The risk factors of children acquiring refractory mycoplasma pneumoniae pneumonia: A meta-analysis.
Medicine
OBJECTIVES:Refractory mycoplasma pneumoniae pneumonia (RMPP) in children has been increasing worldwide. In this study, we conducted a meta-analysis to generate large-scale evidence on the risk factors of RMPP to provide suggestions on prevention and controlling for children. METHODS:Web of Science, PubMed, Embase, Cochrane Library, China National Knowledge Infrastructure, and Wanfang (Chinese) were searched to identify relevant articles. All analyses were performed using Stata 14.0. RESULTS:We conducted a meta-analysis of 15 separate studies. Fever for more than 10 days (odds ratio [OR] 3.965, 95% confidence interval [CI] 2.109-7.456), pleural effusion (OR 6.922, 95% CI 2.058-23.282), extra-pulmonary complications (OR 17.762, 95% CI 11.146-28.305), pulmonary X-ray consolidation ≥2/3 (OR 8.245, 95% CI 1.990-34.153), CRP >40 mg/L (OR 4.975, 95% CI 2.116-11.697) were significantly related to the risk of RMPP. We did not find an association between male sex (OR 0.808, 95% CI 0.548-1.189), LDH >410IU/L (OR 1.033, 95% CI 0.979-1.091) and the risk of RMPP. CONCLUSIONS:Fever for more than 10 days, pleural effusion, extra-pulmonary complications, pulmonary X-ray consolidation≥ 2/3 and CRP >40 mg/L are risk factors for early evaluation of RMPP.
10.1097/MD.0000000000024894
[Clinical characteristics of refractory Mycoplasma pneumoniae pneumonia in children].
Xu Jiang-Jiang,Shu Lin-Hua
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
OBJECTIVE:To provide a basis for early diagnosis and treatment of refractory Mycoplasma pneumoniae pneumonia (RMPP) in children by comparing the clinical characteristics of RMPP and general Mycoplasma pneumoniae pneumonia (MPP). METHODS:Children with MPP hospitalized between October 2015 and December 2016 were selected as study subjects. According to the diagnostic criteria, children were divided into RMPP group (n=152) and MPP group (n=551). The differences between the two groups in the basic situation, clinical manifestations, infection parameters and myocardial enzymes were compared. RESULTS:There were no significant differences in gender and age between the RMPP and MPP groups (P>0.05). The peak temperature in the RMPP group was significantly higher than that in the MPP group on the first day of admission (P<0.01). The percentage of children with augmentation in the RMPP group was lower than that in the MPP group (P=0.009). The percentage of neutrophils [Ne(%)] and serum procalcitonin (PCT) levels in the RMPP group were both higher than those in the MPP group (P<0.05), while the percentage of lymphocytes was significantly lower in the RMPP group (P<0.05). The serum levels of aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) in the RMPP group were also higher than those in the MPP group (P<0.05). Binary logistic regression analysis showed that the peak temperature and LDH were closely related to RMPP in children (P<0.05). Receiver operating characteristic (ROC) curve analysis showed that the area under the curve (AUC) of the peak temperature and LDH for the diagnosis of RMPP was 0.647 and 0.637 respectively. In children ≤2 years old, when the threshold value of LDH was 400 U/L, the diagnostic sensitivity was 52.63% and the specificity was 54.84%. In children above 2 years old, when the threshold value of LDH was 335 U/L, the diagnostic sensitivity was 69.92% and the specificity was 51.55%. CONCLUSIONS:The children with RMPP have a high fever in the early stage. Meanwhile there are abnormal laboratory test results in these children. Elevated serum LDH levels have a high clinical value of early diagnosis of RMPP, especially in children above 2 years.
Potential Causes and Consequences of Gastrointestinal Disorders during a SARS-CoV-2 Infection.
Cell reports
Coronaviruses cause several human diseases, including severe acute respiratory syndrome. The global coronavirus disease 2019 (COVID-19) pandemic has become a huge threat to humans. Intensive research on the pathogenic mechanisms used by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is urgently needed-notably to identify potential drug targets. Clinical studies of patients with COVID-19 have shown that gastrointestinal disorders appear to precede or follow the respiratory symptoms. Here, we review gastrointestinal disorders in patients with COVID-19, suggest hypothetical mechanisms leading to gut symptoms, and discuss the potential consequences of gastrointestinal disorders on the outcome of the disease. Lastly, we discuss the role of the gut microbiota during respiratory viral infections and suggest that targeting gut dysbiosis may help to control the pathogenesis of COVID-19.
10.1016/j.celrep.2020.107915
The microbiome and critical illness.
Dickson Robert P
The Lancet. Respiratory medicine
The central role of the microbiome in critical illness is supported by a half century of experimental and clinical study. The physiological effects of critical illness and the clinical interventions of intensive care substantially alter the microbiome. In turn, the microbiome predicts patients' susceptibility to disease, and manipulation of the microbiome has prevented or modulated critical illness in animal models and clinical trials. This Review surveys the microbial ecology of critically ill patients, presents the facts and unanswered questions surrounding gut-derived sepsis, and explores the radically altered ecosystem of the injured alveolus. The revolution in culture-independent microbiology has provided the tools needed to target the microbiome rationally for the prevention and treatment of critical illness, holding great promise to improve the acute and chronic outcomes of the critically ill.
10.1016/S2213-2600(15)00427-0
Mechanisms linking the human gut microbiome to prophylactic and treatment strategies for COVID-19.
Walton Gemma E,Gibson Glenn R,Hunter Kirsty A
The British journal of nutrition
The recent COVID-19 pandemic has altered the face of biology, social interaction and public health worldwide. It has had a destructive effect upon millions of people and is approaching a devastating one million fatalities. Emerging evidence has suggested a link between the infection and gut microbiome status. This is one of the several factors that may contribute towards severity of infection. Given the fact that the gut is heavily linked to immunity, inflammatory status and the ability to challenge pathogens, it is worthwhile to consider dietary intervention of the gut microbiota as means of potentially challenging the viral outcome. In this context, probiotics and prebiotics have been used to mitigate similar respiratory infections. Here, we summarise links between the gut microbiome and COVID-19 infection, as well as propose mechanisms whereby probiotic and prebiotic interventions may act.
10.1017/S0007114520003980
The Fungal Gut Microbiome Exhibits Reduced Diversity and Increased Relative Abundance of Ascomycota in Severe COVID-19 Illness and Distinct Interconnected Communities in SARS-CoV-2 Positive Patients.
Frontiers in cellular and infection microbiology
Clinical and experimental studies indicate that the bacterial and fungal gut microbiota modulates immune responses in distant organs including the lungs. Immune dysregulation is associated with severe SARS-CoV-2 infection, and several groups have observed gut bacterial dysbiosis in SARS-CoV-2 infected patients, while the fungal gut microbiota remains poorly defined in these patients. We analyzed the fungal gut microbiome from rectal swabs taken prior to anti-infective treatment in 30 SARS-CoV-2 positive (21 non-severe COVID-19 and 9 developing severe/critical COVID-19 patients) and 23 SARS-CoV-2 negative patients by ITS2-sequencing. Pronounced but distinct interconnected fungal communities distinguished SARS-CoV-2 positive and negative patients. Fungal gut microbiota in severe/critical COVID-19 illness was characterized by a reduced diversity, richness and evenness and by an increase of the relative abundance of the Ascomycota phylum compared with non-severe COVID-19 illness. A dominance of a single fungal species with a relative abundance of >75% was a frequent feature in severe/critical COVID-19. The dominating fungal species were highly variable between patients even within the groups. Several fungal taxa were depleted in patients with severe/critical COVID-19.The distinct compositional changes of the fungal gut microbiome in SARS-CoV-2 infection, especially in severe COVID-19 illness, illuminate the necessity of a broader approach to investigate whether the differences in the fungal gut microbiome are consequences of SARS-CoV-2 infection or a predisposing factor for critical illness.
10.3389/fcimb.2022.848650
Shen-ling-bai-zhu-san ameliorates inflammation and lung injury by increasing the gut microbiota in the murine model of Streptococcus pneumonia-induced pneumonia.
Feng Jinli,Dai Weibo,Zhang Cheng,Chen Houjun,Chen Ziliang,Chen Yongfeng,Pan Qianyi,Zhou Yongmao
BMC complementary medicine and therapies
BACKGROUND:Shen-ling-bai-zhu-san (SLBZS) regulates inflammation and gut microbiota which are associated with Streptococcus pneumoniae (Spn)-induced pneumonia. So, we studied the therapeutic effect of SLBZS and evaluated whether gut microbiota is associated with the effects of SLBZS in improving Spn-induced pneumonia. METHODS:Spn-induced pneumonia NIH mice were treated by SLBZS and cefixime. A CT scan was performed and Myeloperoxidase (MPO) activity in lung homogenates was determined using the MPO Colorimetric Assay Kit. Inflammation levels in lung homogenates were measured using ELISA. Bacterial load was coated on a TSAII sheep blood agar. Intestinal gut microbiota information was analyzed according to sequencing libraries. RESULTS:SLBZS decreased bacterial load, reduced wet/dry weight ratio, inhibited myeloperoxidase activity, reduced the neutrophils count, and ameliorated lung injury. Furthermore, SLBZS inhibited interleukin (IL)-1β, IL-6, tumor necrosis factor-α, IL-2, IL-8, IL-12, and interferon-γ secretion and enhanced IL-10 secretion. These results suggest that SLBZS ameliorates lung injury in mice with Spn-induced pneumonia. Moreover, SLBZS reduced inflammatory cytokine levels in a concentration-dependent manner and increased gut microbiota abundance and diversity. After SLBZS treatment, bacteria such as Epsilonbacteraeota, Bacteroidetes, Actinobacteria, Proteobacteria, and Patescibacteria were significantly reduced, while Tenericutes and Firmicutes were significantly increased. CONCLUSION:SLBZS ameliorates inflammation, lung injury, and gut microbiota in mice with S. pneumoniae-induced pneumonia.
10.1186/s12906-020-02958-9
Gut microbiome alterations and gut barrier dysfunction are associated with host immune homeostasis in COVID-19 patients.
Sun Zhonghan,Song Zhi-Gang,Liu Chenglin,Tan Shishang,Lin Shuchun,Zhu Jiajun,Dai Fa-Hui,Gao Jian,She Jia-Lei,Mei Zhendong,Lou Tao,Zheng Jiao-Jiao,Liu Yi,He Jiang,Zheng Yuanting,Ding Chen,Qian Feng,Zheng Yan,Chen Yan-Mei
BMC medicine
BACKGROUND:COVID-19 is an infectious disease characterized by multiple respiratory and extrapulmonary manifestations, including gastrointestinal symptoms. Although recent studies have linked gut microbiota to infectious diseases such as influenza, little is known about the role of the gut microbiota in COVID-19 pathophysiology. METHODS:To better understand the host-gut microbiota interactions in COVID-19, we characterized the gut microbial community and gut barrier function using metagenomic and metaproteomic approaches in 63 COVID-19 patients and 8 non-infected controls. Both immunohematological parameters and transcriptional profiles were measured to reflect the immune response in COVID-19 patients. RESULTS:Altered gut microbial composition was observed in COVID-19 patients, which was characterized by decreased commensal species and increased opportunistic pathogenic species. Severe illness was associated with higher abundance of four microbial species (i.e., Burkholderia contaminans, Bacteroides nordii, Bifidobacterium longum, and Blautia sp. CAG 257), six microbial pathways (e.g., glycolysis and fermentation), and 10 virulence genes. These severity-related microbial features were further associated with host immune response. For example, the abundance of Bu. contaminans was associated with higher levels of inflammation biomarkers and lower levels of immune cells. Furthermore, human-origin proteins identified from both blood and fecal samples suggested gut barrier dysfunction in COVID-19 patients. The circulating levels of lipopolysaccharide-binding protein increased in patients with severe illness and were associated with circulating inflammation biomarkers and immune cells. Besides, proteins of disease-related bacteria (e.g., B. longum) were detectable in blood samples from patients. CONCLUSIONS:Our results suggest that the dysbiosis of the gut microbiome and the dysfunction of the gut barrier might play a role in the pathophysiology of COVID-19 by affecting host immune homeostasis.
10.1186/s12916-021-02212-0
The human microbiome and COVID-19: A systematic review.
PloS one
BACKGROUND:Human microbiotas are communities of microorganisms living in symbiosis with humans. They play an important role in the host immune response to respiratory viral infection. However, evidence on the human microbiome and coronavirus disease (COVID-19) relationship is insufficient. The aim of this systematic literature review was to evaluate existing evidence on the association between the microbiome and COVID-19 in humans and summarize these data in the pandemic era. METHODS:We conducted a systematic literature review on the association between the microbiome and COVID-19 in humans by searching PubMed, Embase, and the Cochrane Library, CINAHL, and Web of Science databases for articles in English published up to October 31, 2020. The results were analyzed qualitatively. This study is registered with PROSPERO (CRD42020195982). RESULTS:Of the 543 articles identified by searching databases, 16 in line with the research objectives were eligible for qualitative review: eight sampled the microbiome using stool, four using nasopharyngeal or throat swab, three using bronchoalveolar lavage fluid, and one using lung tissue. Fecal microbiome dysbiosis and increased opportunistic pathogens were reported in COVID-19 patients. Several studies suggested the dysbiosis in the lung microbiome of COVID-19 patients with an abundance of opportunistic pathogens using lower respiratory tract samples. The association between COVID-19 severity and the human microbiome remains uncertain. CONCLUSION:The human fecal and respiratory tract microbiome changed in COVID-19 patients with opportunistic pathogen abundance. Further research to elucidate the effect of alternation of the human microbiome in disease pathogenesis is warranted.
10.1371/journal.pone.0253293