Comorbidity of purulent meningitis with COVID‐19: A case report

To date, only a few cases of intracranial infection related to severe acute respiratory syndrome‐coronavirus‐2 (SARS‐CoV‐2) were reported. Here we describe a case of coronavirus disease 2019 (COVID‐19) that was comorbid with purulent meningitis. A 62‐year‐old male patient was diagnosed with moderate COVID‐19 and had no fever or cough after treatment. However, he suffered from a head injury and experienced headache and fever immediately after the accident. Computed tomography (CT) of the brain showed bilateral frontal lobe contusion, subdural hematoma, and subarachnoid hemorrhage. In the following days, the patient suffered from recurrent fever, although chest CT did not show evidence of worsening of infection. Several lumbar punctures were made, confirming increased cerebrospinal fluid (CSF) pressure and karyocyte count. SARS‐CoV‐2 nucleic acid was not detected in CSF but revealed the presence of Escherichia coli. Thus, the patient was diagnosed with purulent meningitis, presumably caused by brain trauma or the immunologic dysfunction caused by COVID‐19, which was supported by the significant reduction of all kinds of immune cells. Since immunologic dysfunction is commonly presented in COVID‐19 patients, comorbidity with meningitis should be considered when a COVID‐19 patient presents with headache and fever. Lumbar punctures and CSF cultures may help in the diagnosis.

Meningeal macrophages protect against viral neuroinfection.

The surface of the central nervous system (CNS) is protected by the meninges, which contain a dense network of meningeal macrophages (MMs). Here, we examined the role of tissue-resident MM in viral infection. MHC-II- MM were abundant neonatally, whereas MHC-II+ MM appeared over time. These barrier macrophages differentially responded to in vivo peripheral challenges such as LPS, SARS-CoV-2, and lymphocytic choriomeningitis virus (LCMV). Peripheral LCMV infection, which was asymptomatic, led to a transient infection and activation of the meninges. Mice lacking macrophages but conserving brain microglia, or mice bearing macrophage-specific deletion of Stat1 or Ifnar, exhibited extensive viral spread into the CNS. Transcranial pharmacological depletion strategies targeting MM locally resulted in several areas of the meninges becoming infected and fatal meningitis. Low numbers of MHC-II+ MM, which is seen upon LPS challenge or in neonates, corelated with higher viral load upon infection. Thus, MMs protect against viral infection and may present targets for therapeutic manipulation.

Special Issue: Microbiologists making waves around the South Pacific. (Special Issue: Microbiologists making waves around the South Pacific.)

This special issue includes 11 articles focusing on development of container laboratories in response to COVID-19;COVID-19 in Fiji;Pacific Regional Infectious Disease Association (PRIDA) - capacity-building for microbiology and infectious disease across the Pacific;meningococcal surveillance in Southeast Asia and the Pacific;tropical fever in remote tropics;movement of arboviruses between Indonesia and Western Australia;Rotavirus surveillance informs diarrhoea disease burden in the WHO Western-Pacific region;surveillance for One Health and high consequence veterinary pathogens (Brucellosis, Coxiellosis and Foot and Mouth Disease) in Southeast Asia - Lao PDR and Cambodia in focus and the importance of international partnerships;Avian influenza H5N1.