Gemella morbillorum

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Sharntie Christina Bench E 22 September 2017 [1]

Classification

Higher order taxa

Bacteria – Firmicutes – Bacilli – Bacillales – Gemella – G. morbillorum

Species

Gemella morbillorum. Type Strain: Prévot 2917B = ATCC 27824= CCUG 15561 = CCUG 18164 = CIP 81.10 = DSM 20572 = JCM 12968 = LMG 18985 = NCTC 11323 = VPI 5424

Description and significance

Gemella morbillorum is a facultative anaerobic, gram-positive cocci of the phylum Firmicutes. It is non-motile and non-spore-forming, and can occur singly, in pairs, and in short chains. G. morbillorum was first isolated from a patient with measles in 1917, and was once believed to be associated with measles [1]. G. morbillorum is part of the normal flora of human mucous membranes, found in the oropharynx, upper respiratory, gastrointestinal and female genital tracts [2]. However, G. morbillorum is an opportunistic pathogen, able to cause severe localised and generalised infections. Reported clinical disease cases for G. morbillorum are low, but these numbers could be misrepresentative due to these bacteria being commonly misidentified or left unidentified due to easy decolourisation during gram staining, by which they can appear gram-variable or gram-negative, and sometimes as elongated cocci [3]. Nevertheless, G. morbillorum has been known to cause endocarditis, meningitis, brain abscess, pleural empyema, nephritis, mediastinitis, and liver abscess [4]. G. morbillorum was previously named Diplococcus morbillorum, Peptococcus morbillorum, Peptostreptococcus morbillorum, then Streptococcus morbillorum. It was transferred from the genus Streptococcus to Gemella in 1988 when studies of 16S rRNA catalogues, DNA filter hybridization, and biochemical activities showed a closer relation to Gemella haemolysans than the Streptococcus genus [1]. G. morbillorum naturally produces an antimicrobial peptide, giving it prospects of being developed as a probiotic [5]. However, G. morbillorum can also transfer antibiotic resistance genes with disease-causing Streptococcus species [6], which poses a potential threat of antibiotic resistant G. morbillorum infections.

Genome structure

G. morbillorum strain M424 has a single circular genome of 1.75 Mb, containing 1,676 genes. Of these genes, 1,548 are protein-coding, 42 are tRNA genes, and 4 are non-coding RNAs. There are 7 rRNA genes, 1 gene forming 5S rRNA, 5 genes forming 16S rRNA, and 1 gene forming 23S rRNA. This genome information was obtained by shotgun sequencing for The Gemella morbillorum M424 whole genome shotgun (WGS) project, partner of the Human Microbiome Project. [7]

Cell structure and metabolism

Cell wall

As common with Gram-positive bacteria, the cell wall is composed of three main layers: A thin cytoplasmic lipid membrane, followed by a layer of periplasm, and a thick peptidoglycan layer on the outside. The cell walls of G. morbillorum contain peptidoglycan of the L-Lys-Ala1-3 type [1]. The cell walls of G. morbillorum are thinner than most gram-positive bacteria, ranging from 10-20nm, which is thought may contribute to their easy decolourisation during gram staining, and often misidentification as Gram-variable [3]. G. morbillorum also has a fibrous outer layer, which is said to be an extensively cross-linked polyanionic polysaccharide [3].

Motility

G. mobillorum is non-motile [1].

Metabolism

G. mobillorum is obligately fermentative. From the fermentation of glucose it produces L-lactic acid, with smaller amounts of acetic acid. Trace amounts of succinic, pyruvic acids, and ethanol have also been detected [1]. Formic acid is also sometimes produced. G. mobillorum can also produce acid from maltose and sucrose, and mannitol and sorbitol in some strains. Unlike G. haemolysans, G. morbillorum does not reduce nitrite, and are alkaline phosphatase negative [3]. Cell-free extracts from the bacteria also contain superoxide dismutase activity [1].

Virulence and Biofilm formation

Virulence in G. mobillorum is rarely investigated. A study in 2001 on a case of shunt nephritis showed the organism was responsible for the triggering of autoantibody production against proteinase 3 (PR3-ANCA). These antibodies are known to induce small vessel vasculitis associated with necrotising damage via release of PR3 from neutrophils and monocytes, which cases the detachment of and cytolysis of endothelial cells - likely through apoptosis [8]. A 2002 study inoculated healthy mice with G. mobillorum samples isolated from patients with pulpal necrosis, where they observed resulting down-regulation of IL-12 and IFN-γ. IL-12 and IFN-γ are important cytokines that enhance cytolytic activity of immune system natural killer and T cells, a process which is essential to the eradication of many pathogens [9]. A study from 2005 investigated the mechanism by which G. morbillorum induced apoptosis of lymph node cells, which was observed in periradicular disease (infection in tooth pulp, just above the root). Under their conditions, it was determined that this apoptosis was in some way dependent on TNFRp55 (tumour necrosis factor receptor p55) [10]. Members of the genus Gemella have also been shown to produce a specific IgA1 protease, destroys the host’s secretory Immunoglobulin A (IgA) [11]. This allows the bacteria to evade the adherence-inhibitory activity of secretory IgA, which is the main immunoglobulin found in mucous secretions [12]. These virulence factors assist G. mobillorum in the formation of biofilms. These can lead to diseases such as endocarditis, meningitis, brain abscess, pleural empyema, nephritis, mediastinitis, liver abscess [4]. However, disease-causing G. mobillorum biofilms very rarely occur in a healthy individual, and predominately correlate to poor dental health, dental manipulation or surgery, colorectal disease or procedures, steroid therapy, diabetes mellitus, or hepatorenal dysfunction [13]. Non-disease forming G. mobillorum biofilms occur commonly in the form of subgingival dental plaque [14].

Ecology

G. morbillorum is a facultative anaerobe. This means it utilised aerobic respiration to produce ATP in the presence of oxygen, but can survive on fermentation or anaerobic pathway when oxygen is not available [15]. G. morbillorum thrives in capnophilic (high CO2) environments, and prefers a microaerophilic (low O2) environments [3]. It is a microbiota of the human mucous membranes, found in the oropharynx, upper respiratory, gastrointestinal and female genital tracts [2]. As such, it is found commonly in the mouth and cause plaque in the subgingival area [14]. G. morbillorum is also among the most common bacteria present in teeth with cysts that do not resolve after repeated root canal treatments [16]. In subgingival plaques, G. morbillorum exist in co-aggregations with other bacteria, including V. parvula, Streptococcus sanguinis, Actinomyces naeslundii, Actinomyces viscosus, and Actinomyces odontolyticus [17]. Contact with disease-causing Streptococcus, such as S. pneumoniae and S. pyogenes can be worrying however, as these species of Streptococcus and G. morbillorum are able to transfer resistance genes because of their genomic similarity. Antibiotic resistance genes, which are a serious and growing problem in disease-causing Streptococcus, could be transferred to G. morbillorum populations, making infection harder to treat. In a study of resistance gene transfer between these organisms, G. morbillorum was found to be an important reservoir of genes conferring resistance to macrolides and related antibiotics in Streptococcus [6].

Pathology

G. mobillorum has been implicated in endocarditis, meningitis, brain abscess, pleural empyema, nephritis, mediastinitis, and liver abscess [4]. Poor dental health, dental manipulation or surgery, colorectal disease or procedures, steroid therapy, diabetes mellitus, and hepatorenal dysfunction are all recognised as predisposing factors for infection. G. mobillorum infection can also occur in immunocompromised patients. The most common cause of G. morbillorum-associated endocarditis is poor dental health or dental procedures [13]. In cases of G. mobillorum infection, a definite entry point, such as a dental defect, oral piercing, or gastrointestinal carcinoma is observed [18]. One case of G. mobillorum infection on the chest wall identified the entry point of the infection as acupuncture therapy the patient had received [19]. G. mobillorum is also being investigated as a potential tumour biomarker in oral squamous cell carcinoma (OSCC). G. mobillorum were found to be highly associated to the OSCC tumour site, and their fermentative nature has been theorised to contribute to the acidic and hypoxic microenvironment of tumours, and promote bacterial colonisation [20].

Application to biotechnology

G. mobillorum M242 strain produces subtilosin A, an AMP. AMPs are small secreted peptides that are toxic to some bacteria, often presenting antibacterial activity towards closely-related strains. AMPs are being investigated in therapeutic and agricultural fields, in the hope of developing novel microecologics or probiotic supplements [5].

Current research

A recent case report of a clinical infection due to G. mobillorum following a laparoscopic hysterectomy for uterine corpus cancer warned that “Surgeons in such cases should therefore give greater attention to the spread of normal flora microbes into the blood stream”, concluding that “the genital tract should be better cleaned and sterilized before surgery.” Cases of these infection may bring attention to surgical procedures that can be revised and improved [13]. As mentioned above, G. mobillorum is being investigated as a potential tumour biomarker in oral squamous cell carcinoma [20], and a possible microecologic or probiotic due to its production of the Antimicrobial Peptide subtilosin A [5].

References

1. Kilpper-balz, R. and Schleifer, K. (1988). Transfer of Streptococcus morbillorum to the Genus Gemella as Gemella morbillorum comb. nov. International Journal of Systematic Bacteriology, 38(4), pp.442-443.

2. Kofteridis, D., Anastasopoulos, T., Panagiotakis, S., Kontopodis, E. and Samonis, G. (2006). Endocarditis caused by Gemella morbillorum resistant to β-lactams and aminoglycosides. Scandinavian Journal of Infectious Diseases, 38(11-12), pp.1125-1127.

3. Dworkin, M. (2007). The prokaryotes. 4th ed. New York: Springer, pp.513-515.

4. Borro, P., Sumberaz, A. and Testino, G. (2014). Pyogenic liver abscess caused by Gemella morbillorum. Colomb Med (Cali), 45(2), pp.81-84.

5. Dong, B., Yi, Y., Liang, L. and Shi, Q. (2017). High Throughput Identification of Antimicrobial Peptides from Fish Gastrointestinal Microbiota. Toxins, 9(9), p.266.

6. Cerda Zolezzi, P., Laplana, L., Calvo, C., Cepero, P., Erazo, M. and Gomez-Lus, R. (2004). Molecular Basis of Resistance to Macrolides and Other Antibiotics in Commensal Viridans Group Streptococci and Gemella spp. and Transfer of Resistance Genes to Streptococcus pneumoniae. Antimicrobial Agents and Chemotherapy, 48(9), pp.3462-3467.

7. NCBI Reference Sequence: NZ_ACRX00000000.1

8. Nagashima, T., Hirata, D., Yamamoto, H., Okazaki, H. and Minota, S. (2001). Antineutrophil cytoplasmic autoantibody specific for proteinase 3 in a patient with shunt nephritis induced by Gemella morbillorum. American Journal of Kidney Diseases, 37(5), pp.e38.1-e38.4.

9. Ribeiro Sobrinho, A., de Melo Maltos, S., Farias, L., de Carvalho, M., Nicoli, J., de Uzeda, M. and Vieira, L. (2002). Cytokine production in response to endodontic infection in germ-free mice. Oral Microbiology and Immunology, 17(6), pp.344-353.

10. Ribeiro-Sobrinho, A. (2005). Bacteria recovered from dental pulp induce apoptosis of lymph node cells. Journal of Medical Microbiology, 54(4), pp.413-416.

11. Lomholt, J. and Kilian, M. (2017). Immunoglobulin A1 Protease Activity in Gemella haemolysans. Journal of Clinical Microbiology, 38(7), pp.2760–2762.

12. Macpherson, A. and Slack, E. (2007). The functional interactions of commensal bacteria with intestinal secretory IgA. Current Opinion in Gastroenterology, 23(6), pp.673-678.

13. Miyoshi, A., Miyatake, T., Nishimura, M., Tanaka, A., Kanao, S., Takeda, M., Mimura, M., Nagamatsu, M. and Yokoi, T. (2017). Gemella morbillorum bacteremia following total laparoscopic hysterectomy for uterine corpus cancer. Gynecology and Minimally Invasive Therapy, 6(2), pp.79-81.

14. Kamma, J., Diamanti-Kipioti, A., Nakou, M. and Mitsis, F. (2000). Profile of subgingival microbiota in children with primary dentition. Journal of Periodontal Research, 35(1), pp.33-41.

15. Ruoff, K. (n.d.). Aerococcus, Abiotrophia, and Other Aerobic Catalase-Negative, Gram-Positive Cocci. Manual of Clinical Microbiology, 10th Edition, pp.365-376.

16. Signoretti, F., Gomes, B., Montagner, F. and Jacinto, R. (2017). Investigation of Cultivable Bacteria Isolated from Longstanding Retreatment-resistant Lesions of Teeth with Apical Periodontitis. Journal of Endodontics, 39(10), pp. 1240-1244.

17. Carrouel, F., Viennot, S., Santamaria, J., Veber, P. and Bourgeois, D. (2016). Quantitative Molecular Detection of 19 Major Pathogens in the Interdental Biofilm of Periodontally Healthy Young Adults. Frontiers in Microbiology, 7.

18. Vossen, M., Gattringer, K., Khalifeh, N., Koreny, M., Spertini, V., Mallouhi, A., Willeit, M., Volc-Platzer, B., Asboth, F., Graninger, W., Thalhammer, F. and Lagler, H. (2011). Gemella morbillorum Bacteremia after Anti-Tumor Necrosis Factor Alpha as Acne Inversa Therapy. Journal of Clinical Microbiology, 50(3), pp.1109-1112.

19. Cho, H., Kwon, S. and Chung, S. (2015). Gemella morbillorumInfection after Acupuncture Therapy. Archives of Plastic Surgery, 42(1), p.95.

20. Pushalkar, S., Ji, X., Li, Y., Estilo, C., Yegnanarayana, R., Singh, B., Li, X. and Saxena, D. (2012). Comparison of oral microbiota in tumor and non-tumor tissues of patients with oral squamous cell carcinoma. BMC Microbiology, 12(1), p.144.

21. Sahm, K., MacGregor, B.J., Jørgensen, B.B., and Stahl, D.A. (1999) Sulphate reduction and vertical distribution of sulphate-reducing bacteria quantified by rRNA slotblot hybridization in a coastal marine sediment. Environ Microbiol 1: 65-74.

  1. MICR3004

This page is written by Sharntie Christina for the MICR3004 course, Semester 2, 2017