Nocardia seriolae: a serious threat to the largemouth bass Micropterus salmoides industry in Southwest China

2020 ◽  
Vol 142 ◽  
pp. 13-21
Author(s):  
X Lei ◽  
R Zhao ◽  
Y Geng ◽  
K Wang ◽  
PO Yang ◽  
...  
Keyword(s):  
Largemouth Bass ◽  
Southwest China ◽  
Micropterus Salmoides ◽  
Clinical Signs ◽  
Antibacterial Activities ◽  
Phenotypic Characterization ◽  
Diseased Fish ◽  
Bacterial Aggregates ◽  
Nocardia Seriolae

Nocardia seriolae is the causative agent of nocardiosis in both marine and freshwater fish. Here, we report on multiple outbreaks of nocardiosis associated with elevated mortality (23-35%) in farmed largemouth bass in Sichuan, China, from 2017 to 2018. A total of 9 strains isolated from diseased largemouth bass were identified as N. seriolae by phenotypic characterization, 16S rRNA and hsp65 gene sequence analysis. The clinical signs of infected largemouth bass included hemorrhage, skin ulcers and prominent tubercles varying in size in the gill, liver, spleen and kidney. Experimental infection indicated that these isolates were the pathogens responsible for the mortalities. In vitro antibacterial activities of 12 antibiotics against N. seriolae isolates were determined as minimum inhibitory concentrations. Histopathological observation of diseased fish infected with N. seriolae showed necrotizing granulomatous hepatitis, nephritis, splenitis, epithelial hypertrophy and hyperplasia with degenerative changes of the epithelium in the gill. Large quantities of bacterial aggregates were found in the necrotic area of the granuloma by Lillie-Twort Gram stain and immunocytochemistry. Our findings indicated that N. seriolae is a serious threat to the largemouth bass Micropterus salmoides industry in Southwest China.

scholarly journals A new ranavirus of the Santee-Cooper group invades largemouth bass (Micropterus salmoides) culture in southwest China

Aquaculture ◽  
2020 ◽  
Vol 526 ◽  
pp. 735363
Author(s):  
Ruoxuan Zhao ◽  
Yi Geng ◽  
Zhenyang Qin ◽  
Kaiyu Wang ◽  
Ping Ouyang ◽  
...  
Keyword(s):  
Largemouth Bass ◽  
Southwest China ◽  
Micropterus Salmoides

scholarly journals CXCL14 deficiency does not impact the outcome of influenza or Escherichia coli infections in mice

2014 ◽  
Vol 8 (10) ◽  
pp. 1301-1306 ◽  
Author(s):  
Abubaker ME Sidahmed ◽  
Alberto J Leon ◽  
David Banner ◽  
Alyson A Kelvin ◽  
Thomas Rowe ◽  
...  
Keyword(s):  
Viral Infections ◽  
Influenza Infection ◽  
Clinical Signs ◽  
Influenza Virus Infection ◽  
Antibacterial Activities ◽  
Phenotypic Characterization ◽  
E Coli ◽  
Small Proteins ◽  
Conserved Gene ◽  
Deficient Mice

Introduction: Chemokines are small proteins that regulate different cellular functions, such as leukocyte activation, chemoattraction and inflammation. The chemokine CXCL14 (BRAK) is a highly conserved gene among species and through evolution. It has been shown that CXCL14 is locally upregulated during viral infections, also, it has been found that this chemokine possesses direct antibacterial activities. Nonetheless, the exact role that CXCL14 plays during infection remains elusive. Methodology: CXCL14 deficient mice were generated in a C57B6/129 background and followed by phenotypic characterization. Later, the effect of CXCL14 deficiency during influenza infection and E. coli challenge was assessed. Results: Other than a slight weight reduction, CXCL14 deficient mice exhibited no phenotypic alterations. CXCL14 deficiency did not influence the outcome of influenza virus infection or challenge with E. coli, and no statistically significant differences in clinical signs, cellular responses and histopathological findings were observed. Conclusions: CXCL14 does not seem to play a pivotal role during influenza and E. coli infections of the lung; these results are suggestive of functional overlap between CXCL14 and other chemokines that are present during lung infection.

Immune response of largemouth bass, Micropterus salmoides, to whole cells of different Nocardia seriolae strains

2010 ◽  
Vol 76 (3) ◽  
pp. 489-494 ◽  
Author(s):  
Yoshiko Shimahara ◽  
Yun-Fen Huang ◽  
Ming-An Tsai ◽  
Pei-Chi Wang ◽  
Shih-Chu Chen
Keyword(s):  
Immune Response ◽  
Largemouth Bass ◽  
Micropterus Salmoides ◽  
Whole Cells ◽  
Nocardia Seriolae

scholarly journals Interleukin 34 Serves as a Novel Molecular Adjuvant against Nocardia Seriolae Infection in Largemouth Bass (Micropterus Salmoides)

Vaccines ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 151
Author(s):  
Huy Hoa Hoang ◽  
Pei-Chi Wang ◽  
Shih-Chu Chen
Keyword(s):  
Dna Vaccine ◽  
Largemouth Bass ◽  
Teleost Fish ◽  
Bacterial Infections ◽  
Micropterus Salmoides ◽  
Cell Mediated Immunity ◽  
Molecular Adjuvant ◽  
Genes Encoding ◽  
Immune Related Genes ◽  
Nocardia Seriolae

DNA vaccines have been widely employed in controlling viral and bacterial infections in mammals and teleost fish. Co-injection of molecular adjuvants, including chemokines, cytokines, and immune co-stimulatory molecules, is one of the potential strategies used to improve DNA vaccine efficacy. In mammals and teleost fish, interleukin-34 (IL-34) had been described as a multifunctional cytokine and its immunological role had been confirmed; however, the adjuvant capacity of IL-34 remains to be elucidated. In this study, IL-34 was identified in largemouth bass. A recombinant plasmid of IL-34 (pcIL-34) was constructed and co-administered with a DNA vaccine encoding hypoxic response protein 1 (Hrp1; pcHrp1) to evaluate the adjuvant capacity of pcIL-34 against Nocardia seriolae infection. Our results indicated that pcIL-34 co-injected with pcHrp1 not only triggered innate immunity and a specific antibody response, but also enhanced the mRNA expression level of immune-related genes encoding for cytokines, chemokines, and humoral and cell-mediated immunity. Moreover, pcIL-34 enhanced the protection of pcHrp1 against N. seriolae challenge and conferred the relative percent survival of 82.14%. Collectively, IL-34 is a promising adjuvant in a DNA vaccine against nocardiosis in fish.

Molecular characterization and biological function of CXCR1 in Nocardia seriolae-infected largemouth bass (Micropterus salmoides)

2021 ◽  
Vol 72 ◽  
pp. 101551
Author(s):  
Jiaqian Feng ◽  
Tao Han ◽  
Yuexing Zhang ◽  
Bing Zhang ◽  
Dexiang Huang ◽  
...  
Keyword(s):  
Molecular Characterization ◽  
Largemouth Bass ◽  
Biological Function ◽  
Micropterus Salmoides ◽  
Nocardia Seriolae

scholarly journals Modeling red muscle power output during steady and unsteady swimming in largemouth bass

1994 ◽  
Vol 267 (2) ◽  
pp. R481-R488 ◽  
Author(s):  
T. P. Johnson ◽  
D. A. Syme ◽  
B. C. Jayne ◽  
G. V. Lauder ◽  
A. F. Bennett
Keyword(s):  
Power Output ◽  
Largemouth Bass ◽  
Muscle Power ◽  
Micropterus Salmoides ◽  
Cycle Frequency ◽  
Red Muscle ◽  
Slow Twitch ◽  
Work Done

We recorded electromyograms of slow-twitch (red) muscle fibers and videotaped swimming in the largemouth bass (Micropterus salmoides) during cruise, burst-and-glide, and C-start maneuvers. By use of in vivo patterns of stimulation and estimates of strain, in vitro power output was measured at 20 degrees C with the oscillatory work loop technique on slow-twitch fiber bundles from the midbody area near the soft dorsal fin. Power output increased slightly with cycle frequency to a plateau of approximately 10 W/kg at 3-5 Hz, encompassing the normal range of tail-beat frequencies for steady swimming (approximately 2-4 Hz). Power output declined at cycle frequencies simulating unsteady swimming (burst-and-glide, 10 Hz; C-start, 15 Hz). However, activating the muscle at 10 Hz did significantly increase the net work done compared with the work produced by the inactive muscle (work done by the viscous and elastic components). Thus this study provides further insight into the apparently paradoxical observation that red muscle can contribute little or no power and yet continues to show some recruitment during unsteady swimming. Comparison with published values of power requirements from oxygen consumption measurements indicates a limit to steady swimming speed imposed by the maximum power available from red muscle.

Sign in / Sign up

Export Citation Format

Share Document