In 1890, Von Ratz studied a micro-organism isolated by Schütz from milk and noted its characteristic variability in power of slime production. This organism was later described as Micrococcus mucilaginosus in 1900 by Migula [1]. It was renamed to Stomatococcus mucilaginosus in 1982 based on various characteristics differentiating it from Micrococcus [2]. Finally in 2000, it was reclassified to the genus of Rothia as Rothia mucilaginosa based on 16S rRNA sequencing [3]. Rothia mucilaginosa can be isolated from the oral cavity and upper respiratory tract [4]. Rothia mucilaginosa forms 3.4% of the total cultivable aerobic bacteria present in the oral cavity flora [5]. It is a Gram positive, non-motile, encapsulated, non-spore forming bacteria and their size varies from 0.9 to 1.3 μm in diameter. They are arranged in clusters mostly, rarely in pairs and tetrads [2].
Identification of Rothia mucilaginosa as a possible human pathogen occured for the first time in 1978, when it was isolated from a case of endocarditis in a patient after cardiac catheterization [6]. Over the years, R. mucilaginosa has emerged as an opportunistic pathogen which can cause severe infections including sepsis, endocarditis, pneumonia, acute respiratory distress syndrome (ARDS) and meningitis in immunocompromised patients [7,9,10]. Some literature even mention R. mucilaginosa as a causative pathogen causing disease in immuno-competent patients [8]. It’s role as an opportunistic bacteria can be emphasized further as a study found it to be a cause of secondary pneumonia in a H1N1 positive patient in 2011 [11]. The number of infections caused by R. mucilaginosa is likely to be under-reported, since the bacteria can be misidentified as coagulase-negative staphylococci or micrococci [9,10].
On 31 December 2019, the Wuhan Health Commission reported a cluster of atypical pneumonia cases in Wuhan, China caused by an unknown organism. The organism was later identified as a novel coronavirus and was finally named as SARS CoV-2 by the Coronavirus Study Group (CSG) of the International Committee and the disease which it causes was called ‘COVID-19’ by the World Health Organization (WHO) [12]. As of 8th April 2020, there have been 1,353,361 confirmed COVID-19 cases globally which has accounted for 79, 235 deaths globally [13]. The most common causes of death in SARS CoV-2 patients included acute respiratory distress syndrome, type I respiratory failure, sepsis and acute cardiac injury [14]. Lung biopsy of COVID-19 patients have shown presence of bilateral alveolar damage with cellular fibromyxoid exudates suggestive of changes of acute respiratory distress syndrome. Also, interstitial mononuclear inflammatory infiltrate has been noted in the lungs [15]. Immunological dysfunction in COVID-19 patients can be demonstrated by presence of overactivation of T cells with increase of Th17 and high cytotoxicity of CD8 T cells [15]. Such widespread inflammatory changes and immune dysfunction can be considered as an open ground for secondary opportunistic bacterial infections. A study of 191 patients conducted in two hospitals in Wuhan showed that nearly one in seven COVID-19 patients (28 patients out of 191) developed secondary bacterial infections and about 50 percent of the patients who died had secondary bacterial infections [16].
Thus, we can conclude that the presence of secondary opportunistic bacterial infections can significantly affect the outcome of COVID-19 patients in terms of morbidity and mortality and measures need to be undertaken to promptly diagnose and treat such infections as early as possible. Even in the past influenza pandemics, the majority of deaths were caused from secondary bacterial pneumonia caused by commensals of the upper respiratory-tract [17]. Immune dysfunction in COVID-19 can also pave the way for opportunistic bacterial infections which would rarely occur in immunocompetent patients. There has been a study which showed COVID-19 co-infection with Mycoplasma pneumoniae [18]. To the best of our knowledge, there has not been any study described in which Rothia mucilaginosa was isolated from a COVID-19 patient. Here, we are presenting a case of a COVID-19 positive patient in which Rothia mucilaginosa was isolated from sputum culture resulting in a secondary pneumonia.
References
[1] Migula, W. 1900. System der Bakterien. Gustav Fischer, Jena.
[2] Bergan T., Kocur M., Stomatococcus mucilaginosus gen. nov., sp. nov.,
ep. rev., a member of the family Microcoecaceae. Int. J. sysl. Bact., 1982,
32, 374-377.
[3] Collins MD, Hutson RA, Båverud V, Falsen E. Characterization of a Rothia-like organism from a mouse: Rothia nasimurium sp. nov. and reclassification of Stomatococcus mucilaginosus as Rothia mucilaginosa comb. nov. Int J Syst Evol Microbiol 2000;3:1247–51.
[4] Stackebrandt E. The Genus Stomatococcus: Rothia mucilaginosa, basonym Stomatococcus mucilaginosus. The Prokaryotes [Internet]. Springer New York; 2006;975–82.
[5] Kobayashi T, Uchibori S, Tsuzukibasi O, Goto H, Aida M: A selective medium for Rothia mucilaginosa and its distribution in oral cavities. JMicrobiol Methods. 91:364-365, 2012.
[6] Rubin SJ., et al. “Endocarditis associated with cardiac catheterization due to a gram-positive coccus designated Micrococcus mucilaginosus incertae sedis”. Journal of Clinical Microbiology 7.6 (1978): 546-549.
[7] Henwick S, Koehler M, Patrick CC. Complications of bacteremia due to Stomatococcus mucilaginosus in neutropenic children. Clin Infect Dis 1993;17:667–71.
[8] Faiad G, Singh M, Narasimhan A, Mendez M, Shama S, Nassar N. Rothia mucilaginosa life threatening infections in non-neutropenic hosts. Open Journal of Internal Medicine 2011;1:68–71.
[9] Korsholm, T. L., Haahr, V., & Prag, J. (2007). Eight cases of lower respiratory tract infection caused by Stomatococcus mucilaginosus. Scandinavian Journal of Infectious Diseases, 39(10), 913–917.
[10] Sofia Maraki & Ioannis S. Papadakis (2015) Rothia mucilaginosa pneumonia: a literature review, Infectious Diseases, 47:3, 125-129.
[11] Prakash, R., Sangeetha, S., Lakshminarayana S, A., & Chavan, S.K. (2015). Secondary Pneumonia due to Rothia mucilaginosa in a H1N1 patient.
[12] Gorbalenya AE, Baker SC, Baric RS et al. Severe acute respiratory syndrome-related coronavirus: the species and its viruses – a statement of the Coronavirus Study Group.
bioRxiv. 2020; (published online Feb 11.) (preprint).
DOI: 10.1101/2020.02.07.937863
[13] World Health Organization (WHO). Novel coronavirus (2019-nCoV). Situation report.
[14] Chen T, Wu D, Chen H, et al. Clinical characteristics of 113 deceased patients with coronavirus disease 2019: retrospective study [published correction appears in BMJ. 2020 Mar 31;368:m1295]. BMJ. 2020;368:m1091. Published 2020 Mar 26. doi:10.1136/bmj.m1091
[15] Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. The Lancet Respiratory medicine. 2020. https://doi.org/10.1016/S2213-2600(20)30076-X.
[16] Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study
Zhou, Fei et al.
The Lancet, Volume 395, Issue 10229, 1054 – 1062
[17] Morens DM, Taubenberger JK, Fauci AS. Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemic influenza preparedness. J Infect Dis. 2008;198(7):962–970. doi:10.1086/591708
[18] Fan BE, Lim KGE, Chong VCL,
Chan SSW, Ong KH, Kuperan P. COVID-19 and mycoplasma pneumoniae coinfection. Am J Hematol. 2020;1.
https://doi.org/10.1002/ajh.25785
2020-4-10-1586504948