Proliferative kidney disease in Switzerland: current state of knowledge

The myxozoan Tetracapsuloides bryosalmonae is the causative agent of proliferative kidney disease (PKD), a widespread and serious condition in salmonid fishes in Europe and North America. In Europe, PKD is primarily reported affecting farmed rainbow trout Oncorhynchus mykiss, but limited information exists on the occurrence and effects of T. bryosalmonae in wild salmonids. We investigated the presence of T. bryosalmonae in salmonids in Denmark and found that the parasite is common in the dominant wild Danish salmonid, brown trout Salmo trutta, and that it also appears in wild Atlantic salmon S. salar. Clinical signs of PKD were present in some brown trout, but in most cases the parasite was found through histology and/or PCR investigations of kidney tissue in fish that showed no signs of infection. Even though there was high similarity between internal transcribed spacer 1 (ITS1) sequences of T. bryosalmonae from wild brown trout, Atlantic salmon and farmed rainbow trout, a geographic pattern was indicated among T. bryosalmonae ITS1 phylotypes. None of the investigated streams were found free of T. bryosalmonae, but prevalence of the parasite was highly variable.

Section: Effects Of Pkd In Wild Fishesmentioning

confidence: 88%

Section: Effects Of Pkd In Wild Fishesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Tetracapsuloides bryosalmonae and PKD in juvenile wild salmonids in Denmark

Skovgaard¹,

Buchmann²

2012

“…In Switzerland, several populations of brown trout are declining. This decline was linked to an increasing occurrence of PKD, which in turn was connected to higher temperatures in several Swiss rivers (Wahli et al 2002). An increase in prevalence and severity of PKD in northerly regions as a direct consequence of temperature increase due to climate changes has been predicted (Tops et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Severe mortality in wild Atlantic salmon Salmo salar due to proliferative kidney disease (PKD) caused by Tetracapsuloides bryosalmonae (Myxozoa)

Sterud¹,

Forseth²,

Ugedal³

et al. 2007

110

Extensive mortality in Atlantic salmon fry was reported in the River Åelva from 2002 to 2004. Dead fish were collected in late summer 2006, and live fish were sampled by electrofishing in September the same year. At autopsy and in histological sections, the fish kidneys were found to be pale and considerably enlarged. Proliferative lesions with characteristic PKX cells were seen in a majority of the fish. DNA from kidney samples of diseased fish was subjected to PCR and sequencing, and the amplified sequences matched those of Tetracapsuloides bryosalmonae. We concluded that this myxozoan transmitted from bryozoans was the main cause of the observed mortality in salmon fry in 2006. Results from quantitative electrofishing in 2005 and 2006, combined with the observed fry mortality from 2002 to 2004, show that the smolt production in the river is severely reduced and that T. bryosalmonae is the most likely explanation for this decline. The present study is the first to report a considerable negative population effect in wild Atlantic salmon due to proliferative kidney disease (PKD). It also represents the northernmost PKD outbreak in wild fish. The river is regulated for hydroelectric power purposes, causing reduced water flow and elevated summer temperatures, and the present PKD outbreak may serve as an example of increased disease vulnerability of northern fish populations in a warmer climate.

“…This parasite can be found in Europe and North America and may cause high losses in trout aquaculture (Hedrick et al 1993). Additionally, PKD is suspected to be responsible for the decline of wild brown trout Salmo trutta and salmon Salmo salar populations (Wahli et al 2002, Sterud et al 2007). The development of T. bryosalmonae in the kidney of the fish host has been described in detail by Ferguson & Needham (1978), Kent & Hedrick (1986), Clifton-Hadley et al (1987) and Morris & Adams (2008), whereas the route of entry of the sporoplasm into the fish is widely unknown.…”

Section: Introductionmentioning

confidence: 99%

Tetracapsuloides bryosalmonae (Myxozoa: Malacosporea) portal of entry into the fish host

Grabner¹,

El-Matbouli²

2010

The portal of entry and the penetration process of the myxozoan parasite Tetracapsuloides bryosalmonae are still poorly understood. In the present study, spores of T. bryosalmonae derived from the bryozoan host (malacospores) were activated chemically and mechanically to investigate their reaction after attachment to the fish host in vitro. Amoeboid movement of both sporoplasms was shown for the first time. The morphology of malacospores was assessed using scanning electron microscopy (SEM). Openings of the polar capsules and released polar filaments were visible. One sporoplasm was observed leaving the spore shell. Laboratory exposure experiments of juvenile rainbow trout Oncorhynchus mykiss to spores of T. bryosalmonae were also conducted. Single fish were incubated with 1000 to 2000 spores in 100 ml of water for 5 to 60 min. Immunohistochemically stained sections of skin and gills were examined using light microscopy, as well as ultra thin sections using transmission electron microscopy (TEM), to investigate attachment and early penetration. Whole fish and excised gills of fish exposed to a spore suspension were fixed and prepared for scanning electron microscopy. Attached and penetrating stages were found only on or in the gills, and not in the skin. Due to the low overall number of spores, only a few spores were found adjacent to the gill epithelium in TEM. No parasite stages were found on the samples used for SEM. These results indicate that the gills are the preferred entry loci for the amoeboid sporoplasms of T. bryosalmonae into the fish host. KEY WORDS: Myxozoa · Malacosporea · Penetration · PKD · Portal of entry · InfectionResale or republication not permitted without written consent of the publisher Dis Aquat Org 90: 197-206, 2010 site enters the fish host. However, visualization of developmental stages of T. bryosalmonae in the previous studies did not provide adequate information about the mode of penetration and the chronological progression of early development. As the abundance of Malacosporea-infected bryozoans is usually low (Anderson et al. 1999, Okamura et al. 2001, the attachment to the host and the penetration process of these few spores must be achieved by an efficient mechanism. It has already been shown that a single spore is sufficient to infect a fish and to cause clinical symptoms of PKD (McGurk et al. 2006). In the present study, we investigated whether the skin, gills or both organs are the main portals of entry for T. bryosalmonae into the fish and attempted to characterize the attachment and penetration process in detail. Stages during and shortly after penetration were visualized using light and electron microscopy. To show the reaction of T. bryosalmonae spores from bryozoans after contact with the host, in vitro activation experiments were conducted. Additionally, the malacospores were examined using scanning electron microscopy (SEM) for the first time. MATERIALS AND METHODSFish and infected Bryozoa. For the experiments, specific pathogen free (SPF) rainbow trout...