Health and survival of red abalone, Haliotis rufescens, under varying temperature, food supply, and exposure to the agent of withering syndrome

被引:81
作者
Braid, BA
Moore, JD
Robbins, TT
Hedrick, RP
Tjeerdema, RS
Friedman, CS
机构
[1] Univ Calif Bodega, Davis Bodega Marine Lab, Bodega Bay, CA 94923 USA
[2] Univ Calif Davis, Sch Vet Med, Dept Med & Epidemiol, Davis, CA 95616 USA
[3] Calif Dept Fish & Game, Bodega Marine Lab, Bodega Bay, CA 94923 USA
[4] Univ Calif Davis, Dept Environm Toxicol, Davis, CA 95616 USA
[5] Univ Washington, Sch Aquat & Fishery Sci, Seattle, WA 98195 USA
关键词
Candidatus Xenohaliotis californiensis; WS-RLP; abalone; starvation; temperature; El Nino;
D O I
10.1016/j.jip.2005.06.004
中图分类号
Q95 [动物学];
学科分类号
071002 ;
摘要
Withering syndrome (WS) is a disease of wild and cultured abalone caused by a Rickettsiales-like prokaryote (WS-RLP). This study compared the pathologic changes that occur during the progression of WS in red abalone to those caused by environmental stresses consisting of elevated temperature and food limitation and determined the impact of these stressors on WS prevalence and intensity. Farmed red abalone were administered a feed-based oxytetracycline therapeutic treatment to assure WS-RLP-free status prior to initiation of the experiment. Groups were then held in each of eight combinations of exposed vs. unexposed to WS-RLP, elevated vs. ambient temperature, and high vs. low food supply, for 447 days. Mortality was associated with starvation and disease but not elevated temperature alone. Elevated temperature significantly affected WS-RLP transmission: only 1.7% of WS-RLP-exposed abalone held at ambient temperature (12.3 degrees C) became infected compared to at least 72% of those held at elevated temperature (18.7 degrees C). Among exposed abalone at elevated temperature, fed animals exhibited greater infection prevalence but not greater infection intensity or digestive gland changes than starved animals, suggesting that abalone acquire infections by ingesting contaminated food. Food, temperature, WS-RLP exposure, and most of their interactions had significant effects on body condition and foot atrophy. Immunohistochemical detection of cell proliferation and apoptosis revealed no differences between normal digestive gland and that infected with WS-RLP. Body mass shrinkage, foot atrophy, elevated mortality, and decreased foot and digestive gland glycogen were observed in both WS-affected and starved, unexposed abalone, with the WS-RLP-exposed, starved group held at elevated temperature faring worst. Among exposed and unexposed animals, food Supply but not temperature affected body mass and growth. These data demonstrate that the high morbidity and mortality exhibited by WS-RLP-infected abalone is a consequence of disease and not direct thermal stress. Drug residue analysis indicated oxytetracycline concentrations of up to 600 ppm in the digestive gland at 38 days post-treatment, an unusual degree of tissue retention of this therapeutant. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:219 / 231
页数:13
相关论文
共 43 条
[1]  
Andree KB, 2000, J SHELLFISH RES, V19, P213
[2]  
Bevelander G., 1988, ABALONE GROSS FINE S
[3]   SEARCH FOR DIFFERENTIAL POLYPEPTIDE-SYNTHESIS THROUGHOUT THE CELL-CYCLE OF HELA-CELLS [J].
BRAVO, R ;
CELIS, JE .
JOURNAL OF CELL BIOLOGY, 1980, 84 (03) :795-802
[4]  
Burton SA, 1997, J SHELLFISH RES, V16, P435
[5]  
Caceres-Martinez J, 2001, J SHELLFISH RES, V20, P875
[6]  
CACERESMARTINEZ JC, 2000, MEXICO J SHELLFISH R, V19, P503
[7]   EFFECT OF STARVATION ON ENERGY RESERVES AND METABOLISM IN THE NORTHERN ABALONE, HALIOTIS-KAMTSCHATKANA [J].
CAREFOOT, TH ;
QIAN, PY ;
TAYLOR, BE ;
WEST, T ;
OSBORNE, J .
AQUACULTURE, 1993, 118 (3-4) :315-325
[8]   NF-κB-dependent inhibition of apoptosis is essential for host cell survival during Rickettsia rickettsii infection [J].
Clifton, DR ;
Goss, RA ;
Sahni, SK ;
van Antwerp, D ;
Baggs, RB ;
Marder, VJ ;
Silverman, DJ ;
Sporn, LA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (08) :4646-4651
[9]  
DANIEL WW, 1999, BIOSTAT FDN ANAL HLT
[10]  
Friedman CS, 1997, J SHELLFISH RES, V16, P403