Physiological responses to acute temperature increase in European eels Anguilla anguilla infected with Anguillicola crassus

Gollock, Matthew; Kennedy, C. R.; Brown, J. Anne

doi:10.3354/dao064223

Cited by 16 publications

(11 citation statements)

References 30 publications

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“…Further deaths of infected eels in Lake Balaton occurred in 1992 and 1995 and in the Vranov Reservoir, Czech Republic (Baruš & Prokeš 1996), again associated with high seasonal temperatures. However, our studies of the short‐term effects of an acute temperature rise alone on the physiological responses of A. anguilla did not suggest that A. crassus infection acted as a significant additional stressor to the effects of acute temperature stress (Gollock, Kennedy & Brown 2005), although increased glucose turnover was suggested, and has been reinforced by the results of the present study. Temperature alone does not, therefore, seem likely to be responsible for the mortalities of A. crassus ‐infected eels in Lake Balaton.…”

Section: Discussionsupporting

confidence: 43%

European eels, Anguilla anguilla (L.), infected with Anguillicola crassus exhibit a more pronounced stress response to severe hypoxia than uninfected eels

Gollock

Kennedy

Brown

2005

Journal of Fish Diseases

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The parasite, Anguillicola crassus is a non-native species that infects naive European eels, Anguilla anguilla, and causes pathological damage to the swimbladder, potentially compromising their ability to cope with hypoxic conditions. This study aimed to elucidate whether anguillicolosis exacerbates the stress responses to exposure to hypoxic water, conditions that have been implicated in mass mortalities of wild infected European eels. Blood parameters in infected and uninfected eels were measured during exposure to severe hypoxia over an 8-h period. Infected fish showed significantly higher levels of plasma cortisol compared with uninfected eels after 4 h of hypoxia. Uninfected fish showed an almost twofold increase in plasma glucose after 8-h exposure to hypoxia but infected fish showed no significant change, so that the plasma glucose concentration was significantly higher in uninfected eels than in infected eels. Both groups showed similar elevations in blood haematocrit, suggesting a similar catecholamine response in infected and uninfected eels. The lack of a hyperglycaemic response in infected eels, despite indirect evidence of a catecholamine response to hypoxia, may reflect an increase in glucose turnover. The data suggest that anguillicolosis results in a significantly greater corticosteroid stress response to hypoxia accompanied by a higher metabolic cost.

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Section: Discussionsupporting

confidence: 43%

European eels, Anguilla anguilla (L.), infected with Anguillicola crassus exhibit a more pronounced stress response to severe hypoxia than uninfected eels

Gollock

Kennedy

Brown

2005

Journal of Fish Diseases

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“…Fish were held prone for 3 hours prior to experiments to ensure the heart rate had settled and was constant. A thermocouple (Digitech QM-1600) was then placed inside the fish’s mouth to record temperature that was gradually increased 1°C every 10 minutes in the 20 L reservoir tank using glass aquarium heaters [52]–[54].…”

Section: Methodsmentioning

confidence: 99%

Do Mitochondria Limit Hot Fish Hearts? Understanding the Role of Mitochondrial Function with Heat Stress in Notolabrus celidotus

2013

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Hearts are the first organs to fail in animals exposed to heat stress. Predictions of climate change mediated increases in ocean temperatures suggest that the ectothermic heart may place tight constraints on the diversity and distribution of marine species with cardiovascular systems. For many such species, their upper temperature limits (Tmax) and respective heart failure (HF) temperature (THF) are only a few degrees from current environmental temperatures. While the ectothermic cardiovascular system acts as an “ecological thermometer,” the exact mechanism that mediates HF remains unresolved. We propose that heat-stressed cardiac mitochondria drive HF. Using a common New Zealand fish, Notolabrus celidotus, we determined the THF (27.5°C). Haemoglobin oxygen saturation appeared to be unaltered in the blood surrounding and within heat stressed hearts. Using high resolution respirometry coupled to fluorimeters, we explored temperature-mediated changes in respiration, ROS and ATP production, and overlaid these changes with THF. Even at saturating oxygen levels several mitochondrial components were compromised before THF. Importantly, the capacity to efficiently produce ATP in the heart is limited at 25°C, and this is prior to the acute THF for N. celidotus. Membrane leakiness increased significantly at 25°C, as did cytochrome c release and permeability to NADH. Maximal flux rates and the capacity for the electron transport system to uncouple were also altered at 25°C. These data indicate that mitochondrial membrane integrity is lost, depressing ATP synthesis capacity and promoting cytochrome c release, prior to THF. Mitochondria can mediate HF in heat stressed hearts in fish and play a significant role in thermal stress tolerance, and perhaps limit species distributions by contributing to HF.

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“…stress of infection elevated glucose turnover. In a later study, Gollock, Kennedy & Brown (2005a) showed that acute temperature alone had little effect as an eel stressor, but under such conditions there was a lag in glucose metabolism in infected eels and there was no significant increase in haemoglobin levels when compared with the responses of uninfected eels as both groups showed a significant increase in haemoglobin. Gollock, Kennedy & Brown (2005b) then went on to demonstrate that infected eels exhibited a more pronounced stress response to hypoxia than uninfected individuals.…”

mentioning

confidence: 93%

The pathogenic helminth parasites of eels

Kennedy

2007

Journal of Fish Diseases

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Although 63 and 55 species of helminths have been reported from each species of Atlantic eel and from 29 to 19 for each species of Pacific eel only the monogeneans Pseudodactylogyrus bini and P. anguillae and the nematode Anguillicola crassus, originally specific to species of Pacific eels, can be considered serious pathogens. None of the three are normally pathogenic to their preferred natural eel host species in the wild. Pseudodactylogyrus spp. only cause serious local gill damage when present on a host in large numbers under optimal conditions that facilitate transmission. This is the case in eel aquaculture, where infections can be controlled by drugs. Anguillicola crassus is only pathogenic to Anguilla anguilla and A. rostrata when Atlantic eels are introduced to the far east or when the parasites have been introduced to Europe. Here the parasite life cycle differs in that A. crassus can infect a wide range of intermediate hosts, employ paratenic hosts and survive as larvae for months in the swimbladder wall. This makes it an excellent colonizer. Its major pathogenic effects on eels result from haemorrhaging in, and thickening of, the swimbladder wall. It reduces the oxygen concentration in the swimbladder, reducing its ability to function as a hydrostatic organ, and increases the stress response of eels. In shallow lakes at warm temperatures this can result in mass mortalities. It is also feared that the parasite affects the ability of eels to migrate to the Sargasso Sea and so contributes to the decline in eel populations. Control by drug treatment is possible in culture, but not in the wild.

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Physiological responses to acute temperature increase in European eels Anguilla anguilla infected with Anguillicola crassus

Cited by 16 publications

References 30 publications

European eels, Anguilla anguilla (L.), infected with Anguillicola crassus exhibit a more pronounced stress response to severe hypoxia than uninfected eels

European eels, Anguilla anguilla (L.), infected with Anguillicola crassus exhibit a more pronounced stress response to severe hypoxia than uninfected eels

Do Mitochondria Limit Hot Fish Hearts? Understanding the Role of Mitochondrial Function with Heat Stress in Notolabrus celidotus

The pathogenic helminth parasites of eels

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