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DESCRIPTION OF ACTINOMYCES QIGUOMINGII SP. NOV. Actinomyces qiguomingii (qi.guo.ming��� i.i. N.L. gen. n. qiguomingii, named after Guoming Qi, a prominent microbiologist in the China CDC for his seminal contribution to Vibrio taxonomy and classification). Cells are Gram-stain-positive, catalase- and oxidase-negative, non-motile rods (0.3���0.5��2.1���2.8 ��m). The novel strains grow under anaerobic and in air plus 5% CO 2 condition. The isolates grow at 28���42 ��C (optimum, 37 ��C), at pH 6.0���9.0 (optimum, pH 7.0) and at 0���3 % (w/v) NaCl (optimum, 1%). Colonies are milky white, circular, convex and about 1 mm on BHI-sheep blood agar after 72 h incubation under optimal growth conditions. The end products from glucose fermentation include ethanol and lactic acid. Nitrate is reduced and indole is not produced. When tested with API Rapid ID 32A and ZYM kits, the cells are positive for �� -galactosidase, �� -glucosidase, �� -glucosidase, arginine arylamidase, proline arylamidase, phenylalanine arylamidase, leucine arylamidase, tyrosine arylamidase, glycine arylamidase, histidine arylamidase, alkaline phosphatase, valine arylamidase, acid phosphatase and naphthol-AS-BI-phosphohydrolase. Acid is produced at 48 h incubation from glycerol, D-arabinose,L-arabinose, D-ribose, D-xylose, D-galactose, D-glucose, D-fructose, D-mannose, L-sorbose, L-rhamnose, inositol, D-mannitol, D-sorbitol, amygdalin, arbutin, aesculin, salicin, cellobiose, maltose, lactose, melibiose, sucrose, trehalose, inulin, melezitose, raffinose, starch, glycogen, xylitol, gentiobiose, turanose, D-lyxose and potassium gluconate. The major polar lipids are diphosphatidylglycerol and phosphatidylinositol-mannoside. The main cellular fatty acid is C 16:0, followed by C 18:1 �� 9 c. The main quinones are MK-10 and MK-9. The whole-cell sugars contain rhamnose, ribose and glucose. The diagnostic amino acids of cell-wall peptidoglycan include alanine, lysine, glutamic acid and ornithine. The type strain, 410 T (= CGMCC 1.16361 T = DSM 106201 T), isolated from a Tibetan antelope in Qinghai, PR China, has a G+C content of 67.4 mol%. The 16S rRNA gene and genome sequence accession numbers of strain 410 T are MG 650117 and CP025228, respectively. Strain 553 is classified in this species., Published as part of Zhu, Wentao, Yang, Jing, Lu, Shan, Lai, Xin-He, Jin, Dong, Wang, Xiaoxia, Pu, Ji, Ren, Zhihong, Huang, Ying, Wu, Xiaomin, Zhang, Xiaoyan, Xu, Jianqing & Xu, Jianguo, 2020, Actinomyces qiguomingii sp. nov., isolated from the Pantholops hodgsonii, pp. 58-64 in International Journal of Systematic and Evolutionary Microbiology 70 (1) on page 63, DOI: 10.1099/ijsem.0.003709, http://zenodo.org/record/6048656

Francisella tularensis, the causative agent of tularemia, is a potent human and animal pathogen. Its principal survival mechanism is rapid intracellular multiplication. The mechanisms that enables it to multiply intracellularly have been ill-defined and the thesis focused on characterizing the outcome of the macrophage-Francisella interaction and also if the interactions differ between the various subspecies of F tularensis. The nature of host cell death was examined and the correlation of macrophage killing with intramacrophage Francisella growth was investigated by in vitro infection of J774A.1 macrophages with either the live vaccine (LVS) strain of F. tularensis, belonging to subspecies holarctica, or the subspecies novicida strain U112 Macrophage entry was in both cases cytochalasin D-sensitive but the intramacrophage growth of the two Francisella strains led to distinct types of host cell death, i.e., apoptosis vs. necrosis. The macrophage apoptosis induced by infection with the LVS strain was mediated via the intrinsic pathway with critical involvement of caspase-3 and the mitochondria. The infected and apoptotic macrophages were shrunken, their chromatin was specifically degraded and revealed a typical DNA ladder pattern upon electrophoresis. Moreover, they were TUNEL positive, indicating the occurrence of apoptosis-dependent DNA fragmentation. The necessity of intracellular growth for the apoptosis was shown by the use of an isogenic mutant, denoted iglC, which lacked the ability to multiply intracellularly and this infection did not result in apoptosis. The F. novicida strain U112, on the other hand, inhibited NF- B activity and ultimately induced macrophage necrosis. The infected and necrotic macrophages were enlarged, their chromatin was randomly degraded which gave a diffuse DNA pattern typical of necrosis. There was no apoptosis-specific caspase activation. By the use of an isogenic mutant, denoted mglA, it was shown that intracellular replication was necessary for the induction of necrosis. A hemolytic protein, novilysin A, was found in the F. novicida strain U112 but lacking in other subspecies of F. tularensis. The protein is a putative virulence factor but most likely not involved in the induction of necrosis. Its significance for the pathogenesis of F. novicida remains to be determined. The findings of the thesis provide a detailed picture of the interaction between the host cells and various subspecies of F. tularensis. It also shows that the outcome of the interaction is critically dependent on the type of F. tularensis subspecies. The findings also question the use of F. novicida as a model organism for understanding pathogenicity mechanisms of the species in general. The induction of the host cell death is presumably an important mechanism for the survival of F. tularensis since it allows the bacterium to escape from cells deplete of nutrients and subsequently to invade cells with an intact supply of nutrients necessary for its continuous multiplication.