Choo EJ, et al. Infect Chemother. 2016 Dec;48(4):267-273. https://doi.org/10.3947/ic.2016.48.4.267

Background: Anterior cruciate ligament (ACL) reconstruction failure is relatively common in young high-risk athletes. The purpose of this study was to examine a single center’s 10-year experience with ACL reconstructions in pediatric and adolescent patients to better define short-term failure rates and risk factors for revision ACL surgery. Methods: This institutional review board-approved retrospective study included all patients who underwent a primary ACL reconstruction between 2002 and 2013. Chart and radiographic review was performed to assess patient demographic, injury, and surgical data including growth plate status, concomitant ligament/meniscus/cartilage injury, surgical procedures, femoral drilling technique, graft source and type, femoral and tibial fixation devices, and graft size. Graft failures had to be confirmed both with clinical examination and magnetic resonance imaging or the patient had to undergo a revision ACL reconstruction. Potential factors associated with failure were evaluated using either parametric or nonparametric analysis as appropriate. Results: A total of 561 ACL reconstructions were performed that met our inclusion criteria. The average patient age was 15.4 years (range, 5 to 19 y) and 53% of the patients were male. In all, 54 failures were identified for a 9.6% failure rate. Soft tissue grafts were twice as likely to fail compared with patellar tendon grafts (13% vs. 6%; P<0.001). Multivariate analysis revealed that graft choice (soft tissue vs. patellar tendon) was the primary variable predictive of failure (P<0.05), with interactions/mediating effects contributed by maturity (growth plate status) and ACL technique (P<0.05). The average time to failure was 13.6 months and hamstring grafts and anatomic femoral tunnels were both found to fail earlier (P<0.05). During the study period, approximately 8% of patients sustained a contralateral ACL injury. Conclusions: ACL failure rates in adolescent and pediatric patients vary based on patient age, graft selection, and surgical technique. Bone patellar tendon bone autografts had the lowest failure rate in this high-risk population. Level of Evidence: Level IV—retrospective case series.

Background: Cerebral palsy (CP) is an upper motor neuron disease that results in a progressive movement disorder. Secondary to the neurological insult, muscles from CP patients often become spastic. Spastic muscle is characterized by an increased resistance to stretch, but often develops the further complication of contracture which represents a prominent disability in children with CP. This study's purpose is to characterize alterations of spastic muscle on the transcriptional level. Increased knowledge of spastic muscle may lead to novel therapies to improve the quality of life for children with CP. Method: The transcriptional profile of spastic muscles were defined in children with cerebral palsy and compared to control patients using Affymetrix U133A chips. Expression data were verified using quantitative-PCR (QPCR) and validated with SDS-PAGE for select genes. Significant genes were determined using a 2 × 2 ANOVA and results required congruence between 3 preprocessing algorithms. Results: CP patients clustered independently and 205 genes were significantly altered, covering a range of cellular processes. Placing gene expression in the context of physiological pathways, the results demonstrated that spastic muscle in CP adapts transcriptionally by altering extracellular matrix, fiber type, and myogenic potential. Extracellular matrix adaptations occur primarily in the basal lamina although there is increase in fibrillar collagen components. Fiber type is predominately fast compared to normal muscle as evidenced by contractile gene isoforms and decrease in oxidative metabolic gene transcription, despite a paradoxical increased transcription of slow fiber pathway genes. We also found competing pathways of fiber hypertrophy with an increase in the anabolic IGF1 gene in parallel with a paradoxical increase in myostatin, a gene responsible for stopping muscle growth. We found evidence that excitation-contraction coupling genes are altered in muscles from patients with CP and may be a significant component of disease. Conclusion: This is the first transcriptional profile performed on spastic muscle of CP patients and these adaptations were not characteristic of those observed in other disease states such as Duchenne muscular dystrophy and immobilization-induced muscle atrophy. Further research is required to understand the mechanism of muscle adaptation to this upper motor neuron lesion that could lead to the development of innovative therapies.

Background: The prevalence of infections caused by extended-spectrum beta-lactamase producingEscherichia coli(ESBL-E. coli) is increasing worldwide, but the setting in which this increase is occurring is not well defined. We compared trends and risk factors for ESBL-E. colibacteriuria in community vs healthcare settings.Methods: We collected electronic health record data on all patients withE. coliisolated from urine cultures in a safety-net public healthcare system from January 2014 to March 2020. All analyses were stratified by healthcare-onset/associated (bacteriuria diagnosed > 48 h after hospital admission or in an individual hospitalized in the past 90 days or in a skilled nursing facility resident, N = 1277) or community-onset bacteriuria (bacteriuria diagnosed < 48 h after hospital admission or in an individual seen in outpatient clinical settings without a hospitalization in the past 90 days, N = 7751). We estimated marginal trends from logistic regressions to evaluate annual change in prevalence of ESBL-E. colibacteriuria among all bacteriuria. We evaluated risk factors using logistic regression models.Results: ESBL-E. coliprevalence increased in both community-onset (0.91% per year, 95% CI 0.56%, 1.26%) and healthcare-onset/associated (2.31% per year, CI 1.01%, 3.62%) bacteriuria. In multivariate analyses, age > 65 (RR 1.88, CI 1.17, 3.05), male gender (RR 2.12, CI 1.65, 2.73), and Latinx race/ethnicity (RR 1.52, CI 0.99, 2.33) were associated with community-onset ESBL-E. coli. Only male gender (RR 1.53, CI 1.03, 2.26) was associated with healthcare-onset/associated ESBL-E. coli.Conclusions: ESBL-E. colibacteriuria frequency increased at a faster rate in healthcare-associated settings than in the community between 2014 and 2020. Male gender was associated with ESBL-E. colibacteriuria in both settings, but additional risks—age > 65 and Latinx race/ethnicity—were observed only in the community.

β-lactam antibiotics are excellent drugs for treatment of staphylococcal infections, due to their superior efficacy and safety compared to other drugs. Effectiveness of β-lactams is severely compromised due to resistance, which is widespread among clinical strains of Staphylococcus aureus. β-lactams inhibit bacterial cells by binding to penicillin binding proteins (PBPs), which perform the penultimate steps of bacterial cell wall synthesis. Among PBPs of S. aureus, PBP2a has received the most attention for the past several decades due to its preeminent role in conferring both high-level and broad-spectrum resistance to the entire class of β-lactam drugs. Studies on PBP2a have thus unraveled incredible details of its mechanism of action. We have recently identified that an uncanonical, low molecular weight PBP of S. aureus, PBP4, can also provide high-level and broad-spectrum resistance to the entire class of β-lactam drugs at a level similar to that of PBP2a. The role of PBP4 has typically been considered not so important for β-lactam resistance of S. aureus, and as a result its mode of action remains largely unknown. In this article, we review our current knowledge of PBP4 mediating β-lactam resistance in S. aureus.

First-time patellar dislocation with an associated chondral or osteochondral loose body is typically treated operatively to address the loose fragment. The incidence of recurrent instability in this patient population if the medial patellofemoral ligament (MPFL) is not reconstructed is unknown. To determine the recurrent instability rate in patients undergoing surgery for patellar instability with chondral or osteochondral loose bodies, as well as to identify and stratify risk factors for recurrent instability. Case series; Level of evidence, 4. This was a retrospective analysis of adolescent patients treated operatively for acute patellar dislocation with associated chondral or osteochondral loose bodies between 2010 and 2016 at a single pediatric level I trauma center with minimum 2-year follow-up. Potential demographic, injury-related, radiographic, and surgical risk factors were recorded. The primary outcome variable was recurrent subluxation and/or dislocation. Secondary outcome variables included need for additional procedures, Kujala score, Single Assessment Numerical Evaluation (SANE) score, and patient satisfaction. Forty-one patients were included. In total, 61% experienced recurrent instability at a mean follow-up of 4.1 years and 39% required subsequent MPFL reconstruction. Tibial tubercle-trochlear groove (TT-TG) distance greater than 15 mm was a risk factor for recurrent instability (P = .03). Patients with TT-TG distance greater than 15 mm and greater than 20 mm had recurrent instability rates of 75% and 86%, respectively. MPFL repair did not reduce the rate of recurrent instability (P = .87). Recurrent instability was associated with significantly worse mean Kujala (93.9 vs 83.0; P = .01), SANE (88.9 vs 73.1; P = .01), and patient satisfaction scores (9.4 vs 7.3; P = .002). If the MPFL is not reconstructed during index loose body treatment, children have a 61% recurrent instability rate. Patients with TT-TG distance greater than 15 mm, and particularly greater than 20 mm, are at highest risk for recurrent instability.