Distribution and structure of lesions in the gills of Atlantic salmon, <i>Salmo salar</i> L., affected with amoebic gill disease

Adams, Mark B.; Nowak, Barbara F.

doi:10.1046/j.1365-2761.2001.00330.x

Cited by 109 publications

(91 citation statements)

References 12 publications

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“…Although fish in this study showed up to 90% AGDaffected filaments, the corresponding respiratory results do not reflect major acid -base disturbance. Experimental infections of AGD are typically far more aggressive compared to wild infections due to the increased pathogen loading that fish in culture conditions would not normally experience (Adams & Nowak 2001). Although the precise cause of AGD-associated mortality remains unknown, this, along with the results from the present study, suggests that AGDassociated mortality in cultured fish is not caused by respiratory failure.…”

Section: Discussionsupporting

confidence: 48%

“…These patches are present histologically as multifocal hyperplastic lesions, generally resulting in the fusion of secondary lamellae (Munday et al 1993, Adams & Nowak 2001. AGD-associated mortality has been presumed to be associated with a respiratory distur-bance, as both lethargy and respiratory distress have been described from salmonid AGD infections (Kent et al 1988).…”

Section: Introductionmentioning

confidence: 99%

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Respiratory pathogenesis of amoebic gill disease (AGD) in experimentally infected Atlantic salmon Salmo salar

Leef

Harris²,

Powell³

2005

Dis. Aquat. Org.

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The aim of this study was to investigate the respiratory responses of Atlantic salmon, Salmo salar, experimentally affected with amoebic gill disease (AGD). In Series I, arterial blood samples were taken over a 96 h period following amoebae addition to examine potential respiratory effects associated with initial exposure. No major significant treatment effects were found between fish exposed to amoebae and control (non-exposed) fish. Arterial pH (pH a ) was seen to be significantly elevated at 48 h in AGD fish relative to the 0 h time point. To investigate the long-term respiratory effects associated with infection, fish were similarly exposed to amoebae and sampled over a 16 d period. As for Series I, caudal blood pH was significantly elevated by Day 2 (48 h) compared to the pre (Day 0)-time point, suggesting that initial exposure to amoebae and/or amoebae attachment may have induced an initial respiratory alkalosis via increased ventilation frequency and/or amplitude. From Day 7 onwards, and coinciding with a significant increase in the percentage of affected gill filaments, blood pH decreased significantly, possibly indicating the onset of the characteristic respiratory acidosis that has previously been described for experimentally AGDaffected Atlantic salmon. Although fish in this study showed up to 90% AGD-affected filaments, the corresponding respiratory results do not reflect a major acid -base disturbance. Therefore, the findings from the present study support the contention that, although AGD only affects the gill, AGDassociated mortality in Atlantic salmon may not be primarily associated with respiratory failure.

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Section: Discussionsupporting

confidence: 48%

Section: Introductionmentioning

confidence: 99%

Respiratory pathogenesis of amoebic gill disease (AGD) in experimentally infected Atlantic salmon Salmo salar

Leef

Harris²,

Powell³

2005

Dis. Aquat. Org.

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“…correlated with a reduced proteolytic profile of the attenuated amoebae (Verissimo et al, 2013). The in vitro CPE identified here and its relevance to AGD is unclear given that extensive histological studies on AGD-affected salmon revealed no evidence of cytolytic activity (Adams and Nowak, 2001). While potential damage to host tissues may be masked by the exuberant proliferative host response it seems likely that the CPE demonstrated in vitro is evidence of an ECP with a less direct virulence mechanism.…”

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confidence: 75%

“…The causative agent of AGD is Neoparamoeba perurans as shown by molecular evidence (Young et al, 2007) and fulfillment of Koch's postulates (Crosbie et al, 2012). AGD is initiated by the association, and presumably attachment, of N. perurans to the gill epithelia (Lovy et al, 2007) which results in extensive gill epithelial hyperplasia and proliferation of amoebae associated with the hyperplastic lesions (Adams and Nowak, 2001). As N. perurans is a free-living amoeba and an opportunistic pathogen, AGD can be transmitted horizontally when N. perurans-containing mucus is sloughed off infected gills into the water column and the amoebae are free to colonise the gills of fish .…”

mentioning

confidence: 99%

Neoparamoeba perurans loses virulence during clonal culture

Bridle

Davenport

Crosbie

et al. 2015

International Journal for Parasitology

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“…All sections were viewed by a light microscope (Olympus) at 4-1000 × and fish with typical AGD lesions characterised by a single or multifocal epithelial hyperplasia of the gill lamellae, focal fusion of secondary lamellae and round to ovate interlamellar vesicles containing amoeba were considered AGD positive. Quantitative analysis of disease severity was conducted by estimating the number and size of AGD lesion on each filament (Adams & Nowak 2001). The percentage of lesioned filaments was determined by estimating the ratio of filaments with typical AGD lesions to filaments with no AGD lesions.…”

Section: Resale or Republication Not Permitted Without Written Consenmentioning

confidence: 99%

Influence of salmonid gill bacteria on development and severity of amoebic gill disease

Embar-Gopinath¹,

Bütler²,

Nowak³

2005

Dis. Aquat. Org.

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ABSTRACT:The relationship between salmonid gill bacteria and Neoparamoeba sp., the aetiological agent of amoebic gill disease (AGD) was determined in vivo. Fish were divided into 4 groups and were subjected to following experimental infections: Group 1, amoebae only; Group 2, Staphylococcus sp. and amoebae; Group 3, Winogradskyella sp. and amoebae; Group 4, no treatment (control). Fish (Groups 1, 2 and 3) were exposed to potassium permanganate to remove the natural gill microflora prior to either bacterial or amoebae exposure. AGD severity was quantified by histological analysis of gill sections to determine the percentage of lesioned filaments and the number of affected lamellae within each lesion. All amoebae infected groups developed AGD, with fish in Group 3 showing significantly more filaments with lesions than other groups. Typically lesion size averaged between 2 to 4 interlamellar units in all AGD infected groups. The results suggest that the ability of Neoparamoeba sp. to infect filaments and cause lesions might be enhanced in the presence of Winogradskyella sp. The possibility is proposed that the prevalence of more severe AGD is due to the occurrence of Winogradskyella sp. at high concentrations on the gills.KEY WORDS: Neoparamoeba · Winogradskyella · AGD · Potassium permanganate · Protozoan diseases · Salmon diseases · Amoeba · Bacteria Resale or republication not permitted without written consent of the publisherDis Aquat Org 67: [55][56][57][58][59][60] 2005 MATERIALS AND METHODS Fish. Atlantic salmon Salmo salar L. (n = 72; mean weight = 88 g) were acclimatised to sea water (35 ‰, 1 µm filtered) over a week in 6 identical recirculating systems each consisting of three 70 l tanks (n = 4 fish per tank) and a 70 l reservoir. A sentinel population (n = 12) of the same body weight was acclimatised in a static tank (210 l). Following acclimatisation, fish in the recirculating systems were divided into 3 treatment groups (n = 12 fish per treatment). Each treatment was duplicated. The 4th group was the sentinel population (n = 12). Fish in Group 1 were exposed to amoebae only (positive control); Group 2, Gram positive bacteria (Staphylococcus sp.) and amoebae; Group 3, Gram negative bacteria (Winogradskyella sp.) and amoebae; Group 4 did not receive any treatment. Sea water temperature was maintained at 16 ± 0.5°C, pH 8.2, dissolved oxygen 7.6 mg l -1 , salinity 35 ‰ and total ammonia-nitrogen below 0.2 mg l -1 . Sufficient air supply was maintained in the tanks throughout the experiment by using aerators.Neoparamoeba sp. isolation. Neoparamoeba sp. were harvested from the AGD affected Atlantic salmon held in the Aquaculture Centre, University of Tasmania, Launceston by a method described by Morrison et al. (2004). In brief, infected gills were removed from AGD affected Atlantic salmon after euthanasia (anaesthetic overdose at 20 ml l -1 Aqui-S ® ). Gills were transported to the laboratory in sterile sea water (SS) containing antibiotic and antimycotic solution (5% v/v 5000 IU ml -1 penicillin and 5 mg...

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Distribution and structure of lesions in the gills of Atlantic salmon, Salmo salar L., affected with amoebic gill disease

Cited by 109 publications

References 12 publications

Respiratory pathogenesis of amoebic gill disease (AGD) in experimentally infected Atlantic salmon Salmo salar

Respiratory pathogenesis of amoebic gill disease (AGD) in experimentally infected Atlantic salmon Salmo salar

Neoparamoeba perurans loses virulence during clonal culture

Influence of salmonid gill bacteria on development and severity of amoebic gill disease

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