Despite advances in preventive, diagnostic, and therapeutic interventions, invasive fungal infections cause significant morbidity and mortality in immunocompromised patients. The burden of antifungal resistance in such high-risk patients is becoming a major concern. A better understanding of the mechanisms and clinical impact of antifungal resistance is essential to the prompt and efficient treatment of patients with invasive mycoses and to improving the outcome of such infections. Although recent guidelines have attempted to standardize antifungal susceptibility testing, limitations still exist as a result of the incomplete correlation between in vitro susceptibility and clinical response to treatment. Four major mechanisms of resistance to azoles have been identified, all of which rely on altered gene expression. Mechanisms responsible for polyene and echinocandin resistance are less well understood. In addition to discussing the molecular mechanisms of antifungal resistance, this article elaborates on the concept of clinical resistance, which is critical to the understanding of treatment failure in patients with invasive fungal infections.

Surgical site infection (SSI) following spine surgery is a dreaded complication with significant morbidity and economic burden. SSIs following spine surgery can be superficial, characterized by obvious wound drainage, or deep-seated with a healed wound. Staphylococcus aureus remains the principal causal agent. There are certain pre-operative risk factors that increase the risk of SSI, mainly diabetes, smoking, steroids, and peri-operative transfusions. Additionally, intra-operative risk factors include surgical invasiveness, type of fusion, implant use, and traditional instead of minimally invasive approach. A high level of suspicion is crucial to attaining an early definitive diagnosis and initiating appropriate management. The most common presenting symptom is back pain, usually manifesting 2 to 4 weeks and up to 3 months after a spinal procedure. Scheduling a follow-up visit between weeks 2 to 4 after surgery is therefore necessary for early detection. Inflammatory markers are important diagnostic tools, and comparing pre-operative with post-operative levels should be done when suspecting SSIs following spine surgery. Particularly, Serum Amyloid A (SAA) is a novel inflammatory marker that can expedite the diagnosis of SSIs. Magnetic resonance imaging remains the diagnostic modality of choice when suspecting a SSI following spine surgery. While 18F-fluorodeoxyglucose-positron emission tomography is not widely used, it may be useful in challenging cases. Despite their low yield, blood cultures should be collected before initiating antibiotic therapy. Samples from wound drainage should be sent for Gram stain and cultures. When there is a high clinical suspicion of SSI and in the absence of superficial wound drainage, CT guided aspiration of paraspinal collections is warranted. Unless the patient is hemodynamically compromised, antibiotics should be deferred until proper specimens for culture are secured.

Introduction: Tedizolid phosphate (TR-701) is a new oxazolidinone prodrug that is transformed in the serum into the active drug tedizolid (TR-700). Tedizolid acts by inhibiting protein synthesis and has broad activity against Gram-positive pathogens, including strains that are resistant to linezolid. Areas covered: This review summarizes the currently available data on this new antimicrobial agent. In vitro activity, pharmacokinetics/pharmacodynamics, clinical efficacy and safety are all addressed. Expert opinion: Tedizolid will provide a useful addition to the antimicrobial armamentarium, particularly in complicated skin and skin structure infections, due to its high oral bioavailability and once-daily dosing. The results of future studies will serve to better position tedizolid among the newly approved agents for infections caused by Gram-positive organisms.

Introduction: Cutibacterium acnes (C. acnes), a Gram-positive biofilm-forming rod implicated in acne vulgaris, is increasingly recognized for its role in implant-associated infections. The diagnosis of C. acnes implant-associated infections remains challenging. The optimal treatment is a combination of both surgical intervention and antibiotic therapy. Areas covered: In this review, we discuss the different types of implant-associated infections caused by C. acnes. We also highlight the clinical manifestations pertaining to the various sites of infection, and identify several risk factors previously reported in the literature. We then cover the diagnostic laboratory markers, such as IL-6 and AD-1, optimizing C. acnes recovery in culture, and the specific molecular techniques. Finally, we examine the various effective antibiotic regimens and identify some preventive methods against C. acnes infections. Expert commentary: Biomarkers such as IL-6 and AD-1 should be further investigated for the diagnosis of C. acnes implant-associated infections. The use of 16S rRNA gene sequencing and other molecular techniques should be further explored in this setting. Longer incubation periods should be requested whenever C. acnes infection is suspected. If the clinical suspicion is high, sonication of the excised implant should be encouraged. Research should focus on developing effective anti-biofilm agents. Finally, preventive methods such as hair removal prior to surgery should be further explored.