Emerging and re-emerging infectious diseases are not episodic events, but manifestations of a continuously evolving interface between humans, pathogens, and the environment. Despite major advances in vaccines, antimicrobial therapy, and public health care, the frequency and impact of these diseases are increasing, driven by globalization, ecological disruption, climate change, and intensified human -animal interactions, alongside declining vaccine coverage and expanding antimicrobial resistance. The predominance of zoonotic origins of infectious diseases highlights the inadequacy of siloed approaches and reinforces the necessity of a One Health perspective. This review synthesizes the conceptual foundations and structural drivers of emerging and re-emerging infectious diseases, situating recent outbreaks within a broader historical and systemic context. The coronavirus disease 2019 (COVID-19) pandemic exemplified a recurring pattern: delayed recognition, rapid global dissemination, and profound societal disruption. At the same time, it demonstrated the unprecedented capacity of modern science to respond, while exposing persistent inequities and fragilities in surveillance, health systems, and global governance. Future threats cannot be mitigated through fragmented interventions. Instead, they demand a paradigm shift towards an integrated, anticipatory framework that aligns early detection, resilient health systems, rapid scientific innovation, and coordinated global action. Such a framework must transcend disciplinary and national boundaries and be grounded in equity, transparency, and sustained investment. Preparedness for emerging and re-emerging infectious diseases is no longer optional; it is an enduring imperative in an increasingly interconnected and unstable world.

The incidence of invasive pneumococcal disease (IPD) is reported to have decreased following introduction of the pneumococcal conjugate vaccine (PCV) for children. However, the detection rate of non-vaccine-serotype pneumococci appears to be gradually increasing. Herein, we report two rare cases of IPD caused by pneumococcal serotype 28F in Shizuoka Prefecture.

The first case was a 7-year-old boy with a 5-year history of treatment with prednisolone and cyclosporine for steroid-resistant nephrotic syndrome, who developed pneumococcal bacteremia. His condition improved with intravenous ampicillin, and he was discharged from the hospital without sequelae. Pneumococcal serotype 28F was isolated from blood culture.

The second case was a 14-year-old boy with bacterial meningitis and an intraventricular abscess. He was treated with intravenous ampicillin and cefotaxime and was discharged from the hospital without sequelae. He had a history of untreated chronic sinusitis, and a minor skull fracture due to sports trauma was presumed to have triggered the infection. Pneumococcal serotype 28F was isolated from the blood and cerebrospinal fluid, that was devoid of penicillin-binding protein gene mutations and therefore penicillin sensitive.

These cases highlight the need for a detailed nationwide investigation of the clinical characteristics of patients with IPD, the isolated pneumococcal serotypes, and their antibiotic susceptibility/resistance patterns.

Actinotignum schaalii is a facultatively anaerobic, gram-positive bacillus which is increasingly being recognized as a uropathogen, particularly in elderly patients with urogenital abnormalities. While A. schaalii is associated with urinary tract infections, its involvement in renal cyst infections is unclear, and a search of past studies failed to reveal any previously reported cases.

An 83-year-old, male patient with a history of bladder cancer and end-stage renal disease who was receiving maintenance hemodialysis presented with a fever and chills. Blood cultures grew A. schaalii, which was identified using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Computed tomography revealed perinephric fat stranding and ureteral wall enhancement, prompting further evaluation with magnetic resonance imaging, which demonstrated findings consistent with a renal cyst infection. Despite initial treatment with vancomycin, the inflammatory markers remained elevated. Given the limited penetration of hydrophilic antibiotics into the cystic fluid, vancomycin was switched to clindamycin, which produced clinical improvement.

Highly pathogenic avian influenza viruses (HPAIVs) of the H5N1 subtype have been reported to infect not only birds, but also humans, cattle, and other mammals, posing a serious public health concern and highlighting the need for effective control measures. Ultraviolet (UV) irradiation is widely known as an effective modality for virus inactivation, and recent advances in LED technology have enabled the generation of UV light of various wavelengths, each with distinct characteristics. In this study, we evaluated the efficacy of four different UV wavelengths (222 nm, 230 nm, 254 nm, and 265 nm) in inactivating HPAIVs. HPAIV at a concentration of 2.0 × 10⁶ plaque-forming units (PFU) /mL was irradiated with UV light at doses ranging from 0 to 7.3 mJ/cm². The UV doses required to achieve a 99.9% reduction in the viral titer were 4.2 mJ, 4.9 mJ, 5.6 mJ, and 4.3 mJ for UV light wavelengths of 222 nm, 230 nm, 254 nm, and 265 nm, respectively. All four UV light wavelengths reduced viral titers by more than 99.9%, demonstrating their effectiveness in inactivating HPAIVs. This study demonstrated that UV light at all the four tested wavelengths effectively inactivated HPAIVs to a comparable extent, suggesting the usefulness of UV light for inactivating HPAIVs in a wide range of environments.