09-11-2007, 08:12 AM
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Hole-in-the-Head Disease Synonyms:
Hexamita, Octomita Symptoms:
Large holes on the fish's head, white stringy feces, decreased activity, loss of appetite, anorexia, listlessness Causes:
This was originally considered a deficiency disease before, however, there are many cases that can cause HITH.
As stated in this article
, Hexamita is a flagellated protozoan found in the gastrointestinal tracts of a variety of cold and warm water fish, including several species of Cichlids which are popular aquarium pets. It can be a serious health problem in angel fish and discus. Occasionally hexamita is found in healthy fish. Stress from malnutrition, shipping, overcrowding, or poor water quality may lead to rapid reproduction of the protozoan, resulting in disease. The genus hexamita was formerly called "Octomitus" because of eight hair-like flagella which project from the organism. Three species of hexamita have been associated with disease in fish, Hexamita salmonis , Hexamita truttae and Hexamita intestinalis . It is unknown whether these species or new species which have not yet been identified are responsible for disease in ornamental fish.
Since hexamita can be kept alive in laboratory media, it is assumed that it is an inhabitant of aquaria where organic material has been allowed to accumulate. Cleaning of gravel and filter materials will assist in eliminating the organism from the environment. It may be advisable to periodically check broodstock for subclinical hexamita infections. Even though the fish may not be sick, low levels of the parasite may have an adverse effect on reproductive performance or may flare up under conditions of stress. These subclinical infections can be easily treated with a medicated feed before real problems develop. Treatment:
Flagyl-a combination of Metronidazole and Praziquantel in the form of 250 mg tablets which is an antibiotic used for the eradication of intestinal flagellates.
I used one tablet per 20 gallons dosage when treating for intestinal flagellates and HITH. Metronidazole can be added as a food addictive. It is generally recommended to train your fish to become accustomed to gelatinized foods where you can slip in a dose of Metronidazole should the fish become sick and refuses to eat its food.
09-11-2007, 09:12 AM
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Whirling Disease (Myxosoma cerebralis) Symptoms:
Clinically fish become deformed about the head and spine with the fish swimming erratically (whirling). Histologically there is necrosis of the cartilage with numerous spores present in the area of inflammation. The necrosis of the cartilage is the cause of the deformation. Causes:
Myxosporidean parasite with a 10 micron oval spore with 2 piriform polar capsules. Parasite affects primarily young salmonids (rainbow trout most susceptible).
Transmission is believed to be by ingestion of spores. The life cycle of this organism is not completely known (believed to be indirect since myxobolus spores do not directly infect the fish) however, there appears to be a tubeficid oligochaetes (tubifex mud worm) as an important intermediate or transport host. It is believed that the parasite undergoes sporulation in the tubiflex worm were the organism takes on the form of a Triactinomyxon sp. It is believed that this parasite is then released from the tubifex worm and infects the trout. (ingestion of infected tubifex worms may also cause the fish to become infected) Morphology
All information retrieved from Wikipedia for reference and archival purposes. Triactinomyxon stage
The stages that infect fish, called triactinomyxon spores, are made of a single style that is about 150 micrometers (µm) long and three processes or "tails" that are each about 200 micrometers long. A sporoplasm packet at the end of the style contains 64 germ cells surrounded by a cellular envelope. There are also three polar capsules, each of which contains a coiled polar filament between 170 and 180 µm long. Polar filaments in both this stage and in the myxospore stage (see picture above) rapidly shoot into the body of the host, creating an opening through which the sporoplasm can enter. Sporoplasm stage
Upon contact with fish hosts and firing of the polar capsules, the sporoplasm contained within the central style of the triactinomyxon migrates into the epithelium or gut lining. Firstly, this sporoplasm undergoes mitosis to produce more amoeboid cells, which migrate into deeper tissue layers, in order to reach the cerebral cartilage. Myxosporean stage
Myxospores, which develop from sporogonic cell stages inside fish hosts, are lenticular. They have a diameter of about 10 micrometers and are made of six cells. Two of these cells form polar capsules, two merge to form a binucleate sporoplasm, and two form protective valves. Myxospores are infective to oligochaetes, and are found among the remains of digested fish cartilage. They are often difficult to distinguish from related species because of morphological similarities across genera. Though M. cerebralis is the only myxosporean ever found in salmonid cartilage, other visually similar species may be present in the skin, nervous system, or muscle. Life cycle
Myxobolus cerebralis has a two-host life-cycle involving a salmonid fish and a tubificid oligochaete. So far, the only worm known to be susceptible to M. cerebralis infection is Tubifex tubifex, though what scientists currently call T. tubifex may in fact be more than one species. First, myxospores are ingested by tubificid worms. In the gut lumen of the worm, the spores extrude their polar capsules and attach to the gut epithelium by polar filaments. The shell valves then open along the suture line and the binucleate germ cell penetrates between the intestinal epithelial cells of the worm. This cell multiplies, producing many amoeboid cells by an asexual cell fission process called merogony. As a result of the multiplication process, the intercellular space of the epithelial cells in more than 10 neighbouring worm segments may become infected.
Around 60–90 days post-infection, sexual cell stages of the parasite undergo sporogenesis, and develop into pansporocysts, each of which contains eight triactinomyxon-stage spores. These spores are released from the oligochaete anus into the water. Alternatively, a fish can become infected by eating an infected oligochaete. Infected tubificids can release triactinomyxons for at least 1 year.The triactinomyxon spores swim through the water to infect a salmonid through the skin. Penetration of the fish by these spores takes only a few seconds. Within five minutes, a sac of germ cells called a sporoplasm has entered the fish epidermis, and within a few hours, the sporoplasm splits into individual cells that will spread through the fish.
Within the fish, there are both intracellular and extracellular stages that reproduce in its cartilage by asexual endogeny, meaning that new cells grow from within old cells. The final stage within fish is the myxospore, which is formed by sporogony. They are released into the environment when the fish decomposes or is eaten. Some recent research indicates that some fish may expel viable myxospores while still alive.
Myxospores are extremely tough: "it was shown that Myxobolus cerebralis spores can tolerate freezing at *-20°C for at least 3 months, aging in mud at 13°C for at least 5 months, and passage through the guts of northern pike Esox lucius or mallards Anas platyrhynchos without loss of infectivity" to worms. Triactinomyxons are much shorter lived, surviving 34 days or less, depending on temperature. Treatment:
Some drugs such as furazolidone, furoxone, benomyl, fumagillin, proguanil and clamoxyquine have been shown to impede spore development, which reduces infection rates. For example, one study showed that feeding Fumagillin to Oncorhynchus mykiss
reduced the number of infected fish from between 73% and 100% to between 10% and 20%. Unfortunately, this treatment is considered unsuitable for wild trout populations, and no drug treatment has ever been shown to be effective in the studies required for United States Food and Drug Administration approval.
Rainbow trout deformed from Whirling Disease
09-12-2007, 12:57 AM
| || | Black Spot Disease (Uvulifer ambloplitis) Symptoms:
Clinically the fish have numerous black to brown spots up to 1 mm (dia) over the skin, gills and eyes. The spots contain a metacercaria surrounded by heavily pigmented fibrous connective tissue. Causes:
Introduction of herons and kingfishers which are the definitive host, snails are the first intermediate host. Fish are the second intermediate host.
Black Spot Disease is more common in ponds compared to the aquaria.
- • Adults found in intestine of kingfishers.
• Unembryonated eggs are shed in water -->> hatch in 3 weeks -->> miracidium emerges.
• Miracidium penetrates snail Helisoma trivolvis (ramshorn snail) -->> mother sporocyst -->> daughter sporocyst -->> furcocercous cercaria are released.
• Cercaria penetrates skin of host and transforms into neascus metacercaria, where there is a strong tissue reaction -->> black spot
• Fish then eaten by bird -->> metacercariae excysts -->> adult in intestine.
Frequent water changes are recommended. Pathology
1. Strong tissue reaction due to mobilization of fibrocytes and melanocytes to create black spot.
2. If reaction is strong enough, total body fat of fish will be driven below 5%.
3. If fish enters winter in this condition, it will not survive because fish does not feed in winter and does not have enough fat reserves to over winter.
4. At least 50 cysts are necessary to cause mortality.
5. At least 10-20% of fish will die each winter.
6. Because of parasite overdispersion, 70-80% of the parasites the pond will also be eliminated in winter.
09-12-2007, 01:37 AM
| || | Diplostomosis (Diplostomum spathaceum) Symptoms:
Cataract, lesions on the gills, body surface and fins, (in newly-infected fish) petechia and exophthalmia, small white opacities in the lens, dark coloration and loss of condition Description:
Very wide host range: recorded in more than 150 species of freshwater and brackish water species. Some of the economically important fish species in which the parasite has been recorded include: cod (Gadus morhua
), flounder (Platichthys flesus
), and salmonids of the genera Salmo, Oncorhynchus, and Coregonus.
The life cycle involves pulmonate snails as first intermediate hosts, fish as second intermediate hosts, and piscivorous birds as final intermediate hosts harbouring the adult worms.
Fish are infected with cercariae. Body length of cercariae is 160-260 µm and the bifurcated tail stem is as long as the body. The area around the mouth and the body is equipped with hooks and spines in a regular pattern. On penetration of the fish, the tail is shed. During its migratory route to the lens, the parasites gradually undergo further change. The established metacercariae are flattened, about 400 µm in length, and possess two suckers and an attachment organ (tribocytic organ).
Infection takes place in areas where the various hosts occur together, i.e. in fresh and brackish standing inshore water. Shedding of the cercariae is associated with a rise in water temperature and normally continues from late spring to early autumn.
On another note, this will not happen in the aquaria without other various hosts. Treatment:
09-13-2007, 04:28 AM
| || | Pop-eye Synonyms:
Lethargy, bulging eyes associated with loss of vision Causes:
Severe stress, various pathogens Treatment:
Broad spectrum antibiotics
Determine your water parameters and perform frequent water changes to improve water quality. Pop-eye is a sign of a number of infections rather than a disease in its own right.
09-13-2007, 04:46 AM
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Camallanus cotti and Camallanus lacustris Symptoms:
Red worms protruding on the fish's anus, inflammation in the vent area, whitish slimy feces Causes:
Camallanus worms can be found protruding out of the fish's anus. They are actually transparent but gained the reddish tint which is actually their victims' blood. Female camallanus worms are over a centimeter in length whereas males are about a third fraction of the females' size.
According to The Skeptical Artist website, most species of Camallanus and its close kin shed eggs, and their life cycle needs an intermediate host, often a copepod or perhaps a cladoceran (such as daphnia); their reproduction gets disrupted in the aquarium, though copepods are everywhere, especially in planted tanks. But C. cotti and the less-common C. lacustris are viviparous: their larvae develop within the adult female worm who sheds them into the water; several successive generations can infect aquarium fish.
The young worms are as likely to be eaten by a copepod as by another fish, but either way they get passed to the next fish host. In the severest cases maybe the best thing you can do is net out the sufferer, gently euthanise it, and concentrate on the other fishes that are infested but not so far gone. Don't try to net the fish and pull off the worms with a tweezer; they are deeply embedded and you'll just tear the intestine wall. Parasitic nematodes weaken the host; what kills it usually are secondary infections.
In retrospect, you may realize that the victim had been showing some inflammation in the vent area and might have been passing whitish, mucusy feces. Too often we let symptoms like these pass unnoticed.
In the wild most fish harbor some parasitic nematodes. Fish populations are diffuse enough that the chances of a nematode egg being successfully transfered are low, and besides, a healthy fish can usually live with the normal range of its familiar co-evolved parasites, just as many humans harbor Giardia without suffering significant ill effects. However, when fish are caught and transported to exporters, then flown from wholesaler to wholesaler, shipped to retailers and at last to hobbyists, they have been put through enormous stresses. To a fish with stress-impaired resistance, even a modestly benign and familiar parasite may become serious. How much more lethal, then, is an alien parasite that has not had time to "learn" not to damage its host.
Camallanus cotti was first described in Japan in 1927, but has been distributed throughout the world, largely from the fish farms of Singapore and Malaysia, especially after 1980. Treatment:
Levamisole hydrochloride (effective as anti-worming agent), fenbendazole, fresh garlic extracts Notice the worms protruding on the fish's anus.
09-13-2007, 04:58 AM
| || | Capillaria Symptoms:
Loss of weight/anorexia, slowing down of growth, malnutrition, whitish and stringy feces, dark coloration Causes:
Fish can get them when they eat the eggs of the worms and even in contact with feces of infected individuals. Crustaceans and copepods serve as intermediate hosts and may be eaten by the fish in the wild thus infecting the fish itself as well. Treatment:
Piperazine, mebendazole, albendazole, levamisole hydrochloride, trichlorfon
Another treatment by Drs. Foster and Smith recommended against nematodes http://www.drsfostersmith.com/Produc...&N=2004+113521 Capillaria egg
09-14-2007, 08:34 AM
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Swim Bladder Disorder
Limited signs of bloat though usually no physical damage is found, fish struggles to balance itself sometimes going “belly up” due to lack of proper buoyancy
Often indigestion with goldfish, blood parrot cichlid and “balloon” strains becoming more vulnerable to the disorder rather than most fish species, bacterial infections, damaged swim bladder, the use of floating foods which when ingested allows entry of air to the digestive system, congenital or development causes, birth defect, sudden trauma from sudden changes in water conditions or failure to acclimatize the fish properly.
Causes can be difficult to determine although possible causes are often leaned on the use of floating foods, indigestion and damaged organs by assumption. It has long been argued that floating foods should never be used at all especially for goldfish. It is in the best interest of the safety of the fish that sinking foods be used instead of floating foods or try to squish the foods until they sink.
I’ve personally seen the crossbreed of the parrot cichlid and flowerhorn struggling to swim properly due to its balloon appearance. It will always be noted that balloon strains are rather deformed and should be avoided at all costs. Their vulnerability for this disorder renders them incapable to live a longer life span in comparison to the normal fish species.
Change of diet with foods containing high fiber content, fasting for several days or antibiotics. Unfortunately, there is no cure for such disorder although in some cases, the fish can recover depending on the cause of the disorder. Fish that suffer from this disorder due to sudden trauma from improper acclimatization usually will never recover at all. In this case, it is recommended to destroy the fish.
09-14-2007, 08:36 AM
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Slightly large abdomen, no feces are excreted.
Incorrect diet or overfeeding. What food are you feeding your fish? How many times do you feed your fish? How long does it take for the fish to consume all the food? It is recommended to minimize the food rations by once or twice a day for fish in their adult stage. A one day fasting per week will certainly compensate for the rest of the days of feeding them. It must be noted there are certain fish species that may eat the food but which is totally not appropriate for them.
Green peas are recommended as they serve as a laxative allowing the fish to excrete their wastes blocked inside their bodies. Always remove the shell and if intended to be fed on fish with small mouth, mash the peas to smaller pieces.
Another alternative is the use of half a level teaspoon magnesium sulfates (Epsom salts) per 4.5 liters. If the fish recovers, improve its diet and change feeding routine.
09-14-2007, 08:41 AM
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Air Bubble Disease
Clear small blisters under the skin (0.5-2 mm)
Oversaturation of the water with gas
Aerate the water very well.
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