Flagellates.

Oodinium ("Gold Dust" or "Velvet"). Oodinium (officially now called Piscinoodinium) is a genus of microscopic parasitic dinoflagellates. Call it "Oh-uh-DINN-ium," not "OOD-in-um" as I miscalled it for years! One species is P. pillularis, which gave the old-fashioned name of "pillularis" to these parasites.

Oodinium is more insidious than Ich-- the individuals are invisible. It's hardier and more resistant to treatment. Oodinium is widespread in aquarium fish, though not common in koi ponds, according to Dr Erik Peterson at www.koivet.com.

Flagellates are single-celled organisms that move around by thrashing their whiplike flagella. (A Latin flagellum is a whip.) The dinoflagellates form a huge class among the flagellate phylum and include the organism associated with the notorious "red tides" of polluted marine waters.

Many species of flagellates are part of the normal intestinal fauna of fishes, and many more kinds of free-living flagellates make a living in the mucus of fish gills and skin, without attaching themselves or causing trouble, but even some ordinarily harmless ones can become pathogenic in stressed hosts. Piscinoodinium is not harmless; it puts down a rootlike extension ("rhizoid") and can burrow into the skin or gill tissues.

Don't ignore early warnings of Piscinoodinium, when fishes "flash" their bellies in attempts to scrape their gills against stones or gravel. They may begin to respire rapidly, hide or sink to the bottom and clamp their fins, in classic symptoms of malaise. Oodinium moves fast, faster than Ich. If you're unwary, you might not realize the fish is being attacked by Oodinium until it begins to lose its glossy shine and seems to have patches of yellowish to golden-brown or rusty-colored varnish. When the lights are on, it's hard to detect, but if you turn out all aquarium and room lights and use a flashlight, the point source of light will make Oodinium more visible. Longterm Oodinium infestation may result in darkened heads and backs of fishes.

What you may not notice until it's too late is damage Oodinium may do to fishes' gills. Oodinium may first attack gills, where the parasites cause both localized and diffuse swelling of the gills and fusion of the gill lamellae. But it may be noticed first round the gill openings, and also near the base of fins. Later, it can even attach to the eyes. Badly infested fish in the late stages of Oodiniasis should probably be euthanized, so that you can concentrate your attention on the more likely survivors. Don't expect to see the individual trophonts, which remain much smaller than Ich.

The dinoflagellate that attaches to the skin contains photosynthesizing chloroplasts that supplement the nutrients it is going to be getting from the host fish. The chloroplasts combine chlorophyll with supplementary yellowish to brownish carotenoids, which mask the chlorophyll's green and give Oodinium communities their characteristic yellow-brownish cast. Any critter that could photosynthesize used to be classed as an alga, so if you hear about "parasitic algae," it's likely to be Piscinoodinium they're talking about.

Oodinium can also settle out on the gills, where it sends down a rootlike extension into the gill lamella and dissolves cells with a histolitic action, to absorb their contents. This causes intense gill itch and swelling. If the infestation is bad enough, the gill-cover itself may seem swollen. But don't wait til the fish is at the surface laboring for oxygen. Fish can be killed by Oodinium in a few days, either directly from suffocation or from secondary bacterial infections of the abrasions.

An abstract of a 1998 article in the journal Diseases of Aquatic Organisms reported that Piscinoodinium was routinely found on wild-caught Brochis and Corydoras catfish imported to Great Britain from South America, where infected fish had trophonts of various sizes embedded in pits in the outer skin or enclosed by enlarged epithelial cells.

Like Ich, the Piscinoodinium trophont matures, then detaches and falls to the substrate, where it rounds up and encysts, in the phase called the tomont. (Ich passes through a comparable phase.) The encysted Oodinium tomont can spend three to five days at normal aquarium temperatures, dividing and dividing again as it forms tomites--— as Ich does--— but then, in an additional transformation, each tomite splits into many dinospores. There may be as many as 256 of these swarmers. Spores or tomites can also mature within the trophont while it's still attached to the fish, I understand. They are tougher than Ich, more tolerant of salt and high temperatures, and they have a longer free-swimming period before they must settle out on a host. The University of Florida Cooperative Extension Service estimates the life
cycle of Oodinium at aquarium temperatures as 10 to 14 days. The ZFIN website estimates the life cycle takes about two weeks at optimum temperatures (23-26°C). During their free-swimming tomite stage, they sustain themselves with photosynthesis. This is why you're advised to darken the tank in which you're battling Oodinium.

A Piscinoodinium infection of the gills may not be noticed for a couple more life-cycles. Advanced gill damage is not usually reversible; a fish may survive Oodinium but spend the rest of its days gasping for oxygen. Unfortunately Oodinium can also infest the intestinal tract, where it's comparatively safe from medication, unless you try the bioencapsulation technique, using brine shrimp. From its secure internal position the parasite is free to pass out with the feces in its spore-releasing stage. My understanding is that this isn't common.

Treatments. Oodinium derives some of its nutrition from its chloroplasts and starch reserves. So, whereas heat and salt may stress it like Ichthyophthirius, complete darkness is especially stressful for Oodinium; still, I wouldn't rely on promises that it can be killed with darkness alone.

Sometimes a saltbath is recommended, at a strength on one teaspoon per 5 gallons, or a salt dip:one to three minutes in full-strength seawater (35 parts/thousand). Salt alone hasn't eliminated Oodinium for me. I combat Oodinium with increased heat and the combination of formalin and malachite green. . Because formalin can only be used on ornamental fish that won't be eaten, the University of Florida Cooperative Extension Service's recommended treatment in food fish is quinine hydrochloride (the hydrochloride simply makes the quinine water-soluble). Greenex combines malachite green with quinine hydrochloride. Acriflavine works for some aquarists. Oldtime recommendations of copper sulfate are too risky, especially in soft acidic waters, I feel.

I got some of these details from Robert J. Goldstein's article in F.A.M.A., Feb. 1999, pp 52ff. I sure wish all the aquarium magazines were more forthcoming about posting archival material at their websites.


Minor Ciliates.

These are "minor" because the "major" ciliate parasite, Ichthyophthirius multifiliis or "Ich," gets its own page here.

Tetrahymena. Tetrahymena is a ciliate, only visible under the microscope (it's an oval shape about 35 to 85 microns in size). It is usually free-living, and harmless enough that some lab researchers on the Zebrafish project culture Tetrahymena as a first food for Zebra fry! Yet it is increasingly seen as a parasite on fishes, and it's endemic on fishes from the Asian fishmills. It's effects are easily misinterpreted and taken for symptoms of mycobacterial infection: sunken necrotic lesions that may be hemorhaging, pop-eye, etc. Tetrahymena is encouraged by high organic load in water of deteriorating quality. A large water change is advisable, perhaps followed by an oxidizing treatment to further reduce dissolved organics, using hydrogen peroxide or potassium permanganate. A recommended treatment is with a formalin/malachite green formulation, combined with 3.7 grams of methylene blue per 100 liters of water. See more about Tetrahymena in Shawn Prescott's Spring 1998 article, part 14 in his series "Diseases in Fish," archived at http://www.aquarium.net

Chilodonella. Chilodonella cyprini is another microscopic ciliate parasite of skin and gills, with a crease at one end that makes it heart-shaped under the electron microscope. I'm reading this: "respiratory distress, clamped fins and depression are the principal signs of infection. Excessive mucus production is commonly observed." in Dr. John B. Gratzek et al., Aquariology: Fish Diseases and Water Chemistry, 1992, p.59. Or, apparently, fish afflicted by Chilodonella can die suddenly without apparent signs of disease. These symptoms of fish malaise are quite generic; only microscopic examination of wet-mounted gill and skin tissue could identify this subversive parasite, but it's susceptible to common formalin/malachite green preparations and also sensitive to salt baths, so you should have eliminated it during Quarantine. The salt bath concentration that inhibits Chilodonella is between 0.1 and 0.2 per cent, that is between 2 and 4 tablespoons of common salt per net gallon. Remove the fish from this bath at the first sign of distress.

I'm mentioning Chilodonella because, like Tetrahymena, it's another source of fish deaths that can appear inexplicable.


Sporideans.

It seems quite likely that the multifarious sporidians 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 sporidians, or spore-producing micro-protists, which have evolved independently from separate evolutionary lines of protozoans. They are Apicomplexa, Microspora such as Pleistophora, and Myxospora, which infest tissues and organ cavities of fish or annelid worms. Whether they invade the cells of the host, like Pleistophora, or live in between the cells like the myxosporidians, all sporidians are parasitic. Many of these sporozoa form a highly-resistant stage, whether technically it's a spore or an "oocyst," which may survive a long while in fecal matter from the host or perhaps 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 the metabolism is very reduced: there's little metabolic exchange with the water.

Pleistophora (P. hyphessobryconis or "Neon disease"). More common than ever, this misleadingly named microsporidian was first identified in Neon Tetras (by the famous fish pathologist Schaperclaus, at the New York Aquarium in 1941), but it also attacks other small tetras and their relatives--— and barbs, danios and rasboras, even angelfish. Signs of pleistophora 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. Later, fishes become emaciated, or have hollows and cyst-like lumps that deform their musculature. Towards the end, the spine may even become deformed, 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. 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. 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 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 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 microsporidians 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 microsporidians, 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.

Microsporidia in fishes are generally rather host-specific. When zebrafish are attacked by sporidian 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'm told that microsporidians 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 take it apart, discard the plants, boil the gravel and disinfect everything.


Other sporidians. Certain other kinds of sporidians enter cells and make the cells enlarge so grossly they become visible to the naked eye, and we call them "cysts" and misidentify them as Lymphocystis. Various sporidians can lodge in fishes' liver, kidney tubules, spleen and other vital organs.

Myxosporidians do infect tropical fish, but there's no effective countermeasure against them, either. The notorious coldwater myxosporidian, Myxobolus cerebralis, that causes the "whirling disease" of salmon and trout 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 sporidians is Plasmodium, transmitted by mosquitos, which is the cause of malaria. Cryptosporidians 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.

Other protists.

There are many other weakly parasitic ciliates and flagellates, both external ones, like Ichthyobodo (formerly known as Costia) and Trichodina, which are treated like Ich, and internal, of which the most notorious is the flagellate Hexamita, which is treated with Metronidazole ("Flagyl") at 250mg/5 gals, in a single dose. Seachem makes a metronidazole for the aquarium market. These others aren't true "obligate" parasites, that must find a host or perish, but merely opportunistic organisms that will take advantage of a fishes' reduced defenses. Most of the "weak" parasites will only trouble fishes in water that is too rich in organics, where they can multiply out of control.