Viral Etiology of Chronic Obstructive Pulmonary Disease Exacerbations during the A/H1N1pdm09 Pandemic and Postpandemic Period.

Viral infections are one of the main causes of acute exacerbations of chronic obstructive pulmonary disease (AE-COPD). Emergence of A/H1N1pdm influenza virus in the 2009 pandemic changed the viral etiology of exacerbations that were reported before the pandemic. The aim of this study was to describe the etiology of respiratory viruses in 195 Spanish patients affected by AE-COPD from the pandemic until the 2011-12 influenza epidemic. During the study period (2009-2012), respiratory viruses were identified in 48.7% of samples, and the proportion of viral detections in AE-COPD was higher in patients aged 30-64 years than ≥65 years. Influenza A viruses were the pathogens most often detected during the pandemic and the following two influenza epidemics in contradistinction to human rhino/enteroviruses that were the main viruses causing AE-COPD before the pandemic. The probability of influenza virus detection was 2.78-fold higher in patients who are 30-64 years old than those ≥65. Most respiratory samples were obtained during the pandemic, but the influenza detection rate was higher during the 2011-12 epidemic. There is a need for more accurate AE-COPD diagnosis, emphasizing the role of respiratory viruses. Furthermore, diagnosis requires increased attention to patient age and the characteristics of each influenza epidemic.

First attempt to implement ophthalmia neonatorum prophylaxis in angola: microorganisms, efficacy, and obstacles.

Purpose. To determine the efficacy of povidone-iodine (P-I) prophylaxis for ophthalmia neonatorum (ON) in Angola and to document maternal prevalence and mother-to-child transmission rates. Methods. Endocervical samples from mothers (n = 317) and newborn conjunctival smears (n = 245) were analysed by multiplex polymerase chain reaction (PCR) for Chlamydia trachomatis (CT), Neisseria gonorrhoeae (NG), and Mycoplasma genitalium (MG). Newborns were randomized into a noninterventional group and an interventional group that received a drop of P-I 2.5% bilaterally after conjunctival smear collection. Mothers were trained to identify signs of ON and attend a follow-up visit. Results. Forty-two newborns had ocular pathology, and 11 (4.4%) had clinical signs of ON at the time of delivery. Maternal PCR was positive for MG (n = 19), CT (n = 8), and NG (n = 2). Six newborns were positive for CT (n = 4), MG (n = 2), and NG (n = 1). Mother-to-child transmission rates were 50% for CT and NG and 10.5% for MG. Only 16 newborns returned for follow-up. Conclusions. Lack of maternal compliance prevented successful testing of prophylactic P-I efficacy in ON prevention. Nevertheless, we documented the prevalence and mother-to-child transmission rates for CT, NG, and MG. These results emphasize the need to develop an effective Angolan educational and prophylactic ON program.

Vertical transmission of bacterial eye infections, Angola, 2011-2012.

To determine transmission rates for neonatal conjunctivitis causative microorganisms in Angola, we analyzed 312 endocervical and 255 conjunctival samples from mothers and newborns, respectively, during 2011-2012. Transmission rates were 50% for Chlamydia trachomatis and Neisseria gonorrhoeae and 10.5% for Mycoplasma genitalium. Possible pathogenic effects of M. genitalium in children's eyes are unknown.

The value of simple microbiological studies for on-site screening of acute neonatal conjunctivitis in Angola.

BACKGROUND: Neonatal conjunctivitis or ophthalmia neonatorum (ON) is an acute bacterial conjunctivitis contracted by newborns during delivery. In non-industrialized countries, detection of the etiological agent is difficult due to the unavailability of modern diagnostic resources. Therefore, we analyzed the effectiveness of Gram and methylene blue staining techniques, which are simple microbiological methods in suspecting the aetiology of ON in a maternity ward in Luanda, Angola. FINDINGS: Neonatal conjunctival smears (n = 95), maternal data, and perinatal factors were collected. Slides were air-dried and sent to the Microbiology Department of the Hospital Clinico Universitario, Valladolid, Spain, where trained personnel performed Gram and methylene blue staining methods. Findings were interpreted by two expert microbiologists. Ophthalmological examination of all children showed five newborns with clinical signs of ON. Fourteen mothers reported were suspected with vulvo-vaginitis, and 27 had a urinary infection during pregnancy. Gram staining revealed the presence of epithelial cells in 87.6% and leukocytes in 15% of the conjunctival smears. These values were significantly higher than those shown by methylene blue staining. No rods, cocci, or yeasts were identified by either staining method. Chlamydia trachomatis DNA was also undetected in a small sub-sample with clinical suspicion of ON. There was no correlation among the presence of ON, ON microbes, maternal data, or perinatal factors. CONCLUSIONS: Basic microbiological techniques did not provide enough information for screening cases of ON in Angola. Therefore, the use of molecular biology or other techniques is warranted for this purpose.

Eosinophil as a protective cell in S. aureus ventilator-associated pneumonia.

Cell counts of leukocytes subpopulations are demonstrating to have an important value in predicting outcome in severe infections. We evaluated here the render of leukogram counts to predict outcome in patients with ventilator-associated pneumonia (VAP) caused by Staphylococcus aureus. Data from patients admitted to the ICU of Hospital Clínico Universitario de Valladolid from 2006 to 2011 with diagnosis of VAP caused by S. aureus were retrospectively collected for the study (n = 44). Leukocyte counts were collected at ICU admission and also at VAP diagnosis. Our results showed that nonsurvivors had significant lower eosinophil counts at VAP diagnosis. Multivariate Cox regression analysis performed by the Wald test for forward selection showed that eosinophil increments from ICU admission to VAP diagnosis and total eosinophil counts at VAP diagnosis were protective factors against mortality in the first 28 days following diagnosis: (HR [CI 95%], P): (0.996 [0.993-0.999], 0.010); (0.370 [0.180-0.750], 0.006). Patients with eosinophil counts <30 cells/mm(3) at diagnosis died earlier. Eosinophil counts identified survivors: (AUROC [CI 95%], P): (0.701 [0.519-0.882], 0.042). Eosinophil behaves as a protective cell in patients with VAP caused by S. aureus.

IgM levels in plasma predict outcome in severe pandemic influenza.

BACKGROUND: Little is known on the participation of immunoglobulin isotypes and subclasses in the pathogenesis of the severe disease caused by the pandemic influenza virus (influenza A(H1N1)pdm09). OBJECTIVES: (1) To evaluate the association between plasma levels of IgG1, IgG2, IgG3, IgG4, IgA, IgM, IgE and outcome in patients with severe pandemic influenza. (2) To evaluate the association between immunoglobulin and cytokine levels in these patients. STUDY DESIGN: 40 critically ill patients with community acquired pneumonia and influenza A(H1N1)pdm09 infection were recruited from November 2010 to February 2011. Plasma samples were collected during the first 24h following admission to the ICU. Immunoglobulins and 17 major cytokines were profiled in plasma. RESULTS: 15 patients died (37.5%). When the association between clinical variables and prognosis was assessed, prior immunosuppression, APACHE II score, levels of IgG2 and levels of IgM were associated with outcome in a univariate Cox regression analysis. Kaplan Meier analysis showed that patients with levels of IgG2 and IgM < 59 and<58 mg/dl respectively died earlier. Multivariate Cox regression analysis showed that APACHE II score and levels of IgM were the best predictors of outcome, being levels of IgM a protective factor against mortality. IgM was the immunoglobulin showing the largest number of negative correlations with cytokine levels. CONCLUSIONS: Our results support a central role of IgM in preventing uncontrolled inflammatory response and mortality in severe pandemic influenza. Early assessment of IgM could contribute to guide clinical decisions in these patients.

Viral infection is associated with an increased proinflammatory response in chronic obstructive pulmonary disease.

The development of new diagnostic methods based on molecular biology has led to evidence of the important role of respiratory viruses in chronic obstructive pulmonary disease (COPD) exacerbations. Cytokines and chemokines are recognized as key actors in the pathogenesis of COPD. The objective of this study was to evaluate the association between viral infection and host cytokine responses in 57 COPD patients hospitalized with an acute exacerbation. Seventeen cytokines were profiled using a Luminex-Biorad multiplex assay in plasma samples collected in the first 24 h following hospital admission. Stepwise linear regression analysis was performed, taking into account the influence of seven potential confounding factors in the results. Twenty-four out of 57 showed radiological signs of community-acquired pneumonia (CAP) at hospital admission, 25 patients required admission to the intensive care unit (ICU), 20 had a bacterial infection, and 20 showed a detectable respiratory virus in pharyngeal swabs. Regression analysis showed that viral infection correlated with higher levels of interleukin-6 (IL-6) (log value of the coefficient of regression B, p=0.47, 0.044), and monocyte chemoattractant protein-1 (MCP-1) (p=0.43, 0.019), and increased admission to the ICU. Viral infection also correlated with higher levels of interferon-γ (IFN-γ) (p=0.70, 0.026), which, in turn, was inversely associated with the severity of illness. Finally, viral infection was independently associated with higher levels of tumor necrosis factor-α (TNF-α) (p=0.40, 0.002). Thus our study demonstrates that in patients with COPD exacerbations, viral infection is directly associated with higher systemic levels of cytokines central to the development of the antiviral response, which are also known to contribute to inflammation-mediated tissue damage. These results reveal a potential specific role of viral infection in the pathogenesis of COPD exacerbations.