A high mortality event of Hong Kong newt (Paramesotriton hongkongensis) occurred during Nov. 2014 to June 2015 in Taipei Zoo. Predominant histopathological findings were multifocal necrotic foci in liver, spleen, and kidney with no or minimal inflammatory cell infiltration and the presence of abundant acid-fast positive bacilli. There were also multifocal to coalescing skin ulcerations with intralesional fungal hyphae morphologically consistent with Saprolegnia spp.1 Diffusely, the skeletal muscles showed varying degrees of degeneration characterized by swelling, increased eosinophilia, vacuolation, and fragmentation. The DNA of Mycobacterium spp. was detected via polymerase chain reaction (PCR) by using the primer sets targeting the heat-shock protein genes (hsp65) and internal transcribed spacer (ITS),2-5 and purified PCR amplicons were directly sequenced. The Mycobacterium spp. was 100% identical to the Mycobacterium marinum (M. marinum). Furthermore, the M. marinum also contained the mycolactone-producing plasmid, suggestive of mycolactone-producing mycobacteria (MPM).6,7 The lesions in these cases caused by MPM were multiple necrotic foci, which are quite different from the conventional granulomatous lesions seen in mycobacteriosis,8,9 which could be associated with the anti-inflammatory and apoptotic effects of mycolactone and the impaired immune function due to natural (decreased temperature) and anthropogenic stressors (inappropriate manipulation).10 Furthermore, the MPM may cause diseases in both ectotherms and endotherms, and is also considered as a zoonotic disease. To the best of our knowledge, this is the first report of MPM infection in Hong Kong newt.
The authors' thanks to all the pathology residencies in Graduate Institute of Molecular and Comparative Pathobiology, National Taiwan University (NTU) for helping case/sample collection and idea discussion, to Dr. Albert Taiching Liao and his students in School of Veterinary Medicine, NTU for molecular diagnosis, and to the veterinarians/animal keepers in Taipei Zoo for helping the necropsy and sample collection.
* Presenting author
+ Student presenter
1. Densmore CL, Green DE. Diseases of amphibians. ILAR J. 2007;48:235–254.
2. Devulder G, Perouse de Montclos M, Flandrois JP. A multigene approach to phylogenetic analysis using the genus Mycobacterium as a model. Int J Syst Evol Microbiol. 2005;55:293–302.
3. Haridy M, Tachikawa Y, Yoshida S, Tsuyuguchi K, Tomita M, Maeda S, Wada T, Ibi K, Sakai H, Yanai T. Mycobacterium marinum infection in Japanese forest green tree frogs (Rhacophorus arboreus). J Comp Pathol. 2014;151:277–289.
4. Kim H, Kim SH, Shim TS, Kim MN, Bai GH, Park YG, Le SH, Chae GT, Cha CY, Kook YH, Kim BJ. Differentiation of Mycobacterium species by analysis of the heat-shock protein 65 gene (hsp65). Int J Syst Evol Microbiol. 2005;55:1649–1656.
5. Telenti A, Marchesi F, Balz M, Bally F, Bottger EC, Bodmer T. Rapid identification of mycobacteria to the species level by polymerase chain reaction and restriction enzyme analysis. J Clin Microbiol. 1993;31:175–178.
6. Chemlal K, Huys G, Laval F, Vincent V, Savage C, Gutierrez C, Laneelle MA, Swings J, Meyers WM, Daffe M, Portaels F. Characterization of an unusual Mycobacterium: a possible missing link between Mycobacterium marinum and Mycobacterium ulcerans. J Clin Microbiol. 2002;40:2370–2380.
7. Ranger BS, Mahrous EA, Mosi L, Adusumilli S, Lee RE, Colorni A, Rhodes M, Small PL. Globally distributed mycobacterial fish pathogens produce a novel plasmid-encoded toxic macrolide, mycolactone F. Infect Immun. 2006;74:6037–6045.
8. Ferreira R, Fonseca LdeS, Afonso AM, da Silva MG, Saad MH, Lilenbaum W. A report of mycobacteriosis caused by Mycobacterium marinum in bullfrogs (Rana catesbeiana). Vet J. 2006;171:177–180.
9. Ramakrishnan L, Valdivia RH, McKerrow JH, Falkow S. Mycobacterium marinum causes both long-term subclinical infection and acute disease in the leopard frog (Rana pipiens). Infect Immun. 1997;5:767–773.
10. George KM, Pascopella L, Welty DM, Small PL. A Mycobacterium ulcerans toxin, mycolactone, causes apoptosis in guinea pig ulcers and tissue culture cells. Infect Immun. 2000;68:877–883.