Infant 13-valent pneumococcal conjugate vaccination (PCV13) was introduced to the UK in 2010. Its impact on serotypes implicated in adult non-bacteraemic pneumococcal pneumonia is not known.Beginning in 2008, a 5-year prospective cohort study of adults admitted to hospital with communityacquired pneumonia (CAP) was conducted. Pneumococcal serotype was established using a validated multiplex immunoassay (Bio-Plex; Bio-Rad, Hercules, CA, USA).The overall incidence for hospitalised CAP and pneumococcal CAP was 79.9 (95% CI 76.6-83.3) and 23.4 (95% CI 21.6-25.3) per 100 000 population, respectively. A decline in CAP (incidence rate ratio (IRR) per year 0.96, 95% CI 0.94-0.99; p=0.016) and pneumococcal CAP (IRR per year 0.84, 95% CI 0.80-0.89; p<0.001) was observed over the 5-year period of the study. Between the pre-and post-PCV13 periods of the study, the incidence of CAP due to serotypes included in the PCV7 declined by 88% (IRR 0.12, 95% CI 0.08-0.20; p<0.001), and CAP due to the additional 6 serotypes in PCV13 declined by 30% (IRR 0.70, 95% CI 0.51-0.96; p=0.024).Incidence of adult pneumococcal pneumonia declined over the last 5 years, with serotypes included in PCV13 declining post-PCV13 introduction, indicating early herd protection effects from PCV13 infant vaccination on adult non-bacteraemic disease. These effects may accrue over the coming years with implications for national pneumococcal vaccination policies in adults. @ERSpublications This is the first study to indicate herd protection from infant PCV13 on adult non-bacteraemic pneumococcal pneumonia

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BackgroundChanges over the last 5 years (2013–18) in the serotypes implicated in adult pneumococcal pneumonia and the patient groups associated with vaccine-type disease are largely unknown.MethodsWe conducted a population-based prospective cohort study of adults admitted to two large university hospitals with community-acquired pneumonia (CAP) between September 2013 and August 2018. Pneumococcal serotypes were identified using a novel 24-valent urinary monoclonal antibody assay and from blood cultures. Trends in incidence rates were compared against national invasive pneumococcal disease (IPD) data. Persons at risk of vaccine-type pneumonia (pneumococcal conjugate vaccine (PCV)13 and pneumococcal polysaccharide vaccine (PPV)23) were determined from multivariate analyses.FindingsOf 2934 adults hospitalised with CAP, 1075 (36.6%) had pneumococcal pneumonia. The annual incidence of pneumococcal pneumonia increased from 32.2 to 48.2 per 100 000 population (2013–18), predominantly due to increases in PCV13non7-serotype and non-vaccine type (NVT)-serotype pneumonia (annual incidence rate ratio 1.12, 95% CI 1.04 to 1.21 and 1.19, 95% CI 1.10 to 1.28, respectively). Incidence trends were broadly similar to IPD data. PCV13non7 (56.9% serotype 3) and PPV23non13 (44.1% serotype 8) serotypes were identified in 349 (32.5%) and 431 (40.1%) patients with pneumococcal pneumonia, respectively. PCV13-serotype pneumonia (dominated by serotype 3) was more likely in patients in the UK pneumococcal vaccination clinical risk group (adjusted OR (aOR) 1.73, 95% CI 1.31 to 2.28) while PPV23-serotype pneumonia was more likely in patients outside the clinical risk group (aOR 1.54, 95% CI 1.13 to 2.10).InterpretationThe incidence of pneumococcal CAP is increasing, predominantly due to NVT serotypes and serotype 3. PPV23-serotype pneumonia is more likely in adults outside currently identified clinical risk groups.

BackgroundOver 30% of adult patients with pleural infection either die and/or require surgery. There is no robust means of predicting at baseline presentation which patients will suffer a poor clinical outcome. A validated risk prediction score would allow early identification of high-risk patients, potentially directing more aggressive treatment thereafter.ObjectivesTo prospectively assess a previously described risk score (RAPID - Renal (urea), Age, fluid Purulence, Infection source, Dietary (albumin)) in adults with pleural infection.MethodsProspective observational cohort study recruiting patients undergoing treatment for pleural infection. RAPID score and risk category were calculated at baseline presentation. The primary outcome was mortality at 3 months; secondary outcomes were mortality at 12 months, length of hospital stay, need for thoracic surgery, failure of medical treatment, and lung function at 3 months.ResultsMortality data were available in 542 of 546 (99.3%) patients recruited. Overall mortality was 10% (54/542) at 3 months and 19% (102/542) at 12 months. The RAPID risk category predicted mortality at 3 months; low-risk (RAPID score 0–2) mortality 5/222 (2.3%, 95%CI 0.9 to 5.7), medium-risk (RAPID score 3–4) mortality 21/228 (9.2%, 95%CI 6.0 to 13.7), and high-risk (RAPID score 5–7) mortality 27/92 (29.3%, 95%CI 21.0 to 39.2). C-statistics for the score at 3 and 12 months were 0.78 (95%CI 0.71 to 0.83) and 0.77 (95%CI 0.72 to 0.82) respectively.ConclusionsThe RAPID score stratifies adults with pleural infection according to increasing risk of mortality and should inform future research directed at improving outcomes in this patient population.

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Additive series experiments were conducted under greenhouse conditions to determine the effect of season-long interference of different initial population densities of purple nutsedge on the shoot dry weight and fruit yield of tomato and bell pepper. Purple nutsedge densities up to 200 plants/m2linearly reduced shoot dry weight at flowering and fruit yield of both crops as weed density increased. Both variables were directly correlated, and for each percentage unit of tomato shoot dry weight loss at flowering, fruit yield was reduced 1.24 units, whereas for bell pepper this relationship was 1 to 2.01. Total shoot and tuber biomass of purple nutsedge increased as density increased. The presence of either crop caused a decline in the total shoot dry weight accumulation of purple nutsedge, with tomato producing a higher degree of loss than bell pepper to the weed. Fruit yield losses due to purple nutsedge interference reached 44% for tomato and 32% for bell pepper.

Twelve sweet corn (Zea mays L. var. rugosa Bonaf.) cultivars were tested for response to nicosulfuron at rates of 0, 18, 36, and 72 g a.i./ha. Weight of marketable ears indicated that five cultivars were intolerant to the herbicide. Three of the cultivars that were intolerant contained the shrunken-2 endosperm mutant (sh) and two contained the sugary enhancer endosperm mutant (se). Cultivars that were most tolerant of nicosulfuron contained the sh, gene. Incorporation of terbufos insecticide before planting led to decreased marketable yield when nicosulfuron was applied at 36 g·ha in all cultivars tested. Chlorpyrifos insecticide incorporated before planting did not affect tolerance to nicosulfuron. Neither soil-applied insecticide affected yield when nicosulfuron was not applied. Chemical names used: 2-[[[[(4,6-dimethoxy-2-pyrimidinyl)amino]carbonyl]amino]sulfony]-N,N-dimethyl-3-pyridinecarboxamide (nicosulfuron); S-[[(1,1-dimethylethyl)thio]methyl] O,O-diethylphosphorodithioate (terbufos); O,O-diethyl O-(3,5,6-trichloro-2-pyridyl)phosphorothioate (chlorpyrifos).