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Dacheux, M., Sinou, V., Payre, C., Jeammet, L., Parzy, D., Grellier, P., Deregnaucourt, C., Lambeau, G.
The human group IIA secreted phospholipase A2 (hGIIA sPLA2) is increased in the plasma of malaria patients but its role is unknown. In parasite culture with normal plasma, hGIIA is inactive against Plasmodium falciparum, contrasting with hGIIF, hGV and hGX sPLA2s that readily hydrolyze plasma lipoproteins, release non-esterified fatty acids (NEFAs) and inhibit parasite growth. Here, we revisited the anti-Plasmodium activity of hGIIA in conditions closer to malaria physiopathology where lipoproteins are oxidized. In parasite culture containing oxidized lipoproteins, hGIIA sPLA2 was inhibitory with an IC50 value of 150.0 ± 40.8 nM, in accordance with its capacity to release NEFAs from oxidized particles. With oxidized lipoproteins, hGIIF, hGV and hGX sPLA2s were also more potent, by 4.6-, 2.1- and 1.9-fold, respectively. Using specific immunoassays, we found that hGIIA sPLA2 is increased in plasma from 41 patients with malaria over healthy donors (median (IQR): 1.6 (0.7-3.4) nM, versus 0.0 (0.0-0.1) nM, respectively; P
Holland T, Davis J.
Jorgensen S, Zasowski E, Trinh T, et al.
AbstractBackgroundMounting evidence suggests the addition of a beta-lactam (BL) to daptomycin (DAP) results in synergistic in vitro activity against methicillin-resistant Staphylococcus aureus (MRSA) and bolsters the innate immune response to infection. The objective of this study was to provide clinical translation to this experimental data and determine if DAP+BL combination therapy results in improved clinical outcomes compared to treatment with DAP alone in patients with MRSA bloodstream infections (BSI).MethodsThis was a retrospective, comparative cohort study conducted at two academic medical centers between 2008 and 2018. Adults with MRSA BSI treated with DAP for ≥72 hours and initiated within five days of culture collection were included. Patients who received a BL for ≥24 hours and initiated within 24 hours of DAP comprised the DAP+BL group. The primary outcome was composite clinical failure (60-day all-cause mortality and/or 60-day recurrence). Analyses were adjusted for confounding using inverse probability of treatment weighting (IPTW).ResultsA total of 229 patients were included (72 DAP+BL and 157 DAP). In unadjusted and IPTW-adjusted analyses, DAP+BL was associated with significantly reduced odds of clinical failure (OR 0.362, 95% CI 0.164, 0.801; aOR 0.386, 95% CI 0.175, 0.853). Adjusted analyses restricted to pre-specified subgroups based on infection complexity and baseline health status, were consistent with the main analysis.ConclusionsThe addition of a BL to DAP was associated with improved clinical outcomes in patients with MRSA BSI. This study provides support to ongoing and future studies evaluating the impact of combination therapy for invasive MRSA infections.
Vecchio A, Marra C, Schouten J, et al.
AbstractBackgroundThe prevalence of distal sensory peripheral neuropathy (DSPN) varies among persons living with HIV (PLWH). Here we estimate DSPN prevalence in seven resource limited settings (RLS) for combined antiretroviral therapy (cART)-naive PLWH compared to matched HIV- participants and in PLWH who achieved virologic suppression on one of three cART regimens.MethodsPLWH with a CD4+ count < 300 cells/mm3 underwent standardized neurological examination and functional status assessments before and every 24 weeks after starting cART. Matched HIV- individuals, underwent the same examinations once. Longitudinal analysis was restricted to PLWH who remained virologically suppressed. Associations between covariates with DSPN at entry were assessed by chi square, and with longitudinal DPSN were assessed using generalized estimating equations.ResultsBefore initiating cART, 21.3% of HIV+ participants had DSPN, compared to 8.5% of HIV- people (n = 2400) (χ2(df =1) = 96.5, p< .00001). PLWH with DSPN were more likely to report inability to work (χ2(df =1) = 10.6, p= .001) and depression (χ2(df =1) = 8.9, p= .003) than PLWH without DSPN. After beginning cART, overall prevalence of DSPN decreased: 20.3% at week 48, 15.3% at week 144, 10.3% at week 192. Incident DSPN was seen in 127 PLWH. Longitudinally, DSPN was more likely in older individuals (p
Ahmed S, Pondo T, Xing W, et al.
AbstractBackgroundThe 13-valent pneumococcal vaccine (PCV13) was introduced for U.S. children in 2010, and for immunocompromised adults ≥19 years old in series with the 23-valent polysaccharide vaccine (PPSV23) in 2012. To quantify indirect effects before the 2014 introduction of PCV13 for all adults ≥65 years old, we evaluated PCV13 impact on invasive pneumococcal disease (IPD) among adults with and without PCV13 indications.MethodsWe estimated IPD incidence using Active Bacterial Core surveillance and National Health Interview Survey. We compared incidence in 2013–2014 and 2007–2008, by age and serotype group (PCV13, PPSV23-unique, or types in neither vaccine [NVT]), among adults with and without PCV13 indications.ResultsIPD incidence declined among all adults. Among adults 19–64 years, PCV13-type IPD declined 57% (95%CI:-68,-43) in adults with immunocompromising conditions (IC, indication for PCV13 use), 57% (95%CI:-62, -52) in immunocompetent adults with chronic medical conditions (CMC, indications for PPSV23 use alone), and 74% (95%CI:-78,-70) in adults with neither vaccine indication. Among adults ≥65 years, PCV13-type IPD decreased 68% (95%CI:-76,-60) in those with IC, 68% (95%CI:-72,-63) in those with CMC, and 71% (95%CI:-77,-64) in healthy adults. PPSV23-unique types increased in adults 19‒64 years with CMC, and NVT did not change among adults with or without PCV13 indications. From 2013–2014, non-PCV13 serotypes accounted for nearly 80% of IPD.ConclusionIPD incidence among U.S. adults declined after PCV13 introduction in children. Similar reductions in PCV13-type IPD in those with and without PCV13 indications suggest observed benefits are largely due to indirect effects from pediatric PCV13 use rather than direct use among adults.
Yoshioka T, Yaita K, Mizuta S, et al.
Confounding Factors (Epidemiology)BiasBlood TransfusionRegression Analysis
Wang C, Ware R, Lambert S, et al.
AbstractBackgroundHospital-based studies identify Parechovirus (PeV), primarily PeV-A3, as an important cause of severe infections in young children. However, few community-based studies have been published and the true PeV infection burden is unknown. We investigated PeV epidemiology in healthy children participating in a community-based, longitudinal birth cohort study.MethodsAustralian children (n=158) enrolled in the Observational Research in Childhood Infectious Diseases (ORChID) study were followed from birth until their second birthday. Weekly stool and nasal swabs, and daily symptom diaries, were collected. Swabs were tested for PeV by reverse-transcription polymerase chain reaction and genotypes determined by subgenomic sequencing. Incidence rate, infection characteristics, clinical associations, and virus co-detections were investigated.ResultsPeV was detected in 1,423/11,124 (12.8%) and 17/8,100 (0.2%) stool and nasal swabs, respectively. Major genotypes amongst the 306 infection episodes identified were PeV-A1 (47.9%), PeV-A6 (20.1%), and PeV-A3 (18.3%). The incidence rate was 144 episodes/100 child-years (95% confidence interval 128–160). First infections appeared at a median age of 8.0-months (interquartile range 6.0–11.7). Annual seasonal peaks changing from PeV-A1 to PeV-A3 were observed. Infection was positively associated with age ≥6-months, summer season, non-exclusive breastfeeding at age
Weinberger D, Shapiro E.
Nguyen M, Davis M, Wittenberg R, et al.
AbstractBackgroundPosaconazole tablets are well tolerated and efficacious in the prophylaxis and treatment of aspergillosis, mucormycosis, and other invasive fungal infections. There have been case reports of posaconazole-induced pseudohyperaldosteronism, however, its occurrence and association with serum posaconazole drug levels has not previously been investigated.MethodsIn this single-center retrospective observational study, we examined the occurrence of posaconazole-induced pseudohyperaldosteronism (PIPH) in outpatients newly starting posaconazole and evaluated differences in serum posaconazole concentrations and clinical characteristics between those with and without this syndrome.ResultsSixty-nine patients receiving posaconazole were included, of whom 16 (23.2%) met the definition of PIPH. Patients with PIPH were significantly older (61.1 vs 44.7 years, P=0.007) and more frequently had hypertension prior to starting posaconazole (68.8% vs 32.1%, P=0.009). Patients with PIPH had a significantly higher median serum posaconazole level than those without PIPH (3.0 vs 1.2 µg/mL, P
Harris, G., Holbein, B. E., Zhou, H., Xu, H. H., Chen, W.
Porcine mucin has been commonly used to enhance the infectivity of bacterial pathogens including Acinetobacter baumannii in animal models, but the mechanisms for enhancement by mucin remain relatively unknown. In this study, using the mouse model of intraperitoneal (i.p.) mucin-enhanced A. baumannii infection we characterized the kinetics of bacterial replication and dissemination and the host innate immune responses, as well as their potential contribution to the mucin-enhanced bacterial virulence. We found that mucin, either admixed with or separately injected with the challenge bacterial inoculum, was able to enhance the tissue and blood burdens of A. baumannii strains of different virulence. Intraperitoneal injection of A. baumannii/mucin or mucin alone induced a significant, but comparable reduction of peritoneal macrophages and lymphocytes, accompanied with a significant neutrophil recruitment and early IL-10 responses, suggesting that the resulted inflammatory cellular and cytokine responses were largely induced by the mucin. Depletion of peritoneal macrophages or neutralization of endogenous IL-10 activities showed no effect on the mucin-enhanced infectivity. However, pre-treatment of mucin with iron chelator DIBI, but not deferoxamine, partially abolished its virulence enhancement ability and substitution of mucin with iron significantly enhanced the bacterial burdens in peritoneal cavity and lung. Taken together, our results favour the hypothesis that iron is at least partially contributing to the mucin-enhanced infectivity of A. baumannii in this model.
Olson, M. G., Widner, R. E., Jorgenson, L. M., Lawrence, A., Lagundzin, D., Woods, N. T., Ouellette, S. P., Rucks, E. A.
Many intracellular bacteria, including the obligate intracellular pathogen Chlamydia trachomatis, grow within a membrane-bound "bacteria containing vacuole" (BCV). Secreted cytosolic effectors modulate host activity, but an understanding of the host-pathogen interactions that occur at the BCV membrane is limited by the difficulty in purifying membrane fractions from infected host cells. We used the ascorbate peroxidase proximity labeling system (APEX2), which labels proximal proteins with biotin in vivo, to study the protein-protein interactions that occur at the chlamydial vacuolar, or inclusion, membrane. An in vivo understanding of the secreted chlamydial inclusion membrane protein (Inc) interactions (e.g., Inc-Inc and Inc-eukaryotic protein) and how these contribute to overall host-chlamydial interactions at this unique membrane is lacking. We hypothesize some Incs organize the inclusion membrane whereas other Incs bind eukaryotic proteins to promote chlamydial-host interactions. To study this, Incs fused to APEX2 were expressed in C. trachomatis L2. Affinity purification-mass spectrometry (AP-MS) identified biotinylated proteins, which were analyzed for statistical significance using Significance Analysis of INTeractome (SAINT). Broadly supporting both Inc-Inc and Inc-host interactions, our Inc-APEX2 constructs labeled Incs as well as known and previously unreported eukaryotic proteins localizing to the inclusion. We demonstrate that endogenous LRRFIP1 (LRRF1) is recruited to the inclusion by the Inc, CT226, using bacterial two-hybrid and co-immunoprecipitation assays. We further demonstrate interactions between CT226 and the Incs used in our study to reveal a model for inclusion membrane organization. Combined, our data highlight the utility of APEX2 to capture the complex in vivo protein-protein interactions at the chlamydial inclusion.
Miller, H. E., Hoyt, F. H., Heinzen, R. A.
Coxiella burnetii is an intracellular bacterium that causes query or "Q" fever, a disease that typically manifests as a severe flu-like illness. The initial target of C. burnetii is the alveolar macrophage. Here, it regulates vesicle trafficking pathways and fusion events to establish a large replication vacuole called the Coxiella-containing vacuole (CCV). Similar to a phagolysosome, the CCV has an acidic pH and contains lysosomal hydrolases obtained via fusion with late endocytic vesicles. Lysosomal hydrolases break down various lipids, carbohydrates, and proteins; thus, it is assumed C. burnetii derives nutrients for growth from these degradation products. To investigate this possibility, we utilized a GNPTAB-/- HeLa cell line that lacks lysosomal hydrolases in endocytic compartments. Unexpectedly, examination of C. burnetii growth in GNPTAB-/- HeLa cells revealed replication and viability are not impaired, indicating C. burnetii does not require by products of hydrolase degradation to survive and grow in the CCV. However, although bacterial growth was normal, CCVs were abnormal, appearing dark and condensed rather than clear and spacious. Lack of degradation within CCVs allowed waste products to accumulate, including intraluminal vesicles, autophagy protein-LC3, and cholesterol. The build-up of waste products coincided with an altered CCV membrane, where LAMP1 was decreased, and CD63 and LAMP1 redistributed from a punctate to uniform localization. This disruption of CCV membrane organization may account for the decreased CCV size due to impaired fusion with late endocytic vesicles. Collectively, these results demonstrate lysosomal hydrolases are not required for C. burnetii survival and growth but are needed for normal CCV development. These data provide insight into mechanisms of CCV biogenesis while raising the important question of how C. burnetii obtains essential nutrients from its host.
Roth J, Widmer A.
adjustmentdoor openingsurgical site infection
Achan J, Reuling I, Yap X, et al.
AbstractBackgroundWe assessed the impact of exposure to P. falciparum on parasite kinetics, clinical symptoms, and functional immunity after controlled human malaria infection (CHMI) in two cohorts with different levels of previous malarial exposure.MethodsNine adult males with high (sero-high) and ten with low (sero-low) previous exposure received 3200 PfSPZ of PfSPZ Challenge by direct venous inoculation and were followed for 35 days for parasitemia by thick blood smear (TBS) and quantitative polymerase chain reaction (qPCR). End points were time to parasitemia, adverse events and immune responses.ResultsTen of Ten (100%) volunteers in the sero-low and 7 of 9 (77.8%) in the sero-high group developed parasitemia detected by TBS in the first 28 days (p = 0.125). The median time to parasitemia was significantly shorter in the sero-low group [9 days (7.5-11.0) vs.11.3 days (7.5-18.0), log rank test, p=0.005]. Antibody recognition of sporozoites was significantly higher in the sero-high (median 17.93 AU, IQR 12.95-24) than the sero-low volunteers (median 10.54 AU, IQR 8.36-12.12); p=0.006. Presence of blood-stage antibodies was also significantly higher (p=0.0003) in the sero-high group (median 50.98 AU, IQR 22.46-65.07) than in the sero-low group (median 3.16 AU, IQR 2.43-8.71). Growth inhibitory activity (GIA) was significantly higher in the sero-high (median 21.8%, IQR 8.15-29.65) than in the sero-low (median 8.3%, IQR 5.6-10.23) (p=0.025).ConclusionCHMI was safe and well tolerated in this population. Individuals with serological evidence of higher malaria exposure were able to better control infection and had higher parasite growth inhibitory activity.
White, R. C., Truchan, H. K., Zheng, H., Tyson, J. Y., Cianciotto, N. P.
It was previously determined that the type II secretion system (T2SS) promotes the ability of Legionella pneumophila to grow in co-culture with amoebae. Here, we discerned the stage of intracellular infection that is potentiated, by comparing the wild-type and T2SS mutant legionellae for their capacity to parasitize Acanthamoeba castellanii. Whereas the mutant behaved normally for entry into the host cells and subsequent evasion of degradative lysosomes, it was impaired in the ability to replicate, with that defect being first evident at approx. 9 h post-entry. The replication defect was initially documented in three ways; i.e., determining the numbers of CFU recovered from the lysates of the infected monolayers, monitoring the levels of fluorescence associated with amoebal monolayers infected with GFP-expressing bacteria, and utilizing flow cytometry to quantitate the amounts of GFP-expressing bacteria in individual amoebae. By employing confocal microscopy and newer imaging techniques, we further determined the progression in volume and shape of the bacterial vacuoles and found that the T2SS mutant grows at a decreased rate and does not attain maximally-sized phagosomes. Overall, the entire infection cycle (i.e., entry to egress) was considerably slower for the T2SS mutant than it was for the wild-type strain, and the mutant's defect was maintained over multiple rounds of infection. Thus, the T2SS is absolutely required for L. pneumophila to grow to larger numbers in its intravacuolar niche within amoebae. Combining these results with those of our recent analysis of macrophage infection, T2SS is clearly a major component of L. pneumophila intracellular infection.
Jackson, M. D., Wong, S. M., Akerley, B. J.
Nontypeable Haemophilus influenzae (NTHi) efficiently colonizes the human nasopharynx asymptomatically, but also causes respiratory mucosal infections including otitis media, sinusitis, and bronchitis. Lipooligosaccharide (LOS) on the cell surface of NTHi displays complex glycans that mimic host structures, allowing it to evade immune recognition. However, LOS glycans are also targets of host adaptive and innate responses. To aid in evasion of these responses, LOS structures exhibit inter-strain heterogeneity, and are also subject to phase variation, the random on/off switching of gene expression, generating intra-strain population diversity. Specific LOS modifications, including terminal sialylation of the LOS, which exploits host-derived sialic acid (Neu5Ac), can also block recognition of NTHi by bactericidal IgM and complement by mechanisms that are not fully understood. We investigated LOS sialic acid-mediated resistance of NTHi to antibody-directed killing by serum complement. We identified specific LOS structures extending from heptose III that are targets for binding by naturally occurring bactericidal IgM in serum and are protected by sialylation of the LOS. Phase-variable galactosyltransferases encoded by lic2A and lgtC each add a galactose epitope bound by IgM that results in antibody-dependent killing via the classical pathway of complement. NTHi's survival can be influenced by expression of phase-variable structures on the LOS that may also depend on environmental conditions, such as the availability of free sialic acid. Identification of surface structures on NTHi representing potential targets for antibody-based therapies as alternatives to antibiotic treatment would thus be valuable for this medically important pathogen.
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