly suggested by study participants included using mosquito repellent with DEET, wearing covering clothing such as long sleeves and pants, and avoiding exposure to mosquitoes during peak mosquito activity time periods. The 2004 sero-prevalence study conducted in southern Saskatchewan reported that study participants were highly knowledgeable about personal protective measures with over 95% of participants believing the protective measures prevent WNv; however, less than 50% reported practicing the behaviours all of most of the time [2]. This disconnect between knowledge and action for the personal prevention of WNv makes the introduction of a vaccine an extremely tangible method to prevent all forms of WNv disease which does not have to be applied on a daily basis. The majority of health care professionals felt confident in the potential efficacy of vaccination for prevention of WNv.

It was filtered through Whatmann Paper No 1 To the filtered extr

It was filtered through Whatmann Paper No.1. To the filtered extract, acetic acid and acid ninhydrin (Warm 1.25 g ninhydrin in 30 mL glacial acetic acid and 20 mL 6 M phosphoric acid) were added in the ratio 1:1 and then boiled for 1 h. Reaction was terminated by placing in ice bath after which 4 mL of benzene was added. Benzene layer was separated and warmed to room temperature. The absorbance values were determined at 520 nm.23 and 25 Standard curve was prepared using pure proline and used for the detection of proline in the experimental conditions. Proline accumulation is one of the common characteristics

in many monocotyledons under saline conditions.26 It is well documented that the accumulation of proline is a response of plants to increased noxious elements.27 Among these, sodium ion is known as the most prominent one.8 Very high accumulation PLX4032 datasheet of cellular proline (above 100% of the total amino acid pool under stress

as compared to just 5% under the normal condition) has been earlier reported in many higher plants species due to increased synthesis GSK2118436 molecular weight and decreased degradation under the stress conditions such as water, salt, drought and heavy metal.28 Seedlings of T. aestivum (wheat) was subjected to drought conditions of salinity with different concentrations of NaCl (0.5–5 M). Sample which was treated with 1.0 M NaCl showed high accumulation of proline with 65 times of more than that of the control, whereas at low saline conditions of 0.5 M NaCl it showed only 31.42% of proline. On increasing the saline conditions it was found to be 84.28% and 98.57% at salt concentrations of 2.5 M and 5 M, respectively ( Fig. 1). Above the concentration of 1 M NaCl the decline of proline accumulation at higher values might be some interference of other amino acids with the colorimetric reading. The standard plot was prepared using pure proline which shows the amount of accumulation of proline under various drought conditions of NaCl. From the above result we can conclude that there is accumulation of proline in the plant under induced drought conditions of salinity.

The accumulation is greater at higher concentration of sodium Thalidomide chloride. The expected linear increase in colorimetric absorbance reading at 520 nm may have been affected by other interfering materials. Nevertheless, it has been seen that proline is accumulated under water stress and may have a role in protecting the plant, and helping in its recovery when replenished with water at a later time. All authors have none to declare. Authors are highly thankful to DBT for financial support and Principal, Dr. P. Hemalatha Reddy for providing lab facilities to work. “
“Annona squamosa L. belongs to the family Annonaceae. It is a widely used Indian medicinal plant for the cure of deadly disease, diabetes. 1 In recent decades, a great no. of chemical and pharmacological studies have been done on A. squamosa L.

M Rauscher was involved in analysis of safety data, manuscript w

M. Rauscher was involved in analysis of safety data, manuscript writing, and critically reviewed the manuscript. M.R.Z. Capeding was the principal investigator and E. Alberto co-investigator, and both were involved in data collection, manuscript

writing and critical review. All authors approved the final version of the manuscript. Role of the funding source: Crucell Switzerland AG was involved in study design, analysis and interpretation of data, writing of the report and in the decision to submit the article for publication. “
“Human papillomavirus (HPV) genotypes 16 and 18 are estimated to cause 70% of cervical cancers worldwide [1]. Over 85% of the global burden of cervical cancer occurs in developing selleck products countries and Tanzania reports one of highest rates of cervical cancer Ku-0059436 mouse in Africa [2]. Potent, durable HPV vaccine efficacy will be essential if the vaccine is introduced for the control of

cervical cancer. Endemic infections in sub-Saharan Africa, such as malaria and helminth infections, act as immunological modulators, and have been found to adversely impact immune response to standard immunizations, such as antituberculosis vaccine bacillus Calmette–Guerin (BCG), typhoid fever, tetanus and polio vaccines [3], [4], [5], [6], [7], [8] and [9]. Studies to evaluate the effect of HPV vaccines in populations whose immunological system may be challenged by multiple co-infections such as malaria and helminth infections are needed [10] and [11]. We conducted a study to measure the influence of malaria parasitaemia and helminth infection on the immunogenicity of HPV-16/18 vaccine (GlaxoSmithKline (GSK) Biologicals SA). This study was nested within a cohort recruited for a Phase IIIb immunogenicity and safety trial of the HPV-16/18 vaccine (the HPV 021 trial) conducted in Tanzania and Senegal among HIV-negative girls and young women aged 10–25 years [12]. The HPV 021 trial

(NCT00481767) and the malaria/helminth study were conducted from October 2007 to July 2010 in Mwanza, Tanzania, one of the two participating HPV-021 trial centres. GSK Biologicals was the funding source for the studies. Both studies were approved by the ethics committees of the National Institute Ketanserin for Medical Research (NIMR), Tanzania and the London School of Hygiene & Tropical Medicine (LSHTM), United Kingdom. The helminth/malaria study was registered under ControlledTrials.com (ISRCTN90378590). The HPV 021 trial was a double-blind, randomized, placebo-controlled phase IIIb trial. Eligible participants were randomly assigned (2:1) to receive either three doses of HPV-16/18 AS04-adjuvanted vaccine (vaccine group) or Al(OH)3 (placebo group) at 0,1 and 6 months. After enrolment (Month 0), participants returned to the clinic at Months 1, 2, 4, 6, 7, 8, 10 and 12 for follow-up visit procedures.

The Advisory Committee on Communicable Diseases, established in t

The Advisory Committee on Communicable Diseases, established in the mid-1960s, is responsible for reviewing the status

of communicable diseases – both vaccine-preventable and those for which there are no vaccines – on a regular basis and for making all legally binding policy decisions related to their control and prevention in the country [6]. All policy decisions related to the NPI in the prevention and control of vaccine-preventable diseases come under the purview of the ACCD. Although the mandate of the ACCD has been described in several documents, the Committee does not have formal terms of reference either written in a public document or in documents given to its members. The Quarantine and Prevention of Diseases Ordinance of 1897 mTOR inhibitor [7], is the legal basis for the ACCD, though the act does not specifically mention the establishment of such a committee. The ACCD consists of a Chairperson, a Secretary

and 36 other members. The Director General (DG) of Health Services is always the Chairperson of the Committee and the Chief Epidemiologist – who heads the Epidemiology Unit, under which the NPI is managed – serves, by designation, as the ACCD Secretary. The Secretary convenes the ACCD, prepares the agenda for the meetings, and is responsible for updating members on progress in the national implementation selleck of the Committee’s previous recommendations. The other members of the ACCD consist of academics and experts in a range of disciplines related to communicable diseases, including epidemiology; pharmacology; pharmacovigilance; vaccinology; immunology; and specific infectious diseases of importance to Sri

Lanka, such as malaria, dengue, leprosy, filariasis, HIV/AIDS, and tuberculosis. In addition, there are members with expertise in health education, community medicine, maternal and child health, family health, general practice, paediatrics, microbiology, quarantine services, national drug regulation, medical logistics, and health administration. However, there are as yet no members with expertise Histone demethylase in economics on the Committee. All experts should be either board-certified consultants in their respective fields, with a Ph.D. or MD degree or high-level health administrators in designated ministerial positions (e.g., the Deputy Director General of Health Services) to qualify for membership. The public sector is represented on the ACCD by members from relevant agencies and departments of the Ministry of Health (MOH), as well as from public universities. Members of relevant independent professional organizations, which consist of both public and private sector professionals, such as the colleges of paediatricians, microbiologists and community medicine, represent the interests of their organization on the Committee. In addition, two Committee seats are always allotted to representatives of the World Health Organization (WHO) and UNICEF, as key international partners in immunization.

Email: N [email protected] edu “
“Acute exacerbations are an im

Email: [email protected]
“Acute exacerbations are an important feature of chronic obstructive pulmonary disease (COPD), with long-term implications for patients and the health system. Physiotherapists play an integral role in the treatment of people with exacerbations of COPD, with high-level evidence that physiotherapy interventions can aid recovery and prevent recurrence.

This review summarises the respiratory and systemic consequences of an acute exacerbation of COPD (AECOPD); the burden of exacerbations for individuals and the health system; management of AECOPD, with a focus on important physiotherapy interventions; prevention of AECOPD; and future directions for research and practice. The Global Initiative for Obstructive Lung Disease (GOLD) strategy defines an exacerbation of COPD as ‘an acute

event trans-isomer characterised by a worsening of the patient’s respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication’.1 People with COPD experience between one and four exacerbations per year.2 Important symptoms include dyspnoea (in 84% of individuals), fatigue (81%), runny nose (59%), changes in sputum colour (53%) or amount (47%), and cough (44%).3 As there are no biomarkers that can reliably detect a COPD exacerbation, the diagnosis depends on patient report and clinical presentation. Whilst the GOLD definition suggests that a diagnosis of AECOPD

requires a change in medical GSK-3 phosphorylation management, up to 40% of exacerbations may not be reported to health professionals and these untreated exacerbations may have a significant impact on health status.4 The most common cause of a COPD exacerbation is thought to be viral infection, most often rhinovirus.5 Exacerbations with documented viral infection are associated with more severe symptoms and slower recovery than those without viral infection.5 of Bacterial infection is a less common cause of exacerbation. However, as many COPD airways are colonised with bacteria, secondary bacterial infection occurs in up to 60% of cases.6 Exacerbations have also been attributed to environmental pollution. In one-third of severe exacerbations the cause may be unknown.1 Exacerbations cluster in time7 and the strongest predictor of future exacerbations is a history of exacerbations.8 During an acute exacerbation, exposure to a viral, bacterial or environmental trigger causes worsening airway inflammation, which exacerbates the chronic airway inflammation that is characteristic of stable COPD. Increased inflammation and oxidative stress in the COPD airway are manifested by increased airway oedema and mucus hypersecretion, with worsening airway obstruction, dynamic hyperinflation, dyspnoea and cough.9 Work of breathing may be increased and in severe cases type-II respiratory failure may occur.