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?

Sad about the fish... Been reading the posts and have to say... a) when some species are affected more than others is more likely to be pathogen. Environmental conditions tend to hit all species, thats one of the rules of thumb in investigating fish kills. b) the opacity in the eye probably is just representative of the fish dying...the eyes are clear only because cellular integrity is maintained in a healthy living fish, when that goes, either because of severe disease or death then water penetrates the eye structures and causes cloudiness and opacity. c) the hole in the side of the fish sure looks like infection to me, not a chemical reaction. You cant comment on the gills because the operculum is intact and covering them. d) as has been pointed out - the primary cause of the problem needs to be ascertained as primary pathogens are extremely rare in domestic aquaria - unless new fish have been introduced without quarantine. Just a few thoughts...I wouldn't get too tied up working through the chemical reaction scenario

Haemorrhagic septicaemia is a clinical description, not a specific disease agent. What species are you wanting to treat and what are the clinical signs?

It is probably water quality issue. Check your parameters again. Your fw post said ammonia at 0.25mg/L which is too high - chronic ammonia toxicity can be considered above 0.05mg/L. Ammonia toxicity specifically causes respiratory distress and/or neurological signs. The injected veins in the tail may be due to stress in the fish due to water quality issues but can also be a sign of septicaemia (generalised infection in the fish). In goldfish septicaemia may also be accompanied by brown patches on the fins. Other clinical signs of septicaemia are bulging eyes (sometimes reddened), swollen abdomen, reddening of the fin bases, tiny pinpoint haemorrhages in the skin especially of the belly. Given the phots I think it more likely that the water quality is the problem. Water changes are the answer/

Ammonia test kits measure combined ammonia and ammonium, thats NH3 and NH4+ ions respectively. At pH <7 (i.e more acidic) more of the ammonia/ammonium will be in the NH4+ form which is less toxic than the NH3 ammonia form. If ammonia is a problem you need more acidic water so that a greater proportion is in the NH4+ form rather than the NH3 form. Ammonia is very toxic and will absorb straight through gill cell membranes because it is unionised. Ammonium is less toxic but will still cause respiratory problems and gill irritation at very low ppm levels. The test kit will give you a total NH3 and NH4+ level, but combined with your pH there should be a chart that tells you how much is ionised (NH4+) and howmuch unionised (NH3). Nitrite is also toxic but at slightly higher levels and for a different reason - it forms methaemoglobin in the fish blood stream and cuts down on the oxygen carrying capacity. Neither ammonia/ammonium or nitrite is particularly good for your fish. Water changes necessary until the filter bacteria get up to enough numbers.

Furan-2 with meth blue will work on fungus, but you'll aslo be dosing antibiotics into your system. Wunder tonic or wunder white spot has malachite green which is also effective against fungus. Either way it might be worthwhile dosing anyway to kill off the zoospores from the sap. fungus incase they do infect your other fish. Zoospores much easier to kill than the hyphae (the cottonwool like growth) and of course check your water parameters, I'm seen pepople with fungus infected fish just because thing slike pH were out of whack.

the fungus doesn't mind which fish species it infects

4% is usually w/v...i.e 4g/100mL therefore 100mL contains 4000mg therefore 1 ml contains 40mg if he wants 0.1 mg/L in 200L that is 200 x 0.1 = 20mg therefore 0.5mL The only thing to check is if 4% is 4% w/v

Melafix is indeed derived from tea tree oil. THe active is more active against gram negative than positive. The nitrogen fixing bacteria in your filter are gram negative. Thus it can affect your filter just as most meds will.