My Nanay wild Greens ..Whirling Disease

[fljones3]

I concur Frank.

Do we have any speculation on the cause?

[Willie]

... My guess is its either Viral or parasite similar to the coldwater fish illness, Myxobolus cerebralis. That parasite is passed to the fish when they eat live aquatic worms in their rivers. I suspect this may be the case here at the exporters, if live foods are fed....

I have a different take on this, Al. I've had two cases in ~30 years where the whirling disease moved through an entire tank of discus killing most of them. I've also had 3 - 4 cases where a single discus contracted the whirling disease. In the cases where the disease was contagious, they were fish from the same spawn. When a single discus contracted the whirling disease in a tank of different genetics, the disease rarely, if ever, proved to be contagious. In my case, these were all tank raised discus and all were feeding on beef heart.

[For100]

I am so sorry to hear this happened to you. It is the worst feeling ever see all your fish pass away.

[brewmaster15]

I am so sorry to hear this happened to you. It is the worst feeling ever see all your fish pass away.

Freddy Thanks. I know you had to deal with a tank disaster too recently.

[brewmaster15]

I have a different take on this, Al. I've had two cases in ~30 years where the whirling disease moved through an entire tank of discus killing most of them. I've also had 3 - 4 cases where a single discus contracted the whirling disease. In the cases where the disease was contagious, they were fish from the same spawn. When a single discus contracted the whirling disease in a tank of different genetics, the disease rarely, if ever, proved to be contagious. In my case, these were all tank raised discus and all were feeding on beef heart.

Willie your experiences and observations here definitely complicate identification of a common cause. Its possible theres multiple causes of the same symptoms. Its also possible they have a common factor we are missing. Maybe the vector is another species of fish theyccome in contact with or a snail or even a tiny copepod. I wish I knew. At most I can definitively say this group of wild greens died from something I have never seen before in all my years of discus keeping. It was like something flipped a self destruct switch on these guys.

I'm obsessed now on this subject. Heres something I came across that may also cause this problem....Prions

..

In the past, economically grown fish species were exposed to prions causing bovine spongiform encephalopathy (BSE), and scrapie in cattle, and sheep respectively, through feeding with contaminated meat and bone meal (MBM). It was, however, unknown whether fish genomes encode a homologue of the mammalian prion protein or, in other words, whether fish could theoretically be susceptible to prion infections.

More information
We initially investigated whether fish fulfil the basic precondition of amplifying PrPres: Do fish genomes harbour a gene encoding for a prion protein.
We initially identified two distinct cDNAs coding for homologues to mammalian tetrapod prion protein in Japanese pufferfish (Fugu rubripes) and one in Atlantic Salmon (Salmo salar) (Oidtmann et al. 2003) and subsequently identified further cDNA sequences in other fish species (zebrafish, common carp, stickleback, and rainbow trout) (Maddison et al. 2005, Rivera-Milla, Oidtmann et al. 2006 and unpublished results). In all species investigated to date, we have been able to identify cDNAs for two prion protein genes.<p>
Since the ray fin fish line diverted from the common ancestors of mammals, birds and reptiles, ray fin fish have undergone a genome duplication event. This genome duplication event explains why two PrP genes can be found in fish, compared to only one in mammals. A further genome duplication event has been identified in some salmonid and cyprinid species.

This indicates the culprit could be other fish or even fishmeal used in foods. We know how resistent prions are its something to research further I guess.

[brewmaster15]

More prion research..

https://www.sciencedirect.com/scienc...0communication.

2.2. Prion transmission and the species barrier
Prion transmission across different species is limited by the so-called species barrier. Following primary inoculation between two species, only some animals develop disease, with long incubation periods that may reach the normal life span of the species. This phenomenon is clearly illustrated by the resistance to TSE observed in rabbits, even after intracranial inoculation with TSE agents of sheep, mouse and human origin [70]. It has been suggested that the unique structural characteristics of rabbit PrP make it less prone to pathogenic conversion [70], [71]. Typically, species barriers become attenuated after serial passaging of a prion strain, resulting in shortened incubation times and the consequent adaptation of the host to the specific strain [72]. At the molecular level, the efficiency of interspecies prion transmission appears to depend on the degree of sequence and structural identity between the PrPs of the two species involved [73]. For instance, wild type mice do not become infected with hamster prions, whereas transgenic mice overexpressing hamster PrP do [74]. However, BSE can effectively be transmitted to a wide range of species and maintain its pathogenic characteristics, even when passaged through an intermediate species carrying a different PrP coding gene [75].

4.2. Risk of prion transmission to fish
According to the aforementioned arguments, fish, poultry and pigs represent potential candidate hosts for prion infection. In order to assess the risk of prion transmission to fish, five main parameters should be considered: 1. the potential use of prion-contaminated MBM as a nutritional supplement in aquaculture, 2. the consumption of infected farmed fish by humans, 3. the use of feeds or other products (i.e. gelatin, milk replacers) derived from TSE-affected fish for mammalian or piscine nutrition, 4. the use of fishmeals cross-contaminated with MBM in mammalian diets, and 5. the escape of infected fish, or the release of infected waste from aquaculture facilities into the marine environment. These scenarios are depicted in Fig. 2.

4.3. Transmission studies in commercially important fish species
At present, only a few studies have explored the experimental transmission of TSEs to teleost fish. The first attempts in this direction involved the oral and parenteral inoculation of two commercially important fish species, rainbow trout and turbot, with the 139A mouse-adapted scrapie strain [105]. Although the fish displayed no clinico-histopathological signs during the three month-experimental period, a mouse bioassay revealed that they carried residual infectivity. Specifically, mice intracranially inoculated with trout intestinal extracts one day after oral challenge were positive for brain PrPSc deposition approximately 200 days post inoculation (p.i.), despite the absence of clinical symptoms. Similar results were obtained when mice were intracerebrally (i.c.) inoculated with spleen extracts from trouts and turbots, 15 days after parenteral inoculation of the fish with scrapie material. Finally, brain tissue from parenterally inoculated turbots 15 and 90 days after challenge was also able to elicit PrPSc accumulation in the brains of recipient mice, without causing clinical disease.

Recently, we reported data on the oral transmission of BSE and scrapie to gilthead sea bream (Sparus aurata) [106]. Interestingly, at two years p.i., a number of fish that had been force-fed BSE- or scrapie-infected brain homogenates developed abnormal plaque-like deposits in their brains. Specifically, the brains of two out of five fish inoculated with scrapie developed signs of abnormal protein aggregation at 24 months p.i. These aggregates were positively stained with polyclonal antibodies raised against fish PrPs, but showed no proteinase K (PK)-resistance or Congo red birefringence (Fig. 3A). The brains of the BSE-challenged fish, however, displayed a much more striking picture, having already developed the first signs of abnormal deposition at eight months p.i. A general progression in size, PK-resistance and morphological features was observed thereafter, resulting in an impressive number of aggregates in all the brain regions examined at 24 months p.i. Three out of five fish sacrificed at this time point showed 500–800 deposits per brain section each, 70–85% of which were PK-resistant and had a mean diameter of 30 μm. These aggregates were PAS-positive, congophilic and birefringent in polarized light, indicating an amyloid or amyloid-like fibrillar structure (Fig. 3B). In contrast to the TSE-challenged individuals, no signs of abnormal aggregation or any other lesions were observed in the brains of the control fish “challenged” with bovine or ovine brain homogenates prepared from healthy animals. Altogether, the development of abnormal brain deposits in BSE-challenged sea bream constitutes an unprecedented histopathology in fish.

This research is interesting to me.. especially since it indicates a lengthy period of time where fish are asymptomatic.

[Second Hand Pat]

Al, did you see anywhere in this research which symbols the fish displayed? Also did some fish survive? Since this comes thru the food chain your test fish will never show any symbols (assuming this is the cause)? Sorry for my unscientific view.
Pat

[brewmaster15]

Pat theres really not alot on the prion and fish yet..I have to dig further into the zebra fish research...

What is indicated is the fish can be without symptom for a long time. Im definitely not saying we have mad fish disease just that theres so many things we don't know that in theory could be the cause.

In humans prion disease(mad cow)<mayo clinic source>

People may experience:
Mood: anxiety, apathy, or nervousness
Muscular: problems with coordination or rhythmic muscle contractions
Sensory: pins and needles or uncomfortable tingling and burning
Cognitive: dementia or confusion
Psychological: major depression or psychosis
Also common: insomnia, restlessness, slurred speech, or unresponsiveness

I didnt note any slurred speech in the fish but A bunch of the symptoms do kind of fit.

[brewmaster15]

As for my test fish.. unless its a virus Im not likely to see anything. I think if parasite it maybe a complex lifecycle. Even with Myxobolus cerebralis ,the coldwater fish whirling disease its a complex system. My understanding is the worms pass it to the fish. The fish die and worms are infected by the decaying fish. Its possible I guess for other fish to eat that decaying fish too though I dont know if direct infection has been shown. Either way I wont have decaying fish or live worms feeding on them in my tank. I know the test fish may not give much info in this case but with so many unknowns it was worth trying.

[fljones3]

Thanks Al for the research. From my unknowledgeable reading of what you wrote, there is no way to determine if prion is the cause nor where it entered into their systems. Looks like your test fish will have a lonely life. With what you have written, I don't think I would mix them back into my other stock.

[Johanna]

So sorry to read all this, what a horrible experience! I have to applaud you, Al, for the effort to document and learn about it and share the information. I hope your research pays off and you'll find out something, however unpleasant. It may well help many, many discus hobbyists (and save many fish!) in the long run.

[brewmaster15]

Thanks Al for the research. From my unknowledgeable reading of what you wrote, there is no way to determine if prion is the cause nor where it entered into their systems. Looks like your test fish will have a lonely life. With what you have written, I don't think I would mix them back into my other stock.

Absolutely Frank. They will never come back in to the house.. Weather is warming up here so I hope to be able tp keep them out side at least through the summer and fall. My current setup with insulation all around has kept them mid to high 80s even when we hit below freezing. Im sure my electric bill will creep up a tad but its shouldnt be too bad.

[brewmaster15]

So sorry to read all this, what a horrible experience! I have to applaud you, Al, for the effort to document and learn about it and share the information. I hope your research pays off and you'll find out something, however unpleasant. It may well help many, many discus hobbyists (and save many fish!) in the long run.

I hope something good comes out of it Johanna. Its the best I can do.

[jeep]

What a horrible mystery. There would be at least some sense of accomplishment if you could find a cause, but that doesn't seem probable at this point. For 5 of 6 to be affected, yet none of the test fish, again at this point, is confusing as well as concerning. I wonder if they may have been exposed to some sort of toxin at some point. It also seems that "whirling disease" could have similar effects with different causes since rare reports of successful treatments have been reported...

Part of me hopes this has come to a conclusion for you, but part of me hopes it proves contagious so you can find a definitive answer...

[LizStreithorst]

I've been interested in the Prion diseases almost since they were first identified. Not only is the incubation period long, it's development takes a long time, as well. It first presents as mild cognitive impairment. With you're fish it's like a switch was suddenly turned from off to on. Willie's fish indicate a strong genetic link. I wonder if your fish might have all been siblings.