We found an inverse relationship between pneumonia-associated invasive pneumococcal serotypes and RSV detection during CAAP. This finding may lead to better understanding of the interaction between respiratory viruses and S. pneumoniae in CAAP pathogenesis.
Background
Streptococcus pneumoniae (Pnc) serotypes differ in invasive potential. We examined whether community-acquired alveolar pneumonia (CAAP) in children carrying commonly recognized pneumonia invasive pneumococcal serotypes ([PnIST] 1, 5, 7F, 14, and 19A) differs from CAAP in children carrying less invasive serotypes (non-PnIST) or no Pnc (Pnc-neg).
Methods
Children <5 years, visiting the only regional Pediatric Emergency Room, with radiologically proven CAAP were enrolled. Nasopharyngeal cultures were processed for pneumococcal isolation and serotyping. Clinical and demographic characteristics were recorded. The study was conducted before pneumococcal conjugate vaccine implementation in Israel.
Results
A total of 1423 CAAP episodes were recorded: PnIST, 300 (21.1%); non-PnIST, 591 (41.5%); and Pnc-neg, 532 (37.4%). After adjustment for age, ethnicity, seasonality, and previous antibiotics, the following variables were positively associated with PnIST carriage compared with both groups: temperature ≥39°C, peripheral white blood cell count ≥20 000/mm3, C-reactive protein ≥70.0 mg/L, and serum sodium <135 mEq/L. Lower oxygen saturation, viral detection, and comorbidities were negatively associated with Pn-IST carriage (odds ratios, <1.0). Differences between non-PnIST carriers and Pnc-neg groups were smaller or nonsignificant.
Conclusions
Young children with CAAP carrying common PnIST had a lower proportion of comorbidities, hypoxemia, and viral detection and had more intense systemic inflammatory response than those carrying non-PnIST or not carrying Pnc.
Diabetic foot infections (DFIs) are associated with major morbidity, reduced quality of life and increased mortality. Osteomyelitis is a leading cause of lower-extremity amputation in diabetic patients. We aimed to examine whether a multifaceted strategy for treating hospitalized patients with a DFI effectively influenced microbiological culture results and outcomes. A retrospective cohort-study in a 1100-bed, tertiary-care university hospital was conducted. Adult patients with a DFI admitted to the orthopedics department between 2015 and 2019 were included. During the pre-intervention period (2015-2016), one general orthopedic department was in operation. In the post-intervention period (2017-2019), a second department was created with a designated “complicated wound unit". The multifaceted strategy included revising local guidelines for DFI culturing emphasizing bone cultures, correct sample handling, and adjusting antibiotic treatment to culture results. Additionally, a weekly multidisciplinary-team grand round was instigated and post-discharge outpatient follow-up was scheduled. 652 patients with DFIs were included; 101 during the pre-intervention period and 551 during the post-intervention period. Compared to the pre-intervention, during the post-intervention period mainly bone or deep-tissue cultures were performed (9.7% vs. 98.2%, P < 0.001). Bacteriology cultures in the pre-intervention versus post-intervention period revealed: among staphylococcus isolates, fewer methicillin-resistant Staphylococcus aureus detected (20.4% vs. 9.8%, P = 0.010); within Enterobacteriaceae isolates, fewer extended-spectrum β-lactamase producing bacteria detected (51.6% vs. 23.6%, P < 0.001); a decrease in Pseudomonas aeruginosa isolates (28% vs. 10.6%, P < 0.001) and an increase in anaerobic bacterial isolates (0 vs. 11.1%, P < 0.001). On multivariate regression, the post-intervention period (ie multifaceted strategy) was a protective measure against readmissions (P = 0.007 OR 0.50 95% CI 0.30-0.82). We conclude that our interventive multifaceted strategy led to accurate bacterial diagnosis, de-escalation of antibiotic treatment and readmission reduction.
Aldosterone synthase deficiency (ASD) is a rare potentially life‐threatening genetic disorder that usually presents during infancy due to pathogenic variants in the CYP11B2 gene. Knowledge about CYP11B2 variants in the Arab population is scarce. Here, we present and analyze five Palestinian patients and their different novel pathogenic variants. Data on clinical presentation, electrolytes, plasma renin activity, and steroid hormone levels of five patients diagnosed with ASD were summarized. Sequencing of the CYP11B2 gene exons was followed by evolutionary conservation analysis and structural modeling of the variants. All patients were from highly consanguineous Palestinian families. The patients presented at 1–4 months of age with recurrent vomiting, poor weight gain, hyponatremia, hyperkalemia, and low aldosterone levels. Genetic analysis of the CYP11B2 gene revealed three homozygous pathogenic variants: p.Ser344Profs*9, p.G452W in two patients from an extended family, and p.Q338stop. A previously described pathogenic variant was found in one patient: p.G288S. We described four different CYP11B2 gene pathogenic variants in a relatively small population. Our findings may contribute to the future early diagnosis and therapy for patients with ASD among Arab patients who present with failure to thrive and compatible electrolyte disturbances.
Aim
Telomeres are DNA sequences of tandem TTAGGG repeats that protect chromosome ends from degradation and instability. Constitutional loss‐of‐function telomerase mutations result in rapid telomere shortening, premature senescence and cell death. Liver cirrhosis is rare and has only been reported in adults. We present five family members of Bedouin‐Muslim origin, all of which carry the same mutation, and yet demonstrate an extremely variable phenotypical presentation, including liver cirrhosis during early childhood.
Methods
A multidisciplinary long‐term follow‐up of two healthy and three affected patients was analysed. The mutation (r.95G>C) was identified in all patients using Sanger sequencing. Telomere length samples were obtained and analysed.
Results
Clinical phenotypes were extremely variable, including age at first symptoms, organ involvement, disease severity and patient prognosis. The most prominent clinical phenotype is liver involvement, including end‐stage liver disease early in life, which affects three members of the family. Affected patients had markedly shorter telomeres.
Conclusion
We describe an unusual presentation of early liver failure in telomere disease patients. Little, if any, is known about the association between the genotype and phenotype among children with telomere disease and whether the mutation we have described (r.95G>C) is predisposed to early severe hepatic involvement.
The Nancy Histological Index (NHI) was developed to assess histological disease activity in adult ulcerative colitis (UC) patients. However, data in pediatrics is limited. Our aim was to determine whether the NHI correlates with different indices of disease activity in pediatric UC patients. We retrospectively reviewed the NHI in rectal biopsies from 61 pediatric UC patients (median age 14.3 years), of whom 34 (55.7%) were newly diagnosed. The median Pediatric Ulcerative Colitis Activity Index (PUCAI) score among participants was 30 (interquartile range 5–55). Most patients exhibited an NHI of 3 (41/61, 67.2%) or 4 (8/61, 13.1%), reflecting moderate-severe histologic inflammation. A moderate positive correlation was identified between the NHI and PUCAI, fecal calprotectin, and Mayo endoscopic scores (r = 0.60, 0.54, and 0.56 respectively, P ≤ 0.001), but not with CRP or albumin. These results indicate that the NHI has a modest correlation with clinical, laboratory and endoscopic indices of disease activity in pediatric UC patients.
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