The coronavirus disease 2019 (COVID-19) pandemic caused by the outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). To date, COVID-19 has claimed nearly seven million lives worldwide.
Due to the high mortality, scientists have extensively studied aspects of SARS-CoV-2, adding the body’s reaction to this virus, as well as the possibility of co-infections or secondary infections. The optimal clinical technique to reduce the mortality rate and protect more people from contracting COVID-19 was also explored.
The number one SARS-CoV-2 infection is the human respiratory tract. Clinical outcomes in chronic respiratory diseases are particularly affected due to interactions between the human respiratory microbiota and the host immune system.
Several studies have indicated an alteration of the respiratory microbiota after respiratory viral infections that alters the innate immune reaction of the host, thus facilitating coinfections and superinfections. The respiratory microbiome also affects the colonization and proliferation of pathogens.
SARS-CoV-2 infection promotes microbial dysbiosis through changing the nasal, oropharyngeal and pulmonary microenvironment. This microbial dysbiosis promotes coinfection or secondary infection, resulting in increased morbidity and mortality in patients inflamed by SARS-CoV-2. To design better pharmaceutical approaches and diagnostics, it is to perceive the link between the respiratory microbiota and the pathogenesis of COVID-19.
There remains a lack of studies similar to the lung microbiome due to limitations in sampling techniques and difficulties in assessing respiratory tract decline. Although some small-scale studies have evaluated the bacterial composition in the lungs of COVID-19 patients, the presence of other microbes such as fungi, which can also affect the lungs, has not been discussed. Therefore, there remains a need to explore the prevalence of bacteria and fungi in the lungs of COVID-19 patients.
A recent pathogen study used nanopore sequencing for fungal and bacterial microbiota in the lungs of COVID-19 and non-COVID-19 patients.
Bronchoalveolar lavage fluid (BALF) and sputum samples collected from thirty-eight patients hospitalized due to COVID-19 and twenty-six patients with pneumonia not related to COVID-19. All patients treated at Zhongnan Hospital, Wuhan University, China, between February 1, 2020 and August 15, 2020
Subsequently, the microbial DNA was extracted from the samples and subjected to targeted sequencing in the nanopores according to a standardized procedure.
Both examination teams included participants in terms of average age and gender ratio. More than 75% of patients on either team had comorbidities such as diabetes, coronary artery disease, hypertension, chronic infectious diseases, and chronic lung disease.
Hospitalized patients with SARS-CoV-2 infection required increased oxygen support, invasive ventilation, and noninvasive ventilation compared to patients without COVID-19. Both examination teams underwent antibiotic treatment; however, antiviral and antifungal remedies were more commonly prescribed to COVID-19 patients. A total of 12 COVID-19 patients and six non-COVID-19 patients died during hospitalization.
Consistent with previous studies, laboratory effects of existing ones indicated that COVID-19 patients had significant relief in lymphocyte counts and hemoglobin levels, as well as higher serum amyloid A (ASA) levels and a sliding neutrophil-to-white-to-white blood ratio.
Significant relief in microbial diversity and severe microbial dysbiosis has been observed in COVID-19 patients. In particular, the distribution of bacteria and fungi in COVID-19 patients differed from that of non-COVID-19 patients.
An increased abundance of opportunistic pathogens has been known in patients with COVID-19, which has altered lung ecology. These pathogens can announce co-infections or secondary infections and influence disease severity.
Metagenomic sequencing revealed that, compared to patients who do not have COVID-19, Acinetobacter baumannii provides a particularly superior abundance in most COVID-19 patients. Previous studies have indicated that patients inflamed with this pathogen are vulnerable to severe COVID-19.
More studies are needed to perceive the underlying mechanism through which Acinetobacter proliferates in the COVID-19 lung. This discovery can be used to expand effective treatments targeting this bacteria-virus interaction to clinical outcomes.
A large amount of Candida spp. , particularly Candida glabrata, Candida parapsilosis and Candida albicans, has also been observed in the lungs of COVID-19 patients. In addition, many bacterial taxa discovered in the lungs of COVID-19 patients had strong correlations with signs of inflammation.
SARS-CoV-2 infection can be serious or even fatal in certain populations, such as the elderly, others with underlying physical conditions, and those with weakened immune systems.
In this study, a significant difference in lung microbiome was observed between controls with COVID-19 and those without COVID-19. Specifically, COVID-19 patients had a higher abundance of opportunistic pathogens, namely Acinetobacter baumannii and Candida spp. In particular, certain pathogens found in the lungs of COVID-19 patients have influenced alterations in certain signs of inflammation.
Written by
Priyom holds a PhD in Plant Biology and Biotechnology from the University of Madras, India. She is an active er and an experienced science writer. Priyom is also co-author of several original articles that have been published in renowned peer-reviewed journals. She is also an avid reader and amateur photographer.
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