Otitis media (OM) is an inflammation of the middle ear associated with infection. Despite appropriate therapy, acute OM (AOM) can progress to chronic suppurative OM (CSOM) associated with ear drum perforation and purulent discharge. The effusion prevents the middle ear ossicles from properly relaying sound vibrations from the ear drum to the oval window of the inner ear, causing conductive hearing loss. In addition, the inflammatory mediators generated during CSOM can penetrate into the inner ear through the round window. This can cause the loss of hair cells in the cochlea, leading to sensorineural hearing loss. Pseudomonas aeruginosa and Staphylococcus aureus are the most predominant pathogens that cause CSOM. Although the pathogenesis of AOM is well studied, very limited research is available in relation to CSOM. With the emergence of antibiotic resistance as well as the ototoxicity of antibiotics and the potential risks of surgery, there is an urgent need to develop effective therapeutic strategies against CSOM. This warrants understanding the role of host immunity in CSOM and how the bacteria evade these potent immune responses. Understanding the molecular mechanisms leading to CSOM will help in designing novel treatment modalities against the disease and hence preventing the hearing loss. IntroductionOtitis media (OM) refers to a group of complex infectious and inflammatory diseases affecting the middle ear (Dickson, 2014). OM in general is very common, as studies show that around 80 % of children should have experienced at least one episode by their third birthday (Teele et al., 1989). OM has been broadly classified into two main types, acute and chronic. Acute OM (AOM) is characterized by the rapid onset of signs of inflammation, specifically bulging and possible perforation of the tympanic membrane, fullness and erythema, as well as symptoms associated with inflammation such as otalgia, irritability and fever (Pukander, 1983;Harkness & Topham, 1998). Despite appropriate antibiotic therapy, AOM may progress to chronic suppurative OM (CSOM) characterized by persistent drainage from the middle ear associated with a perforated ear drum (Wintermeyer & Nahata, 1994;Harkness & Topham, 1998). When examined by otoscope, the middle ear looks red and inflamed with purulent discharge in CSOM patients (Figs 1 and 2). It is one of the most common chronic infectious diseases worldwide especially affecting children (Roland, 2002; Verhoeff et al., 2006). Hearing impairment is one of the most common sequelae of CSOM (Aarhus et al., 2015). The resultant hearing loss can have a negative impact on a child's speech development, education and behaviour (Olatoke et al., 2008; Khairi Md Daud et al., 2010). Mortality due to complications of CSOM is typically higher than other types of OM (Yorgancilar et al., 2013a;Qureishi et al., 2014). Intracranial complications like brain abscess and meningitis are the most common causes of death in CSOM patients (Dubey et al., 2010;Chew et al., 2012;Sun & Sun, 2014).In this article, the rec...

Otitis media (OM) is a broad term describing a group of infectious and inflammatory disorders of the middle ear. Despite antibiotic therapy, acute OM can progress to chronic suppurative otitis media (CSOM) characterized by ear drum perforation and purulent discharge. Pseudomonas aeruginosa is the most common pathogen associated with CSOM. Although, macrophages play an important role in innate immune responses but their role in the pathogenesis of P. aeruginosa-induced CSOM is not known. The objective of this study is to examine the interaction of P. aeruginosa with primary macrophages. We observed that P. aeruginosa enters and multiplies inside human and mouse primary macrophages. This bacterial entry in macrophages requires both microtubule and actin dependent processes. Transmission electron microscopy demonstrated that P. aeruginosa was present in membrane bound vesicles inside macrophages. Interestingly, deletion of oprF expression in P. aeruginosa abrogates its ability to survive inside macrophages. Our results suggest that otopathogenic P. aeruginosa entry and survival inside macrophages is OprF-dependent. The survival of bacteria inside macrophages will lead to evasion of killing and this lack of pathogen clearance by phagocytes contributes to the persistence of infection in CSOM. Understanding host–pathogen interaction will provide novel avenues to design effective treatment modalities against OM.

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The Coronavirus disease 2019 (COVID-19) infection has classical symptoms of high fevers, diarrhea, cough, and dyspnea; however, there are cases recording more unconventional features. In this case report, we will discuss recurrent laryngeal nerve palsy as a new and unusual presentation of COVID-19. The patient was a 58-year-old African American male with a history of hypertension, type-2 diabetes mellitus, and obstructive sleep apnea presenting with dyspnea, fatigue, and nausea. The patient was initially admitted to the medical intensive care unit (MICU) for acute hypoxic respiratory failure and completed intravenous Remdesivir for COVID-19. He never got intubated during the ICU stay and his condition improved on the 34th day of admission. However, two weeks later the patient suddenly developed hoarseness of voice. A bedside laryngoscopy revealed a left-sided vocal cord paralysis but patent airway. The computed tomography (CT) scan of the neck did not show any abnormalities, including any impinging masses or structures. The patient did not have any recent intubations to suggest the paralysis was due to traumatic injury, thus favoring that his neurologic injury was likely a post-viral symptom. One possible pathophysiology would be the invasion of nerve fibers (peripheral or cranial nerves) by the virus using the same mechanism as seen in alveolar cells and finally destroying them. Another hypothesis would be the inflammatory response of the host immune system affecting the peripheral and cranial nerves. Therefore, the potential association between neuroinvasiveness of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the recurrent laryngeal nerve palsy resulting in the vocal cord paralysis should be considered and more studies need to be conducted for better understanding.

Figure 1. Strobovideolaryngoscopic examination performed 7 days after the fat injection shows the extensive edemaand erythema of the rightvocal fold and surrounding structures.