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The pathogenesis of chronic wounds (CW) involves a multifaceted interplay of biochemical, immunological, hematological, and microbiological interactions. Biofilm development is a significant virulence trait which enhances microbial survival and pathogenicity and has various implications on the development and management of CW. Biofilms induce a prolonged suboptimal inflammation in the wound microenvironment, associated with delayed healing. The composition of wound fluid (WF) adds more complexity to the subject, with proven pro-inflammatory properties and an intricate crosstalk among cytokines, chemokines, microRNAs, proteases, growth factors, and ECM components. One approach to achieve information on the mechanisms of disease progression and therapeutic response is the use of multiple high-throughput 'OMIC' modalities (genomic, proteomic, lipidomic, metabolomic assays), facilitating the discovery of potential biomarkers for wound healing, which may represent a breakthrough in this field and a major help in addressing delayed wound healing. In this review article, we aim to summarize the current progress achieved in host–microbiome crosstalk in the spectrum of CW healing and highlight future innovative strategies to boost the host immune response against infections, focusing on the interaction between pathogens and their hosts (for instance, by harnessing microorganisms like probiotics), which may serve as the prospective advancement of vaccines and treatments against infections. [ABSTRACT FROM AUTHOR]

Encephalitis is a rare complication of cervical - cranial zoster infection. Myelitis is a similar, severe complication of thoracic zoster. They occur in patients with immune deficiencies, in 5-21 days after the rash and progress in the same time frame. We are presenting the case of a 54 year old male with rapid evolution of an ascending encephalomyelitis with onset at 17 days after a left cervical-thoraco-brachial zoster episode. Neurologic examination: lower limb paresthesia, ascending to the trunk, unstable gait, which becomes impossible with closed eyes, absent deep tendon reflexes, bilateral Babinski sign. After 48 hours, left cerebellar syndrome appears, in one week the patient had asymmetrical tetraparesis and in 11 days he becomes paraplegic, left side more affected than the right one. After 16 days, the clinical state stabilizes, he begins moving his right lower limb. Lumbar puncture on admission: CSF albumin 1220 mg% (after 3 days it becomes normal); 81 cells/mm3, 100% mononuclear cells, 50 cells after 3 days and after a week 23 cells/mm3. Cervical and thoracic spine MRI performed on the 3rd day from admission was normal but after repeating it in 10 days it showed T2, STIR and FLAIR hyper intense intraspinal, infra- and supratentorial lesions, well contoured, with homogenous gadolinium enhancement: demielinating lesions. He received Aciclovir, Solumedrol, Insulin and symptomatic treatment. After 2 weeks from leaving the hospital with symptomatic treatment and kinetic therapy, he returns in a septic state, with deep bed sores, positive blood cultures (Fusobacterium nucleatum, Staphylococcus Epidermidis) and urine cultures (Klebsiella). The outcome was death in 4 days. Differential diagnosis - polyradiculoneuritis, paraneoplastic syndrome, cerebral and vertebral metastases. Pathology exams: low grade acinary adenocarcinoma of the pancreatic head, invasive, with a solid pattern. The particularity of the case: the severity of the acute ascending encephalomyelitis, the fulminant evolution of the pancreatic cancer, the disruption of the blood-brain barrier by an inflammatory and tumoral mechanism, showed on spine and brain contrast MRI. [ABSTRACT FROM AUTHOR]