Dentro de las infecciones nosocomiales más frecuentes asociadas a bacterias multi-resistentes y de peor pronóstico, se encuentran las producidas por Pseudomonas aeruginosa. Esta bacteria posee una alta capacidad de adaptación a condiciones adversas como por ejemplo el pH y la osmolaridad de la orina. Pseudomonas aeruginosa es uno de los principales patógenos implicados en infecciones nosocomiales y de pacientes inmunosuprimidos. Esta bacteria se considera un agente infeccioso oportunista que posee diversos mecanismos de patogenicidad, así como de resistencia a antimicrobianos, lo que contribuye a la dificultad en el tratamiento de estas infecciones. En la presente revisión bibliográfica se analizan la taxonomía, los mecanismos de patogenicidad y genes de resistencia de P. aeruginosa. Así también, se abordan los factores microambientales de la infección urinaria producida por esta bacteria, haciendo un acercamiento al entendimiento de las bases fisiopatológicas de esta infección.

Dry eye disease (DED) can arise from a variety of factors, including inflammation, meibomian gland dysfunction (MGD), and neurosensory abnormalities. Individuals with DED may exhibit a range of clinical signs, including tear instability, reduced tear production, and epithelial disruption, that are driven by different pathophysiological contributors. Those affected often report a spectrum of pain and visual symptoms that can impact physical and mental aspects of health, placing an overall burden on an individual’s well-being. This cumulative impact of DED on an individual’s activities and on society underscores the importance of finding diverse and effective management strategies. Such management strategies necessitate an understanding of the underlying pathophysiological mechanisms that contribute to DED in the individual patient. Presently, the majority of approved therapies for DED address T cell-mediated inflammation, with their tolerability and effectiveness varying across different studies. However, there is an emergence of treatments that target additional aspects of the disease, including novel inflammatory pathways, abnormalities of the eyelid margin, and neuronal function. These developments may allow for a more nuanced and precise management strategy for DED. This review highlights the recent pharmacological advancements in DED therapy in the United States. It discusses the mechanisms of action of these new treatments, presents key findings from clinical trials, discusses their current stage of development, and explores their potential applicability to different sub-types of DED. By providing a comprehensive overview of products in development, this review aims to contribute valuable insights to the ongoing efforts in enhancing the therapeutic options available to individuals suffering from DED.

Objectives Ocular pain symptoms (e.g., hypersensitivity to light and wind, “burning” sensations) can be debilitating and difficult to treat. Neuromodulatory therapies targeting sensory trigeminal and central pain pathways may help treat chronic ocular pain refractory to traditional therapies. The current study evaluates the long-term effects of a trigeminal neurostimulator (TNS) on ocular pain. Materials and Methods Retrospective review of 18 individuals at the Miami Veterans Affairs Eye Clinic with chronic, severe ocular pain who were prescribed and used TNS at home for ≥3 months. The primary outcome measures were 1) ocular symptom intensity over a 24-hour recall period (dryness, pain, light sensitivity, wind sensitivity, burning; rated on 0–10 scales) captured pre-TNS and at monthly follow-up intervals and 2) side effects. The frequency and duration of TNS was a secondary outcome measure. Results The mean age of the population (n = 18) was 57.5 years (range, 34–85 years) with a male majority (67%). Two individuals discontinued use due to lack of efficacy and one due to confounding health issues. Initial mean weekly frequency of TNS use was 3.7 ± 1.9 sessions of 25.8 min at month 1 and 2.7 ± 2.3 sessions of 28.0 min at month 6. At six months, pain intensity (↓ 31.4%), light sensitivity (↓ 36.3%), wind sensitivity (↓ 32.6%), and burning sensation (↓ 53.9%) were all decreased compared to baseline (p < 0.01 for all); greater decreases in ocular pain were noted in individuals with migraine (n = 10) than those without migraine (n = 8). No significant change was noted in mean dryness scores. Fifteen subjects experienced sedation with TNS use, persisting throughout the follow-up visits. No other adverse effects were communicated by any subjects. Conclusion Our study suggests TNS is a safe, adjunctive treatment option in individuals with severe, chronic ocular pain. Individuals demonstrated gradual, continual improvement in pain symptoms over time within a multimodal approach.

Purpose: Gut microbiome alterations have been associated with various autoimmune diseases. There are limited data, however, on relationships between gut dysbiosis and immune-related dry eye (DE). Our aim was to compare the gut microbiome composition of individuals with early and late markers of Sjögren syndrome (SS) with controls without DE. Methods: We compared 20 individuals with positive early markers [antisalivary protein 1 (SP1), antiparotid secretory protein (PSP), anticarbonic anhydrase 6 (CA6) IgG, IgA, and IgM, n = 19)], or late markers (anti-Ro/SS-A and anti-La/SS-B, n = 1) of SS with no comorbid autoimmune diagnoses and 20 age-matched and sex-matched controls. Collected stool samples underwent deep RNA sequencing. The main outcomes measured included gut microbiome composition and diversity. Results: A total of 20 cases [Dry Eye Questionnaire-5 15.2 ± 3.4, Ocular Surface Disease Index 55.1 ± 22.8, and Schirmer 7.1 ± 5.2 mm] were compared with 20 controls (Dry Eye Questionnaire-5 4.8 ± 3.8, Ocular Surface Disease Index 14.2 ± 12.3, and Schirmer 20.4 ± 9.2 mm). No differences were observed in α-diversity (P = 0.97) or overall community structure (P = 0.62). Between groups, 32 species were differentially abundant (P < 0.01). Among cases, 27 were relatively more abundant, including 10 Lactobacillus and 4 Bifidobacterium species. A relative depletion of 5 species was found in cases compared with controls, notably Fusobacterium varium and Prevotella stercorea. Conclusions: Differences in gut microbiome composition were found in individuals with mostly early markers of SS compared with controls. However, their clinical significance to DE manifestations remains unclear. Further studies are needed to elucidate the role of gut dysbiosis on immune dysregulation and disease activity in the various forms of immune-mediated DE.

Autosomal recessive Stargardt disease (STGD1) is an inherited retinal degenerative disease associated with a mutated ATP-binding cassette, subfamily A, member 4 (ABCA4) gene. STGD1 is the most common form of juvenile macular degeneration with onset in late childhood to early or middle adulthood and causes progressive, irreversible visual impairment and blindness. No effective treatment is currently available. In the present article, we review the most recent updates in clinical trials targeting the management of STGD1, including gene therapy, small molecule therapy, and stem cell therapy. In gene therapy, dual adeno-associated virus and non-viral vectors have been successful in delivering the human ABCA4 gene in preclinical studies. For pharmaceutical therapies ALK-001, deuterated vitamin A shows promise with preliminary data for phase 2 trial, demonstrating a decreased atrophy growth rate after two years. Stem cell therapy using human pluripotent stem cell-derived retinal pigment epithelium cells demonstrated long-term safety three years after implantation and visual acuity improvements in the first two years after initiation of therapy. Many other treatment options have ongoing investigations and clinical trials. While multiple potential interventions have shown promise in attenuating disease progression, further exploration is necessary to demonstrate treatment safety and efficacy.

A 28-year-old male presented unilateral visual loss, intense ocular pain, redness and intraocular hypertension in his right eye 2 days after undergoing small-incision lenticule extraction (SMILE) in both eyes. Initial examination of the affected eye revealed the presence of white infiltrates within the corneal interface, as well as a central epithelial defect. The patient was diagnosed with infectious keratitis, posteriorly the eye was irrigated with balanced saline solution and treatment was initiated with hourly moxifloxacin 0.5%. Since this approach failed to resolve symptoms, a sample from the interface was obtained for PCR assay, which revealed the presence of herpes simplex virus DNA, confirming the cause of the infection. The patient was prescribed a regimen of oral acyclovir, topical ganciclovir and prednisolone. Clinical improvement following resolution of the epithelial defect was observed. Although rare, herpetic keratitis following SMILE is best managed via early diagnosis and initiation of appropriate anti-herpetic treatment.