Project description:IntroductionThe novel coronavirus SARS-CoV-2 has spread all over the world causing a global pandemic and representing a great medical challenge. Nowadays, there is limited knowledge on the rate of co-infections with other respiratory pathogens, with viral co-infection being the most representative agents. Co-infection with Mycoplasma pneumoniae has been described both in adults and pediatrics whereas only two cases of Chlamydia pneumoniae have been reported in a large US study so far.MethodsIn the present report, we describe a series of seven patients where co-infection with C. pneumoniae (n = 5) or M. pneumoniae (n = 2) and SARS-CoV-2 was detected in a large teaching hospital in Rome.Results and conclusionAn extensive review of the updated literature regarding the co-infection between SARS-CoV-2 and these atypical pathogens is also performed.
Project description:Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently a serious public health concern worldwide. Notably, co-infection with other pathogens may worsen the severity of COVID-19 symptoms and increase fatality. Here, we show that co-infection with influenza A virus (IAV) causes more severe body weight loss and more severe and prolonged pneumonia in SARS-CoV-2-infected hamsters. Each virus can efficiently spread in the lungs without interference by the other. However, in immunohistochemical analyses, SARS-CoV-2 and IAV were not detected at the same sites in the respiratory organs of co-infected hamsters, suggesting that either the two viruses may have different cell tropisms in vivo or each virus may inhibit the infection and/or growth of the other within a cell or adjacent areas in the organs. Furthermore, a significant increase in IL-6 was detected in the sera of hamsters co-infected with SARS-CoV-2 and IAV at 7 and 10 days post-infection, suggesting that IL-6 may be involved in the increased severity of pneumonia. Our results strongly suggest that IAV co-infection with SARS-CoV-2 can have serious health risks and increased caution should be applied in such cases.
Project description:RATIONALE AND OBJECTIVES:An increasing number of neurological complications and corresponding radiological findings have been reported in patients with COVID-19 infection. The purpose of this study is to systematically review the current literature on COVID-19-associated neuroradiological findings and examine the prevalence of different findings in patients with both severe and mild COVID-19 infection. MATERIALS AND METHODS:A comprehensive literature search of the PubMed and Embase databases was performed. Any studies reporting CT or MRI neuroimaging findings in patients with confirmed COVID-19 infection were included. Patient demographics, main radiological findings, neurological symptoms, and severity of COVID-19 infection were tabulated and quantified according to infection severity. RESULTS:Sixty-one studies published between 2019 and 2020 comprising 711 patients were analyzed according to severity of respiratory symptoms. The main neuroradiological findings for patients with mild classification were cranial nerve abnormalities, ischemic infarction, and white matter abnormalities, while the main findings in patients with severe classification were white matter abnormalities, ischemic infarction, and hemorrhagic events. CONCLUSION:Neuroradiological manifestations in COVID-19 infection are highly heterogeneous and differ based on the severity of COVID-19 infection. Cranial nerve abnormalities appear exclusive to mild infection, with a high degree of olfactory tract involvement, while hemorrhagic events are more common in severe infection. Notably, ischemic infarction was equally prevalent in both mild and severe COVID-19 infection. Healthcare providers treating COVID-19 patients should be aware of these potential complications and consider neurological assessment and neuroimaging studies when indicated.
Project description:Postmortem lung pathology of a patient in Japan with severe acute respiratory syndrome coronavirus 2 infection showed diffuse alveolar damage as well as bronchopneumonia caused by Streptococcus pneumoniae infection. The distribution of each pathogen and the accompanying histopathology suggested the infections progressed in a mutually exclusive manner within the lung, resulting in fatal respiratory failure.
Project description:Hybrid immunity induced by vaccination following recovery from SARS-CoV-2 infection is more robust than immunity induced by either infection or vaccination alone. To investigate how infection severity influenced the strength and character of subsequent vaccine-induced humoral or cellular immune responses against SARS-CoV-2, we assessed humoral and cellular immune responses against SARS-CoV-2 following recovery from infection, vaccine dose 1 and vaccine dose 2 in 35 persons recovered from COVID-19. Persons with polymerase chain reaction or serologically confirmed SARS-CoV-2 infection were recruited into a study of immunity against SARS-CoV-2. Self-reported symptoms categorized them as experiencing asymptomatic, mild, moderate or severe infection based on duration, intensity and need for hospitalization. Whole blood was obtained before vaccination and after first and second doses. Humoral immunity was assessed by ELISA and cellular immunity by ELISpot and intracellular flow cytometry. Responses were compared between groups recovered from either asymptomatic/mild (n = 14) or moderate/severe (n = 21) infection. Most subjects experienced robust increases in humoral and cellular immunity against SARS-CoV-2 spike (S) protein following 1 vaccination. Quantitative responses to second vaccination were marginal when measured 2.5 months afterwards and moderate or severe infection maintained stronger responses. Polyfunctional CD8+ T cell responses were largely restricted to subjects recovered from moderate or severe infection. One vaccine dose triggered stronger immune responses than in a comparable group never infected with SARS-CoV-2, while the second dose produced only minor lasting increases in humoral or cellular responses. Infection history should be considered in planning COVID-19 vaccine administration.
Project description:Community-acquired pneumonia caused by Mycoplasma pneumoniae or Chlamydia pneumoniae is usually mild. Mycoplasma pneumoniae-related and C. pneumoniae-related acute respiratory distress syndromes (ARDSs) are rare. Moreover, to our knowledge, there are no published reports on ARDS caused by M. pneumoniae and C. pneumoniae coinfection. Here, we report a case of an immunocompetent young woman who was co-infected with M. pneumoniae and C. pneumoniae and was started on treatment with piperacillin and clarithromycin. Two days later, she developed ARDS. She recovered rapidly following a change of antibiotic treatment to levofloxacin and was discharged on day 12. We conducted exome sequencing followed by alternative filtering to search for candidate ARDS-related genes. We identified an intronic variant of unknown significance within leucine-rich repeat-containing 16A (LRRC16A), a gene previously identified as a significant locus for platelet count with a possible role in ARDS. This is a rare case of ARDS in a young adult caused by M. pneumoniae and C. pneumoniae coinfection. This case suggests that ARDS in young adults may be correlated with variants in LRRC16A. This requires confirmation by further case reports.
Project description:BackgroundThe H5N1 influenza virus is a cause of severe pneumonia. Co-infection of influenza virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may lead to poor prognosis of patients during the COVID-19 epidemic. However, reports on patients co-infected with avian influenza virus and SARS-CoV-2 are scarce.Case presentationA 52-year-old woman presented with a fever, which has persisted for the past eight days, along with worsening shortness of breath and decreased blood pressure. Computed tomography (CT) revealed an air bronchogram, lung consolidation, and bilateral pleural effusion. The subsequent polymerase chain reaction (PCR) of the bronchoalveolar lavage fluid (BALF) revealed positivity for H5N1 and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).ConclusionThe H5N1 influenza virus is a cause of severe pneumonia. The clinical presentation of the patient had a predomination of H5N1 influenza rather than COVID-19. A PCR analysis for the identification of the virus is necessary to reveal the pathogen causing the severe pneumonia. The patient exhibited an excellent prognosis upon the use of the appropriate antiviral medicine.
Project description:The present study evaluated the association between different Mycoplasma pneumoniae (M. pneumonia) genotypes and clinical features of pediatric patients. Subjects were children diagnosed with community-acquired pneumonia at the Children's Hospital of Soochow University (Suzhou, China) from January 2012 to December 2013. Clinical and laboratory tests were conducted and clinical samples positive for M. pneumoniae were genotyped by nested-multiplex polymerase chain reaction. Three type I strains and three type II strains were also randomly selected for sequencing. A total of 335 clinical samples positive for M. pneumoniae were obtained. The average age of M. pneumonia-infected pediatric patients was 4.8±3.3 (years). Genotyping results identified 304 positive samples as group I strains and 30 samples as group II strains, in which 1 sample was type II variant 2a. It was also observed that point mutations were more likely to occur in type I strains compared with type II strains. Although clinical pulmonary infection scores between patients with type I and type II strains did not significantly differ, patients with type I strains had a higher risk of developing severe M. pneumoniae pneumonia (SMPP) and extrapulmonary complications, and had significantly higher percentages of peripheral blood neutrophils than patients with type II strains (P<0.05). Collectively, these data indicate that the predominant strains of M. pneumoniae in Suzhou between 2012 and 2013 were type I, and that pediatric pneumonia patients with type I strains of M. pneumoniae were more likely to progress to SMPP.
Project description:Dysregulated immune responses contribute to the excessive and uncontrolled inflammation observed in severe COVID-19. However, how immunity to SARS-CoV-2 is induced and regulated remains unclear. Here we uncover a role of the complement system in the induction of innate and adaptive immunity to SARS-CoV-2. Complement rapidly opsonizes SARS-CoV-2 particles via the lectin pathway. Complement-opsonized SARS-CoV-2 efficiently induces type-I interferon and pro-inflammatory cytokine responses via activation of dendritic cells, which are inhibited by antibodies against the complement receptors (CR) 3 and 4. Serum from COVID-19 patients, or monoclonal antibodies against SARS-CoV-2, attenuate innate and adaptive immunity induced by complement-opsonized SARS-CoV-2. Blocking of CD32, the FcγRII antibody receptor of dendritic cells, restores complement-induced immunity. These results suggest that opsonization of SARS-CoV-2 by complement is involved in the induction of innate and adaptive immunity to SARS-CoV-2 in the acute phase of infection. Subsequent antibody responses limit inflammation and restore immune homeostasis. These findings suggest that dysregulation of the complement system and FcγRII signaling may contribute to severe COVID-19.