Sporidea. It seems quite likely that the multifarious microsporideans may be responsible for many more unexplained fish deaths than we realize, especially when the necrosis of a vital organ results in "bloat" or "dropsy," which we conventionally attribute to bacterial infections.
There are three separate phyla of sporideans, or spore-producing micro-protists, which have evolved independently from separate evolutionary lines. Two of the lines developed from single-celled protists, specialized and minimalized for their life as obligate parasites: they are Apicomplexa and Microsporea such as Pleistophora. But the Myxospora originated, astonishingly, as multicellular animals, rather than protozoans, according to Lynn Margulis, in Five Kingdoms. Simplicity is not invariably a primitive trait, but few organisms can have stripped off as much unneeded baggage as the myxosporans. All sporidea infest cells, tissues or organ cavities of fish, arthropods or annelid worms.
Whether they invade and take over the cells of the host, like the myxosporeans, or live diffused in tissue in between the cells like the microsporean Pleistophora, all sporideans are parasitic. Many of these sporozoa form a highly-resistant stage, whether technically it's a spore-like propagule or an "oocyst," which may survive a long while in fecal matter from the host or perhaps free in the substrate. This cyst, only 1 micrometer in diameter, is the infective stage for the next host in the parasite's life cycle. It isn't very susceptible to medications, partly because its metabolism is very reduced: there's little metabolic exchange with the water.
In the aquarium, transmission occurs most easily when fish scavenge the dead bodies of infected fish; this is the vector that spreads the parasite among tetras and danios cultured for the aquarium market in the southeast Asian fish mills. Transmission to the host fish also occurs when the microscopic cyst is ingested directly, or in some cases through the intermediary of an infected invertebrate that the fish eats.
Pleistophora (P. hyphessobryconis or "Neon disease"). More common than ever, this misleadingly named microsporidean was first identified in Neon Tetras and the closely related Hemigrammus erythrozonus by the famous fish pathologist Wilhelm Schäperclaus, at the New York Aquarium in 1941; it isn't so host-specific in actual fact as its common name implies: it also attacks fishes in four families, including other small tetras and their relatives, and barbs (including goldfish), danios and rasboras, even angelfish.
Pleistophora attacks muscle tissue. Signs of pleistophoriasis are greyish-white waxy or opaque areas in muscles that ought to be translucent or transparent. The long iridescent color bands of tetras and rasboras can become pale and patchy. Afflicted fishes are restless and avoid the others. As affected muscle tissues turn white, the bleached areas expand; by this stage you should have already removed and euthanized the fish. Later, fishes become emaciated, or have hollows and cyst-like lumps that deform their musculature. Towards the end, the spine may even become deformed, and swimming movements and swim bladder control can be affected, but these terminal symptoms can also result from secondary bacterial infections in a weakened host fish. Long before these late stages you should have identified the suffering fish and euthanized it.
There is no treatment for Pleistophora; it is always fatal. Susceptible individuals will die like flies at first, then the rest of the infected fish will die more slowly, over a period of weeks. On the other hand, some of their tankmates may never become infected.
Fishes suffering with Pleistophora should be removed and euthanized before they actually die. My reasons for advising this aren't merely fastidious. In its weird and complex, alien and utterly parasitic life cycle, this extremely minute spore-forming protozoan lodges within a cell in the musculature of the host fish and forms a "sporoblast." Protected from the fishes' immune system inside the host's cell, the nucleus of the protist keeps dividing inside its sporoblast. There are many resulting "spores;" Pleistophora means "bearing lots [of spores]." Each spore, only 2 to 20 micrometers across, consists of a nucleus embedded in a minimal amount of amoeba-like protoplasm.
Sometimes the sporoblast settles in kidney tissue, and subequently spores can be shed in the host fishes' urine, I'm told. More commonly, though, the infective spores aren't freed until the host dies and its musculature softens with decomposition, or until the carcase is scavenged by another fish. Within the new host's gut, the spore covering dissolves, and the amoebalike spore is injected through the intestinal wall through a structure like a hypodermic syringe (shiver shiver). Then it travels in blood or lymph fluid to find a suitable lodging in a cell in the muscles.
So, you can interrupt the transmission of Pleistophora by removing the dying victims.
Many microsporideans have co-evolved with their hosts, which also include insects and annelid worms. The globular whitish cysts you might notice in glassworms (Chaoborid larvae) are microsporideans, which can't pass to a fish that eats the larva, by the way. In their "natural" hosts they discreetly form their single-cell cyst in the musculature and never cause any harm.
In general, microsporidea in fishes are generally also rather host-specific. When zebrafish are attacked by sporidean parasites, the organism commonly responsible may be Pseudoloma neurophilia, for instance. It's a clumsy parasite that kills its own host: so, if Pleistophora hasn't co-evolved with the fishes it is attacking in our aquaria, then where is Pleistophora's natural host, I'd like to know?
I'm told that microsporideans can even infect fish eggs. And week-old Neon Tetras have been found bearing fully-developed Pleistophora sporoblasts. How long Pleistophora spores can remain viable at large in the aquarium before being ingested by a new host is an open question. But if your tank has suffered Pleistophora, you must consider it under long-term quarantine. Some fishkeepers would euthanize the fishes exposed to Pleistophora, take the tank apart, discard the plants, boil the gravel and disinfect everything.
Other sporideans. Certain other kinds of sporideans enter cells and make the cells enlarge so grossly they become visible to the naked eye, and we call them "cysts" (''xenomas" would be more accurate) and misidentify them as Lymphocystis. Various sporideans can lodge in fishes' liver, kidney tubules, spleen and other vital organs.
Myxosporideans do infect tropical fish, but there's no effective countermeasure against them, either. The notorious coldwater myxosporidean, Myxobolus cerebralis, that causes the "whirling disease" of salmon and trout in hatchery fingerlings, survives freezing and drying and may persist in coldwater streams for 20-30 years. But it doesn't affect any tropical fishes. That parasite is transmitted through tubifex worms, however, sparking some unfounded tubifex fears.
For non-aquarists, the most notorious of all sporideans is Plasmodium, transmitted by mosquitos, which is the cause of malaria. Cryptosporideans have become prominent with the spread of AIDS; they live inside cells lining the intestine, and sometimes the lungs, of people with compromised immune systems.
Link. FishChannel has Dt Neale Monk's good article on "Neon Tetra Disease".