- Volume 3, Issue 9, 2021

During an outbreak of invasive meningococcal disease (IMD) at the University of Southampton, UK, in 1997, two Neisseria meningitidis serogroup C isolates were retrieved from a student (‘Case’), who died of IMD, and a close contact (‘Carrier’) who, after mouth-to-mouth resuscitation on the deceased, did not contract the disease. Genomic comparison of the isolates demonstrated extensive nucleotide sequence identity, with differences identified in eight genes. Here, comparative proteomics was used to measure differential protein expression between the isolates and investigate whether the differences contributed to the clinical outcomes. A total of six proteins were differentially expressed: four proteins (methylcitrate synthase, PrpC; hypothetical integral membrane protein, Imp; fructose-1,6-bisphosphate aldolase, Fba; aldehyde dehydrogenase A, AldA) were upregulated in the Case isolate, while one protein (Type IV pilus-associated protein, PilC2) was downregulated. Peptides for factor H binding protein (fHbp), a major virulence factor and antigenic protein, were only detected in the Case, with a single base deletion (ΔT366) in the Carrier fHbp causing lack of its expression. Expression of fHbp resulted in an increased resistance of the Case isolate to complement-mediated killing in serum. Complementation of fHbp expression in the Carrier increased its serum resistance by approximately 8-fold. Moreover, a higher serum bactericidal antibody titre was seen for the Case isolate when using sera from mice immunized with Bexsero (GlaxoSmithKline), a vaccine containing fHbp as an antigenic component. This study highlights the role of fHbp in the differential complement resistance of the Case and the Carrier isolates. Expression of fHbp in the Case resulted in its increased survival in serum, possibly leading to active proliferation of the bacteria in blood and death of the student through IMD. Moreover, enhanced killing of the Case isolate by sera raised against an fHbp-containing vaccine, Bexsero, underlines the role and importance of fHbp in infection and immunity.

COVID-19 severity and progression are determined by several host and virological factors that may influence the final outcome of SARS-CoV-2-infected patients. The objective of this work was to determine a possible association between viral load, obtained from nasopharyngeal swabs, and the severity of the infection in a cohort of 448 SARS-CoV-2-infected patients from a hospital in Madrid during the first outbreak of the pandemic in Spain. To perform this, we clinically classified patients as mild, moderate and severe COVID-19 according to a number of clinical parameters such as hospitalization requirement, need of oxygen therapy, admission to intensive care units and/or death. Also, Ct values were determined using SARS-CoV-2-specific oligonucleotides directed to ORF1ab. Here we report a statistically significant association between viral load and disease severity, a high viral load being associated with worse clinical prognosis, independently of several previously identified risk factors such as age, sex, hypertension, cardiovascular disease, diabetes, obesity and lung disease (asthma and chronic obstructive pulmonary disease). The data presented here reinforce viral load as a potential biomarker for predicting disease severity in SARS-CoV-2-infected patients. It is also an important parameter in viral evolution since it relates to the numbers and types of variant genomes present in a viral population, a potential determinant of disease progression.

Reverse-transcription quantitative PCR (RT-qPCR) is currently the most sensitive method to detect severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19). We analysed 1927 samples collected in a local public hospital during the autumn 2020 peak of the pandemic in the Czech Republic. The tests were performed using the Seegene Allplex 2019-nCov assay, which simultaneously detects three SARS-CoV-2 genes. In all samples analysed, 44.5 % were negative for all three genes, and 37.6 % were undoubtedly positive, with all three viral genes being amplified. A high degree of correlation between C t values among the genes confirmed the internal consistency of testing. Most of the positive samples were detected between the 15th and 35th cycles. We also registered a small number of samples with only one (13.2 %) or two (4.7 %) amplified genes, which may have originated from either freshly infected or already recovering patients. In addition, we did not detect any potentially false-positive samples from low-prevalence settings. Our results document that PCR testing represents a reliable and robust method for routine diagnostic detection of SARS-CoV-2.

Pancreatic necrosis infection (PNI) accounts for about 20–40 % of severe acute pancreatitis. PNI caused by anaerobic bacteria is unusual but when they present, Clostridium perfringens is the microorganism most commonly involved. We present a 60-year-old patient with a previous history of SARS-CoV-2, diagnosed with acute pancreatitis. During the hospitalisation he developed Clostridium perfringens bacteraemia. A CT-scan showed pancreatic gas gangrene and a surgical necrosectomy was performed. Clostridium perfringens was isolated in cultures of the pancreatic tissue and collections. The patient’s clinical status improved after surgery and the appropriate medical therapy. He was discharged 76 days after admission. Nowadays, the ‘step-up approach’ is an accepted therapeutic tool in treatment of pancreatic necrosis and peripancreatic fluid collections. However, most authors suggest that Clostridum perfringens infection requires a more aggressive approach due to the high mortality associated to clostridial infection.

Introduction. Disseminated sporotrichosis is an incapacitating infection caused by the dimorphic fungus Sporothrix schenckii. Because this condition may mimic the presentation of tuberculosis, syphilis and other bacterial infections, the diagnosis may be missed or delayed.

Case Presentation. We describe a case of disseminated sporotrichosis in a patient with poorly controlled human immunodeficiency virus infection. The patient was initially treated for bacterial skin infections. The differential diagnosis also included tuberculosis and syphilis. Only after appropriate specimens had been sent for microbiological and histopathological investigations was the diagnosis of disseminated sporotrichosis made and appropriate treatment started. The patient showed a good clinical response to itraconazole.

Conclusion. This report highlights the importance of having a high index of suspicion of endemic mycoses when managing immunocompromised patients. The report also demonstrates that a delay in the diagnosis of sporotrichosis increases morbidity and results in unnecessary and inappropriate treatment with associated costs and adverse effects.

Streptococcus lutetiensis has been known to cause sepsis in adults, but only one case regarding neonatal sepsis has been reported internationally, with no sequelae. We report the first case of neonatal bacteremia and meningitis with empyema caused by S. lutetiensis in the United States.