cadeusus

It wont be Myxobolus cerebralis - that is a salmonid disease

Putting in ice water is not considered really acceptable anymore. FIsh placed in very cold water become immobile before they become insensible. So just becaue they've stopped moving doesn't mean that they are not aware of all the sensory stimuli coming from their thermoreceptors. What that feels like no one knows but benefit of the doubt...? Use clove oil or percussive stunning (whack them on the head)

I was querying the metro with respect to the suggestion of bacterial gill disease, not your earlier suggestion for internal problems.

Chloramine-T is a marketed fish treatment used in aquaculture, benzalkonium chloride also - I've used both without killing fish. Certainly wouldn;t use savlon though!!

Why would u want to go straight to metronidazole? even if it is bacterial gill disease? Metronidazole is designed for use against obligate anaerobic bacteria (those that can't use oxygen) so unlikely obligate anaerobes would be on the gills really. One could try a salt bath, or something like chloramine-T or benzalkonium chloride bath and make sure oxygen levels are good in the tank.

Just to clarify this relates to the original posting that started this thread. Cheers

Could be a nematode such as Philometra sp. which has been reported in subcutaneous tissues in ornamental fishes. If it is then it is likely that those big white ones are adult females, rather than larvae. The males are teeny, less than 2mm long, so the females can become gravid (egg bearing) then they pop their ovipositor out through the skin and lay their eggs into the water. Daphnia and branchurians in your tank water act as intermediate hosts allowing the lifecycle to complete in you other fish. So, if they were my fish I'd get them out of the tank, change the water and monitor the other fish. Treatment with levamisole has been reported to be successful in early stages of infection. There are reports of resistance to prazi, droncit etc.

Possibly an intussusception? Where the gut folds in on itself, then the blood supply to the inner part gets cut off slowly and it becomes necrotic and dark bloody colour. Fibrous tissues develops at the upper end of it blocking the gut and quite often the inner dead part (the intussusceptum) sloughs off and is passed, but the gut is still fibrosed almost shut by that time. Nothing you could have done if that is the case aside of whipping the bd down to a vet for laparotomy, excision of the intussusception and surgical anastomosis of the remaining bits of gut.

Hi, I don't post much, but don't please treat what you read with some scepticism sometimes... quote: "Prazi is probably the best choice here because it’s safe for adults and young and definitely kills the flukes by rupturing the outer membrane (skin) causing then to be totally destroyed. The hooks they hold on with aren’t destroyed and will fall or decompose out on there [sic] own. " Praziquantel acts on the calcium channels in the parasites. It results in paralysis of the parasite, which in many cases, unless the fish has encapsulated the parasite in an exuberrant epithelial response on the gills, means that the haptors (hooks) that it uses to hold on relax and the parasite falls off. In terrestrial animals prazi causes gut parasites to fall asleep, and when they wake up the animal is no longer there :-). (i.e. they are in the poo!) Prazi does not cause the parasite to explode or disintegrate...in fact in aquaculture one problem with prazi is that at low doses the flukes can wake up again after the fish have been treated. Anyway, the statement after that about eggs not being affected is actually true and so repeated doses are indeed needed. Great to see peoples' experience being shared, but lets get the facts right.

Stella It is not unheard of for fish species to have more than one lateral line. It depends on the embryologicla development of the fish and how and where the neuromast precursors migrate to. Eigenmannia species have 3 separate phases of neuromast development and migration - a ventral line, a midline and a dorsal line which develop as larvae and juvenile stages. The lungfish has 2 distinct lateral lines reported ventrolateral and dorsolateral. The upper one linking to the 3 channels on the head (above the eye, between the eys and the mouth and under the mouth [mandibular branch]) with the lower lateral line joining to the mandibular branch. So I suppose long story short is don;t be surprised...

My pleasure Stella (some sort....)

Stella, you hit the proverbial nail on the proverbial head. Hypoxia can be absolute or relative - absolute = lack of oxygen in the water, but relative = inability to take up the oxygen in the water. This could be caused by either gill pathology (decreased blood flow due to loss of lamellae or decreased gas exchange due to increased thickness of repiratory epithelium) or cardiovascular compromise leading to decreased gill perfusion and thus less blood passing through gill to exchange gases. Some chronic (or even acute I suppose) pathologies can result in cardiovascular compromise and thus hypoxia. As a professor I once knew said - "one only dies for 3 reasons...the heart stops working, the brain stops working or the lungs stop working" in the case of fish substitute gills for lungs

high

Gaping post mortem is a recognised differential for hypoxia. Like anything else these signs are clues to investigate not definitive things. But the vast majority of dead fish I've seen, and I've seen thousands, do not develop gaping purely because of post mortem muscular contraction. It would be unusual for rigor to result in gaping as the temporal and masseter muscles that shut the jaw are more powerful than those that assist in opening the jaw.

Did the dead ones have a wide open mouth? perhaps hypoxia (oxygen deficiency) was involved?