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Alejandro Jaime-Villalonga, Zane Saul, Goran Miljkovic
Many large series studies have reported that non-tuberculous mycobacteria (NMT) can be attributed to both pulmonary and extrapulmonary diseases. Of the extrapulmonary diseases caused by NMT, skin and soft tissue infection was the most common (Chen et al., 2011). These infections were usually associated with surgical procedures or trauma (Senda et al., 2011; Beam et al., 2014; Legout et al., 2012; Chen et al., 2011). Mycobacteria arupense is an extremely rare cause of soft tissue infection and osteomyelitis.
Adeel A. Butt, Peng Yan, Samia Aslam, Kenneth E. Sherman, Dawd Siraj, Nasia Safdar, Bilal Hameed
Miguel Angel Aguilar-Luis, Juana del Valle-Mendoza, Wilmer Silva-Caso, Tamara Gil-Ramirez, Saul Levy-Blichtein, Jorge Bazán-Mayra, Victor Zavaleta-Gavidia, Daniel Cornejo-Pacherres, Carlos Palomares-Reyes, Luis J. del Valle
Infection caused by Mayaro virus (MAYV) is considered a neglected tropical disease by the World Health Organization (WHO) and represent an important public health challenge (Marcondes et al., 2017). MAYV cases in humans have been limited to Central and South America, particularly in regions around of the Amazon basin, with some exported cases by travelers (Mackay and Arden, 2016). It was first isolated in Trinidad and Tobago from the blood of five symptomatic infected humans during August and September of 1954 (Anderson et al., 1957) and later native human cases have happened in Brazil (1955), Bolivia (1959) Surinam (1964), Peru (1965), Ecuador (1997), Venezuela (2000), Mexico (2001) and Haiti (2015).
Kacper Toczylowski, Sambor Grygorczuk, Joanna Osada, Malgorzata Wojtkowska, Ewa Bojkiewicz, Marta Wozinska-Klepadlo, Paulina Potocka, Artur Sulik
Kingbherly L. Li, Cybele Lara R. Abad
Fengmin Huo, Fuzhen Zhang, Yi Xue, Yuanyuan Shang, Qian Liang, Yifeng Ma, Yunxu Li, Liping Zhao, Yu Pang
The global control of tuberculosis (TB) remains a major challenge due to the epidemic of drug-resistant tuberculosis, especially multidrug-resistant tuberculosis (MDR-TB), which is resistant to rifampin and isoniazid (Zhao et al., 2012; Zhang et al., 2014b). According to recent WHO global estimates, there were 480,000 MDR-TB cases in 2017 (WHO,2018). Almost half of the global MDR-TB cases occurred in China and India (WHO,2018). Due to resistance to both of the most effective antituberculosis drugs, the treatment of MDR-TB requires the use of the less effective and more toxic second-line drugs; approximately half of MDR-TB patients achieve favorable outcomes by the end of prolonged treatment (Velasquez et al., 2014; Xu et al., 2018).
Boris Shaskolskiy, Ekaterina Dementieva, Ilya Kandinov, Alexander Chestkov, Alexey Kubanov, Dmitry Deryabin, Dmitry Gryadunov
Hatch, N. D., Ouellette, S. P.
Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infections, and C. pneumoniae causes community-acquired respiratory infections. In vivo, the host immune system will release interferon-gamma (IFN) to combat infection. IFN activates human cells to produce the tryptophan (trp) catabolizing enzyme, IDO. Consequently, there is a reduction in cytosolic trp in IFN-activated host cells. In evolving to obligate intracellular dependence, Chlamydia has significantly reduced its genome size and content as it relies on the host cell for various nutrients. Importantly, C. trachomatis and C. pneumoniae are trp auxotrophs and are starved for this essential nutrient when the human host cell is exposed to IFN. To survive this, chlamydiae enter an alternative developmental state referred to as persistence. Chlamydial persistence is characterized by a halt in the division cycle, aberrant morphology, and, in the case of IFN-induced persistence, trp codon-dependent changes in transcription. We hypothesize that these changes in transcription are dependent on the particular amino acid starvation state. To investigate the chlamydial response mechanisms acting when other amino acids become limiting, we tested the efficacy of prokaryotic specific tRNA synthetase inhibitors, indolmycin and AN3365, to mimic starvation of trp and leucine, respectively. We show that these drugs block chlamydial growth and induce changes in morphology and transcription consistent with persistence. Importantly, growth inhibition was reversed when the compounds were removed from the medium. With these data, we find that indolmycin and AN3365 are valid tools that can be used to mimic the persistent state independently of IFN.
Delbaz, A., Chen, M., Jen, F. E.- C., Schulz, B. L., Gorse, A.-D., Jennings, M. P., St John, J. A., Ekberg, J. A. K.
Neisseria meningitidis, a common cause of sepsis and bacterial meningitis, infects the meninges and central nervous system (CNS) primarily via paracellular traversal across the blood-brain or blood-cerebrospinal fluid barrier. N. meningitidis is often present asymptomatically in the nasopharynx, and the nerves extending between the nasal cavity and the brain constitute an alternative route by which the meningococci may reach the CNS. To date, the cellular mechanisms involved in nerve infection are not fully understood. Peripheral nerve glial cells are phagocytic and capable of eliminating microorganisms, but some pathogens may be able to overcome this protection mechanism and instead infect the glia, causing cell death or pathology. Here, we show that N. meningitidis readily infects trigeminal Schwann cells (the glial cells of the trigeminal nerve) in vitro in both two-dimensional and three-dimensional cell cultures. Infection of trigeminal Schwann cells may be one mechanism by which N. meningitidis is able to invade the CNS. Infection of the cells led to multinucleation and the appearance of atypical nuclei, with the presence of horseshoe nuclei and budding of nuclei increasing over time. Using SWATH-MS proteomics followed by bioinformatics pathway analysis, we showed that N. meningitidis induced protein alterations in the glia associated with altered intercellular signalling, cell-cell interactions and cellular movement. The analysis also suggested that the alterations in protein levels were consistent with changes occurring in cancer. Thus, infection of the trigeminal nerve by N. meningitidis may have ongoing adverse effects on the biology of Schwann cells, which may lead to pathology.
Lupianez, C. B., Martinez-Bueno, M., Sanchez-Maldonado, J. M., Badiola, J., Cunha, C., Springer, J., Lackner, M., Segura-Catena, J., Canet, L. M., Alcazar-Fuoli, L., Lopez-Nevot, M. A., Fianchi, L., Aguado, J. M., Pagano, L., Lopez-Fernandez, E., Alarcon-Riquelme, M., Potenza, L., Goncalves, S. M., Luppi, M., Moratalla, L., Solano, C., Sampedro, A., Gonzalez-Sierra, P., Cuenca-Estrella, M., Lagrou, K., Maertens, J. A., Lass-Flörl, C., Einsele, H., Vazquez, L., PCRAGA Study Group, Loeffler, J., Rios-
Invasive Aspergillosis (IA) is a life-threatening infection that affects an increasing number of patients undergoing chemotherapy or allo-transplant and recent studies have shown that genetic factors contribute to disease susceptibility. In this two-stage population-based case-control study, we evaluated whether 7 potentially functional single nucleotide polymorphisms (SNPs) within the ARNT2 and CX3CR1 genes influence the risk of IA in high-risk haematological patients. We genotyped selected SNPs in a cohort of 500 haematological patients (103 of those diagnosed with proven or probable IA) and we evaluated their association with the risk of developing IA. The association of the most interesting markers with IA risk was then validated in a replication population including 474 subjects (94 IA and 380 non-IA). Functional experiments were also performed to confirm the biological relevance of the most interesting markers. The meta-analysis of both populations showed that carriers of the ARNT2rs1374213G, CX3CR1rs7631529A and CX3CR1rs9823718G alleles had a significantly increased risk of developing IA according to a log-additive model (PMeta=9.8•10-5; PMeta=1.5•10-4 and PMeta=7.9•10-5). Haplotype analysis also confirmed the association of the CX3CR1AGCGG haplotype with an increased risk of IA (P=4.0•10-4). Mechanistically, we observed that monocyte-derived macrophages (MDM) from subjects carrying the ARNTR2rs1374213G allele or the GG genotype showed a significantly impaired fungicidal activity whereas MDM from carriers of the ARNT2rs1374213G and CX3CR1rs9823718G or CX3CR1rs7631529A alleles had deregulated immune responses against Aspergillus conidia. These results together with those from eQTL data browsers showing a strong correlation of the CX3CR1rs9823718G allele with lower levels of CX3CR1 mRNA in whole peripheral blood (P=2.46•10-7) and primary monocytes (P=4.31•10-7), highlight the role of ARNT2 and CX3CR1 loci in modulating and predicting IA risk and provide new insights into the host immune mechanisms involved in IA development.
Ji, X., Zhang, X., Li, H., Sun, L., Hou, X., Song, H., Han, L., Xu, S., Qiu, X., Wang, X., Zheng, N., Li, Z.
The mechanism underlying the pathogenesis of Nocardia is not fully known. The Nfa34810 protein of Nocardia farcinica has been predicted to be a virulence factor. However, relatively little is known regarding the interaction of Nfa34810 with host cells, specifically invasion and innate immune activation. In this study, we aimed to determine the role of recombinant Nfa34810 during infection. We demonstrated that Nfa34810 is a immunodominant protein located in the cell wall. Nfa34810 protein was able to facilitate the uptake and internalization of latex beads coated with Nfa34810 protein into HeLa cells. Furthermore, the deletion of the nfa34810 gene in N. farcinica attenuated the ability of the bacteria to infect both HeLa and A549 cells. Moreover, stimulation with Nfa34810 triggered macrophages to produce TNF-α, and it also activated mitogen-activated protein kinase (MAPK) and nuclear factor B (NF-B) signaling pathways by inducing the phosphorylation of ERK1/2, p38, JNK, p65, and AKT in macrophages. Specific inhibitors of ERK1/2, JNK, and NF-B significantly reduced the expression of TNF-α, which demonstrated that Nfa34810-mediated TNF-α production was dependent upon the activation of these kinases. We further found that neutralizing antibodies against TLR4 significantly inhibited TNF-α secretion. Taken together, our results indicated that Nfa34810 is a virulence factor of N. farcinica and plays an important role during infection. Besides, Nfa34810 induced production of TNF-α in macrophages involves ERK, JNK, and NF-B via the TLR4 pathway.
Igietseme, J. U., Partin, J., George, Z., Omosun, Y., Goldstein, J., Joseph, K., Ellerson, D., Eko, F. O., Pohl, J., Bandea, C., Black, C. M.
Human genital Chlamydia infection is a major public health concern due to the serious reproductive system complications. Chlamydia binds several receptor tyrosine kinases (RTKs) on host cells, including the epidermal growth factor receptor (EGFR) and activates cellular signaling cascades for host invasion, cytoskeletal remodeling, optimal inclusion development, and induction of pathogenic epithelial-mesenchyme transition (EMT). Chlamydia also upregulates TGF-β expression whose signaling pathway synergizes with the EGFR cascade, but its role in infectivity, inclusions and EMT induction is unknown. We hypothesized that the EGFR and TGF-β signaling pathways cooperate during chlamydial infection for optimal inclusion development and stable EMT induction. The results revealed that Chlamydia upregulated TGF-β expression as early as 6 h post-infection of epithelial cells and stimulated both the EGFR and TGF-β signaling pathways. Inhibition of either the EGFR or TGF-βR1 signaling substantially reduced inclusions development; however, the combined inhibition of both EGFR and TGF-βR1 signaling reduced inclusions by over 90% and prevented EMT induction. Importantly, EGFR inhibition suppressed TGF-β expression, and an inhibitory thrombospondin-1 (Tsp1)-based peptide inhibited chlamydia-induced EMT, revealing a major source of active TGF-βduring infection. Finally, TGF-βR signaling inhibition suppressed the expression of transforming acidic coiled-coil protein-3 (TACC3) that stabilizes EGFR signaling, suggesting a reciprocal regulation between TGF-β and EGFR signaling during chlamydial infection. Thus, RTK-mediated host invasion by chlamydia upregulated TGF-β expression and signaling, which cooperated with other cellular signaling cascades and cytoskeletal remodeling to support optimal inclusion development and EMT induction. The finding may provide new targets for chlamydial disease biomarkers and prevention.
Garcia-Senosiain, A., Kana, I. H., Singh, S. K., Chourasia, B. K., Das, M. K., Dodoo, D., Singh, S., Adu, B., Theisen, M.
Development of a successful blood-stage vaccine against Plasmodium falciparum malaria remains a high priority. Immune-epidemiological studies are effective tools for the identification of antigenic-targets of naturally acquired immunity (NAI) against malaria. However, differences in study design and methodology may compromise inter-study comparisons. Here, we assessed antibody responses against intact merozoites and a panel of 24 recombinant merozoite antigens in longitudinal cohort studies of Ghanaian (n = 115) and Indian (n=121) populations using the same reagents and statistical methods. Anti-merozoites antibodies were associated with NAI in both the Indian (hazard ratio [lsqb]HR[rsqb] = 0.41, p = 0.020) and the Ghanaian (HR = 0.17, p < 0.001) participants. Of the 24 antigen-specific antibodies quantified, 12 and 8 were found to be protective in India and Ghana, respectively. Using LASSO regression, a powerful variable sub-selection technique, we identified subsets of four (MSP6, MSP3.7, MSPDBL2, and Pf12) and five (cMSP33D7, MSP3.3, MSPDBL1, GLURP-R2, and RALP-1) antigens which explained NAI better than the individual antibodies in India (HR=0.18, p< 0.001) and Ghana (HR=0.31, p< 0.001), respectively. IgG1 and/or IgG3 subclasses against five antigens from these subsets were associated with protection. Through this comparative study, maintaining uniformity of reagents and methodology, we demonstrate that NAI across diverse geographic regions may result from antibodies to multiple antigenic targets which constitute the peripheral merozoite surface protein complexes.
Granland, C. M., Scott, N. M., Lauzon-Joset, J.-F., Langereis, J. D., de Gier, C., Sutherland, K., Clark, S. L., Pickering, J. L., Thornton, R. B., Richmond, P. C., Strickland, D. H., Kirkham, L.-A. S.
Background: Nasopharyngeal colonisation with nontypeable Haemophilus influenzae (NTHi) is a prerequisite for developing NTHi-associated infections, including otitis media. Therapies that block NTHi colonisation may prevent disease development. We previously demonstrated that Haemophilus haemolyticus, a closely related human commensal, can inhibit NTHi colonisation and infection of human respiratory epithelium in vitro. We have now assessed whether Muribacter muris (a rodent commensal from the same family) can prevent NTHi colonisation and disease in vivo using a murine NTHi otitis media model.Methods: Otitis media was modelled in BALB/c mice using coinfection with 1x104.5 plaque-forming units of Influenza A virus MEM H3N2, followed by intranasal challenge with 5x107 CFU of NTHi R2866SpecR. Mice were pre-treated or not with an intranasal inoculation of 5x107 CFU M. muris 24h before coinfection. NTHi and M. muris viable counts and inflammatory mediators (IFN, IL-1β, IL-6, KC and IL-10) were measured in nasal washes and middle ear tissue homogenate.Results: M. muris pre-treatment decreased the median colonisation density of NTHi from 6x105 CFU/mL to 9x103 CFU/mL; p=0.0004. Only 1/12 M. muris pre-treated mice developed otitis media on Day 5 compared to 8/15 mice with no pre-treatment; 8% vs 53%, p=0.0192. Inflammation, clinical score and weight loss were also lower in M. muris pre-treated mice.Conclusion: We have demonstrated that a single dose of a closely related commensal can delay onset of NTHi otitis media in vivo. Human challenge studies investigating prevention of NTHi colonisation are warranted to reduce the global burden of otitis media and other NTHi diseases.
Derrick, T., Ramadhani, A. M., Macleod, D., Massae, P., Mafuru, E., Aiweda, M., Mbuya, K., Makupa, W., Mtuy, T., Bailey, R. L., Mabey, D. C. W., Holland, M. J., Burton, M. J.
Trachoma is initiated during childhood following repeated conjunctival infection with Chlamydia trachomatis, which causes a chronic inflammatory response in some individuals that leads to scarring and in-turning of the eyelids in later life. There is currently no treatment to halt the progression of scarring trachoma due to an incomplete understanding of disease pathogenesis.A cohort study was performed in northern Tanzania in 616 children aged 6-10 at enrolment. Every three months for four years, children were examined for clinical signs of trachoma and conjunctival swabs were collected for C. trachomatis detection and to analyse the expression of 46 immuno-fibrogenic genes. Data were analysed in relation to progressive scarring status between baseline and the final time-point.Genes that were significantly associated with scarring progression included pro-inflammatory chemokines (CXCL5, CCL20, CXCL13, CCL18), cytokines (IL23A, IL19, IL1B), matrix modifiers (MMP12, SPARCL1), immune-regulators (IDO1, SOCS3, IL10) and pro-inflammatory antimicrobial peptide S100A7. IL23A and PDGF were significantly upregulated in scarring progressors in response to C. trachomatis infection relative to non-progressors.Our findings highlight the importance of innate pro-inflammatory signals from the epithelium and implicate IL-23A-responsive cells in driving trachomatous scarring, with potential key mechanistic roles for PDGFB, MMP12 and SPARCL1 in orchestrating fibrosis.
Gjonbalaj, M., Keith, J. W., Do, M. H., Hohl, T. M., Pamer, E. G., Becattini, S.
The complex bacterial populations that constitute the gut microbiota can harbor antibiotic-resistance genes (ARGs), including those encoding for β-lactamase enzymes (BLA), which degrade commonly prescribed antibiotics such as ampicillin. Prevalence of such genes in commensal bacteria has been increased in recent years by the wide use of antibiotics in human populations and in livestock. While transfer of ARGs between bacterial species has well-established dramatic public health implications, these genes can also function in trans within bacterial consortia, where antibiotic-resistant bacteria can provide antibiotic-sensitive neighbors with leaky protection from drugs, as shown both in vitro and in vivo, in models of lung and subcutaneous co-infection.However, whether expression of ARGs by harmless commensal bacterial species can destroy antibiotics in the intestinal lumen and shield antibiotic-sensitive pathogens is unknown. To address this question, we colonized GF or WT mice with a model intestinal commensal strain of E. coli that produces either functional or defective BLA. Mice were subsequently infected with Listeria monocytogenes or Clostridioides difficile followed by treatment with oral ampicillin. Production of functional BLA by commensal E. coli markedly reduced clearance of these pathogens and enhanced systemic dissemination during ampicillin treatment. Pathogen resistance was independent of ARG acquisition via horizontal gene transfer but instead relied on antibiotic degradation in the intestinal lumen by BLA. We conclude that commensal bacteria that have acquired ARGs can mediate shielding of pathogens from the bactericidal effects of antibiotics.
Mojca Maticic, Andrea Lombardi, Mario U. Mondelli, Massimo Colombo, ESCMID Study Group for Viral Hepatitis (ESGVH)
Chronic hepatitis C virus (HCV) infection affects 71 million people worldwide. The availability of highly efficient direct acting antivirals has revolutionized the treatment landscape with over 95% cure rates. World Health Organization (WHO) has launched a global program to achieve rather ambitious HCV elimination targets for 2030.
Cryptococcal meningitis (CCM) is a common and deadly disease among HIV-infected patients. Notable about CCM is its association with the immune reconstitution inflammatory syndrome (IRIS). Though it has been posited a switch from first to second-line antiretroviral therapy (ART) can induce CCM IRIS, a case presentation of CCM IRIS has not been published.
A 10-year-old, HIV-infected girl who initially presented with severe headache and new-onset seizures, with cerebrospinal fluid that returned antigen, India Ink, and culture positive for Cryptococcus neoformans. Notably, 8 weeks prior to seizures, she had switched from first line to second-line ART (abacavir-lamivudine-efavirenz to zidovudine-lamivudine-lopinavir/ritonavir) due to virologic failure, with a viral load of 224,000 copies/milliliter. At time of seizures and 8 weeks on second-line ART, her viral load had reduced to 262 copies/milliliter.
Her hospital course was prolonged, as she had ongoing headaches and developed bilateral cranial nerve VI palsies despite clearance of Cryptococcus from cerebrospinal fluid on antifungal therapy and therapeutic lumbar punctures. However, symptoms stabilized, and she was discharged with oral fluconazole. Cranial nerve palsies resolved 10 weeks post discharge and she has remained disease free.
We describe a case of CCM IRIS in a 10-year-old HIV infected child after changing to second-line ART. This case provides evidence that screening for cryptococcal antigenaemia prior to switch from first-line to second-line ART could be an important measure to prevent cryptococcal disease.
The impact of HIV-1 subtype (CRF01_AE and non-CRF01_AE) on HIV-1 DNA levels in HIV-1 chronically infected patients with suppressive antiretroviral therapy (ART) remains poorly understood. To evaluate the correlation of HIV-1 subtype with DNA level, and identify baseline predictors of HIV-1 DNA decay.
ART-naïve HIV-1-infected patients from two large multi-center studies in China were classified into CRF01_AE and non-CRF01_AE subtype groups. Peripheral blood samples were collected at baseline and week 12, 24, 48 and 96 after ART initiation and total HIV-1 DNA levels were quantified by real-time PCR. HIV-1 DNA levels at week 96 were categorized into high, moderate, and low levels, reflecting HIV-1 DNA ≥ 3, 2–3, ≤ 2 log10 copies/106 PBMCs, respectively, and the corresponding proportion of CRF01_AE and non-CRF01_AE subtype were compared. The baseline predictors of low HIV-1 total DNA levels (≤ 2 log10 copies/106 PBMCs) at week 96 were evaluated using a logistic regression model.
Compared to the non-CRF01_AE subtypes (n = 185), patients with CRF01_AE subtype (n = 188) harboured a higher level of HIV-1 DNA (median: 3.19 vs. 2.95 log10 copies/106 PBMCs, P
The aim of our study was to analyze the risk factors of nosocomial infection after cardiac surgery in children with congenital heart disease (CHD).
We performed a retrospective cohort study, and children with CHD who underwent open-heart surgeries at Shanghai Children’s Medical Center from January 1, 2012 to December 31, 2018 were included. The baseline characteristics of these patients of different ages, including neonates (0–1 months old), infants (1–12 months old) and children (1–10 years old), were analyzed, and the association of risk factors with postoperative nosocomial infection were assessed.
A total of 11,651 subjects were included in the study. The overall nosocomial infection rate was 10.8%. Nosocomial infection rates in neonates, infants, and children with congenital heart disease were 32.9, 15.4, and 5.2%, respectively. Multivariate logistic regression analysis found age (OR 0798, 95%CI: 0.769–0.829; P
The immune response during falciparum malaria mediates both harmful and protective effects on the host; however the participating molecules have not been fully defined. Interleukin (IL)-27 is a pleiotropic cytokine exerting both inflammatory and anti-inflammatory effects, but data on IL-27 in malaria patients are scarce.
Clinical data and blood samples were collected from adults in Mozambique with P. falciparum infection, with (n = 70) and without (n = 61) HIV-1 co-infection, from HIV-infected patients with similar symptoms without malaria (n = 58) and from healthy controls (n = 52). In vitro studies were performed in endothelial cells and PBMC using hemozoin crystals. Samples were analyzed using enzyme immunoassays and quantitative PCR.
(i) IL-27 was markedly up-regulated in malaria patients compared with controls and HIV-infected patients without malaria, showing no relation to HIV co-infection. (ii) IL-27 was correlated with P. falciparum parasitemia and von Willebrand factor as a marker of endothelial activation, but not with disease severity. (iii) In vitro, IL-27 modulated the hemozoin-mediated cytokine response in endothelial cells and PBMC with enhancing effects on IL-6 and attenuating effects on IL-8.
Our findings show that IL-27 is regulated during falciparum malaria, mediating both inflammatory and anti-inflammatory effects, potentially playing an immune-regulatory role during falciparum malaria.
Timely infant testing for HIV is critical to ensure optimal treatment outcomes among exposed infants. While world health organization recommends HIV exposed infants to be tested between 4 to 6 weeks of age, in developing countries like Ethiopia, access to timely infant testing is still very limited. The study is intended to assess timely infant testing, testing for HIV at the 18th month, test results and factors influencing HIV positivity among infants born to HIV positive mothers in public hospitals of Mekelle, Ethiopia.
A cross-sectional study design was employed on 558 HIV exposed infants, using consecutive sampling technique. A checklist was used to extract 4 years (January 2014–December 2017) secondary data, collected from January–April 2018. Data were analyzed using SPSS version 20, and binary logistic regression model was used to examine the association of independent variables with the outcome variables.
Timely infant testing for HIV accounted for 346(62.0%). Mothers who attended antenatal care (AOR: 2.77; 95% CI: 1.17, 6.55) and who were counselled on feeding options (AOR: 2.01; 95% CI: 1.11, 3.65) were strongly associated with timely infant testing. Poor maternal adherence status was associated with infants’ HIV positivity at the 18th month of antibody test (AOR: 15.93; 95% CI: 2.21, 94.66). Being rural resident (AOR: 4.0; 95% CI: 1.23, 13.04), being low birth weight (AOR: 5.64; 95% CI: 2.00, 16.71) and not receiving ARV prophylaxis (AOR: 4.70; 95% CI: 1.15, 19.11) were positively associated with the overall HIV positivity.
A considerable proportion of exposed infants did not undergo timely testing for HIV. Antenatal care follow-up and counselling on feeding options were associated with timely infant testing. Mother’s poor adherence status was associated with infant’s HIV positivity at the 18th month of antibody testing. Being rural resident, being low birth weight, and not receiving ARV prophylaxis were the factors that enhance the overall HIV positivity. Timely infant testing, counselling on feeding options and adherence should be intensified, and prevention of mother-to-child transmission program in rural settings need to be strengthened.
P. A. Minchella,
E. R. Rottinghaus,
G. L. Ouedraogo,
J. N. Nkengasong
Tropical Medicine &International Health, EarlyView.
Following publication of the original article , it was brought to the authors’ attention that one of the names in the author list had been provided with the incorrect spelling.
Because clustering of Plasmodium falciparum infection had been noted previously, the clustering of infection was examined at four field sites in West Africa: Dangassa and Dioro in Mali, Gambissara in The Gambia and Madina Fall in Senegal.
Clustering of infection was defined by the percent of persons with positive slides for asexual P. falciparum sleeping in a house which had been geopositioned. Data from each site were then tested for spatial, temporal and spatio-temporal clustering in relation to the prevalence of infection from smear surveys.
These studies suggest that clustering of P. falciparum infection also affects the effectiveness of control interventions. For example, the clustering of infection in Madina Fall disappeared in 2014–2016 after vector control eliminated the only breeding site in 2013. In contrast, the temporal clustering of infection in Dioro (rainy season of 2014, dry season of 2015) was consistent with the loss of funding for Dioro in the second quarter of 2014 and disappeared when funds again became available in late 2015. The clustering of infection in rural (western) areas of Gambissara was consistent with known rural–urban differences in the prevalence of infection and with the thatched roofs, open eaves and mud walls of houses in rural Gambissara. In contrast, the most intense transmission was in Dangassa, where the only encouraging observation was a lower prevalence of infection in the dry season. Taken together, these results suggest: (a) the transmission of infection was stopped in Madina Fall by eliminating the only known breeding site, (b) the prevalence of infection was reduced in Dioro after financial support became available again for malaria control in the second half of 2015, (c) improvements in housing should improve malaria control by reducing the number of vectors in rural communities such as western Gambissara, and (d) beginning malaria control during the dry season may reduce transmission in hyperendemic areas such as Dangassa.
From a conceptual perspective, testing for spatial, temporal and spatio-temporal clustering based on epidemiologic data permits the generation of hypotheses for the clustering observed and the testing of candidate interventions to confirm or refute those hypotheses.
International Congress on Infectious Diseases (ICID) 2020
Kuala Lumpur, Malaysia
20.02.2020 - 23.02.2020
Dansk Selskab for Intern Medicin (DSIM) årsmøde og overrækkelse af Hagedorn prisen 2020
Novo Nordisk Fonden, Tuborg Havnevej 19, 2900 Hellerup
Conference on Retroviruses and Opportunistic Infections (CROI) 2020
Boston, Massachusetts, USA
8.03.2020 - 11.03.2020
Når CROI går i fisk - med transmissioner fra CROI 2020
10.03.2020 - 11.03.2020
World TB day 2020
National handlingsplan for antibiotika til mennesker (2017)
Retningslinjer til sundhedsprofessionelle vedr. håndtering af infektion med zikavirus (2019)
Antiviral behandling af hiv smittede personer (2019)
Yield, Efficiency and Costs of Mass Screening Algorithms for Tuberculosis in Brazilian Prisons
17.02.2020Clinical Infectious Diseases Advance Access
Detecting Tuberculosis in Prisons: Switching Off the Disease at its Source
17.02.2020Clinical Infectious Diseases Advance Access
Effect of diabetes mellitus on short-term prognosis of 227 pyogenic liver abscess patients after hospitalization
17.02.2020Latest Results for BMC Infectious Diseases
Terlipressin Increases Systemic and Lowers Pulmonary Arterial Pressure in Experimental Acute Pulmonary Embolism
15.02.2020Critical Care Medicine - Online First
Sustained reduction in third-generation cephalosporin usage in adult inpatients following introduction of an antimicrobial stewardship program in a large urban hospital in Malawi
15.02.2020Clinical Infectious Diseases Advance Access
Hvorfor anbefaler Professor Jens Lundgren artiklen"Dolutegravir plus Two Different Prodrugs of Tenofovir to Treat HIV."?
Hvad mener Professor Troels Lillebæk om artiklen"The global prevalence of latent tuberculosis: a systematic review and meta-analysis."?
Hvorfor anbefaler Professor Lars Østergaard artiklen"Efficacy of antibiotic treatment in patients with chronic low back pain and Modic changes (the AIM study): double blind, randomised, placebo controlled, multicentre trial."?
Hvorfor anbefaler Professor Thomas Benfield artiklen"Oral versus Intravenous Antibiotics for Bone and Joint Infection."?
Hvad mener Professor Niels Obel om artiklen"Early, Goal-Directed Therapy for Septic Shock - A Patient-Level Meta-Analysis."?
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