According to new research presented by Dehai Xu, Ph.D. at the 240th National Meeting of the American Chemical Society (ACS)*, a vaccine against the feared ich disease might be available in the foreseeable future.
Ich is a disease dreaded by hobby aquarists and professional fish farmers alike. It is caused by the ciliated protozoan Ichthyophthirius multifiliis (hence the name ich) and can easily kill of all the fish in an aquarium or fish pond. Fortunately, it seems to be unable to infect humans. Among aquarists, it is chiefly known as White Spot Disease since the parasites cause small white nodules to form on the skin and in the gills of infested fish.
Today, ich outbreaks in large commercial fish farms are often treated by adding hundreds of gallons of a formaldehyde solution to the water. This is far from an ideal solution, since formaldehyde can be toxic to both humans and fish. It is classified as a known human carcinogen by the WHO International Agency for Research on Cancer (IARC) and is associated with both nasal sinus cancer and nasopharyngeal cancer. And as anyone who has ever combated ich in an aquarium knows, ich treatment is something you have to do over and over again since the parasite is usually only sensitive to treatment during one of its multiple life stages. This means repeatedly adding large quantities of formaldehyde solution to the pond. Even when formaldehyde ich treatment is successful, it provides no long-lasting effects since the fish develops no immunity. If new outbreaks occur, a new treatment cycle has to be carried out.
It is therefore no surprise that the series of vaccine tests carried out by Dr. Xu and his colleagues Dr. Phillip Klesius and Dr. Craig Shoemaker, who are with the U. S. Department of Agriculture’s Agricultural Research Service (ARS) in Alabama, have sparked vibrant interest within the aquatic world. For anyone from commercial fish farmers to public aquaria and hobby fish keepers, an ich vaccine would be a dream come true.
“Outbreaks of the parasitic disease caused by Ichthyophthirius (Ich) can result in losses of 50-100 percent of fish,” Dr Xu explained while presenting the team’s findings at the ACS meeting. “The disease is very common, and almost every home fish hobbyist has encountered it. Once the parasite infects fish, and starts growing in the skin, fins, and gills, there is no really effective treatment. Ich causes losses estimated at $50 million annually. It would be much better to prevent the disease. To vaccinate against Ich, you would need much less medication, and it would not pose an apparent threat to the environment. And you would need just one treatment to make the fish immune for life.”
In their efforts to develop a vaccine, Xu and his colleagues have focused on the use of so-called trophonts.
The ich protozoa goes though three life stages:
• The ich trophozoite feeds inside the nodule (”the white spot”) on the skin or gill of the fish.
• The ich trophozoite falls off and becomes an ich tomont, i.e. it enters an encapsulated dividing stage. During this stage, the tomont is attached to plants, gravel or other objects in the environment.
• The ich parasite will then start dividing itself, producing trophonts. The trophonts will move around freely in the water, looking for fish to infect.
Trophonts burrow into the skin and fills of a fish and start to feed, thus completing the cycle. When Xu, Klesius and Shoemaker began their research project very little was known about how fish develop protective immunity to trophonts, so the researchers basically had to start from scratch.
Eventually, they were able to show that vaccination with live ich theronts and trophonts killed with high-frequency sound waves stimulated production of protective antibodies in channel catfish (Ictalurus punctatus)
“This study demonstrated that vaccines against Ich induced protective immunity and could provide a unique solution to prevent this parasitic disease through vaccination,” Xu said. “An Ich vaccine would have great impact by preventing the disease, minimizing loss of valuable fish and increasing profitability of aquaculture.”
Injecting fish in a laboratory setting is one thing, administering a vaccine to thousands or even millions of fish in a huge commercial farm is another, so the next goal will be to find a way of carrying out large-scale vaccinations. It might for instance be possible to produce a large quantity of Ich antigen and then creating a vaccine that can be administered as food or in a “bath”.
For aquarists however, injecting each fish with the vaccine might actually be a feasible solution, provided of course that an injectable vaccine would be produced for the aquarium market.
The controversial use of live fish to chew away dead skin in pedicures may be banned in New York State for health and safety issues which have been proposed in a new bill.
The procedure in question was actually developed in Turkey, as a way to take care of a variety of ailments of the skin, such as psoriasis, consists of the feet being plunked into a tank of water which contains two different kinds of small fish. These rather hungry fish then proceed to eat away dead skin while leaving the healthy skin alone.
These “Fish Pedicures” are illegal in at least 14 different states, comments Senator Jeff Klein, of the Bronx and Westchester, who originally proposed the ban. The basis of the ban rests on the concern that fungal infections may be passed by unsanitized fish in unclean water. Of course the animal rights groups have jumped on the band wagon, pushing to outlaw the use of fish in pedicures as it is inhumane.
Robin Ross, the president of the New York Podiatic Medical Association, had this to say during a telephone interview: “I do not recommend it to anyone who has any diabetes or any immuno-compromised condition such as AIDS or cancer, because of the risk of infection. The fish are defecating and urinating in that water and you’re sticking your feet in it.” ”
The New York Department of State has gone on the record, saying that it is not aware of any of the 20,000 plus licensed nail salons engaging in such an activity. Apparently it is only being done on the down low, in backrooms of New York City.
Viral hemorrhagic septicaemia (VHS) is a disease caused by a negative-sense single-stranded RNA virus of the genus Novirhabdovirus. Infected fish suffer from haemorrhaging of their internal organs, skin and muscles. Symptoms that can be observed from the outside includes reddened eyes, gills, skins and fin, opens sores, a bloated abdomen, and bulging eyes, but some fish show no outward signs at all.
The virus can spread through water transfer and through the consumption of infected eggs or fish, which means that baitfish can introduce the fish to new localities. A fish that manages to survive the disease can become a lifelong carrier of the virus, excreting it through its urine and sperm or ovarian fluids. In Europe, the gray heron is known to spread the virus without being infected; the virus appears to remain inactive as long as it resides in the digestive tract of the bird.
Different strains with different properties
Historically, VHS was associated with Western Europe where it was documented as a pathogenic disease among cultured salmonids as early as the 1950s. In 1963, the viral cause of the disease was discovered by M. H. Jenson. Until late 1988, VHSv Type I was the only known strain of the disease and it appeared to be contained within freshwater fish farms in continental Europe, affecting primarily rainbow trout and only occasionally brown trout and pike.
In 1988 the first case of VHS was reported from the United States and the culprit turned out to be a distinct, more marine-stable strain of VHSv than the European variant. The virus was present in salmon returning to Washington State from the Pacific Ocean. Today, we know of four different main strains and except for type IV, all of them are endemic to Europe.
The type IV virus can be divided into two subtypes: IV-a and IV-b. IV-a has been reported from marine fish living in the Northwest Pacific, along the North American north Atlantic coast, and along the shores of Japan and Korea. IV-b is the type causing problems for freshwater fish in the North American Great Lakes region.
The IV-b strain was first isolated from fish living off Canada’s Atlantic coast where it did not cause any high mortality rates. This strain is capable of infecting not only salmonids but a long row of warm-water freshwater species previously assumed to be resistant to VHS. The European strains are particularly deadly do rainbow trout, but the IV-b strain only have a mild affect on this species. It is on the other hand capable of killing fish such as chinook salmon, lake trout, steelhead trout, gobies, emerald shiners, yellow perch, walleye, muskies and whitefish.
First of let me say that I am sorry for the lack of post these last weeks. Internet problems. Will hopefully be back to normal soon. Now to the story
Hearing impairment caused by damage to hail cells in the inner ear is by far the most common cause of hearing loss, but research carried out on Zebrafish might be able to show us how these hair cells can be re-grown.
Scientists involved in the experiments say there could be therapeutic trials to prevent hearing loss using drugs within a decade, while finding a cure for hearing loss using hair-cell regeneration is probably at least 20 years away.
Hair cells in the inner ear can be damaged by a long row of factors, such as noise, drugs, disease and ordinary aging. Once a hair cell dies, mammals – including us humans – aren’t able to replace that hair cell with a new one. Until the mid-1980’s, researchers thought that this was true for all warm-blooded vertebrates, but we now know that birds are able to grow new hair cells and that this hair-cell regeneration can result in improved hearing.
Among the so called cold-blooded animals, aquatic creatures like the zebrafish are equipped with clusters of hair cells running along the outside of the body to help the animal sense vibrations in the water. Just like the birds, zebrafish are capable of regenerating these hair cells if there’re damaged and this has attracted the attention of U.S. researchers looking for a cure for hearing loss.
Why some animals can regenerate hair cells while other can’t, and why some animals – even within the same species – are more vulnerable to hair-cell death, remains a mystery.
“I literally walked around for years wondering about this variability,” says Ed Rubel, a professor of hearing sciences who leads part of a University of Washington research effort in Seattle.
The Seattle research teams are currently using zebrafish to gain a better understanding of hair cell generation in hope of figuring out how to protect human hair cells from becoming damaged and how to stimulate the cells to regenerate. The project is focused on understanding the molecules and genetics involved with hair cell regeneration, and how to mimic this process in animals that don’t spontaneously regenerate hair cells.
In collaboration with Dr. David Raible, another University of Washington scientist, Professor Rubel has already identified chemicals that seem to protect hair cells from damage. Those chemicals are now being tested on mice and rats to see if they will have an affect on warm blooded mammals and not just on zebrafish. The goal is to develop a medicine that can be administered to patients receiving drugs known to kill hair cells, e.g. chemotherapeutic agents.
Dr. Rubel’s and Dr. Raible’s teams also are studying the genetics of zebrafish to identify markers that confer hair-cell protection. The teams are also working on a separate group of studies regarding the genes and other molecules that make the regeneration of hair cells possible in zebrafish, birds and mice. In 2008, the teams jointly indentified several genetic mutations and drug-like compounds that seemed to protect hair cells from death, publishing their findings in the journal PLoS Genetics.
In addition to this, Dr. Rubel’s lab is investigating the role of the so called support cells; cells that surround the hair cells and are capable of both turning into hair cells and generate new hair cells. “If we understand the template of genes that are expressed by the cells we would want to divide, then we could tap into that template to mimic regeneration efforts in mammals”, Dr. Rubel explains.
How do hair cells work?
Hair cells are called hair cells since they look like cells with little hairs growing out of them when you look at them through a microscope. Hair cells are found in our inner ears and damage to these cells is a major cause of irreversible hearing loss. The filament hairs, also known as cilia, bend as sound waves enter the ear, prompting the hair cell to send an electrical signal to the auditory nerve from which it continues to the brain.
A team of U.S. scientists has documented the first transmission of the lethal phocine distemper virus from the Atlantic Ocean to a population of sea otters living along the coast of Alaska.
The presence of phocine distemper virus has been confirmed in nasal swabs take from live otters and through necropsies conducted on dead otters found along the Alaskan coast. The findings also indicate that the virus was passed between seal species across Northern Canada or Arctic Eurasia before reaching the otters in Alaska’s Kachemak Bay.
Prior to this study, PDV had never been identified as the cause of illness or death in the North Pacific Ocean and researchers suggest that diminishing Arctic sea ice may have opened a new migration route for both animals and pathogens.
The study was carried out by researchers from two California universities and the Alaskan branch of the U.S. Fish and Wildlife Service. It has been published in ”Emerging Infectious Diseases”, a journal published by the U.S. Centers for Disease Control and Prevention.
What is phocine distemper virus (PDV)?
Phocine distemper virus (PDV) is a paramyxovirus of the genus Morbillivirus. It is dangerous for pinniped species, especially seals, and is a close relative of the canine distemper virus (CDV).
PDV was first identified in 1988 when it caused the death of approximately 18,000 harbour seals, Phoca vitulina, and 300 grey seals, Halichoerus grypus, in northern Europe. In 2002, the North Sea lost approximately 21,700 harbour seals in new a PDV outbreak – estimated to be over 50% of the total population.
Infected seals normally develop a fever, laboured breathing and nervous symptoms.
Several types of commonly used fish egg disinfectants increase the risk of swim bladder disorder in fish, a new study from Israel reveals.
In an effort to prevent fungal growth, many fish breeders use various chemicals, such as methylene blue, hydrogen peroxide, acriflavine and chloramine-T to aquariums where eggs are kept. This practise is especially common among breeders who will not let the parents stay with eggs and fry. Many fish species carry out parental care and eggs from such species often depend on one or both parents gently fanning fresh water over them and manually removing any unfertilized eggs from the batch. Without such parental care, the eggs easily succumb to fungi unless the fish breeder adds some type of fungicide to the water.
The new Israeli study, which focused on Angelfish (Pterophyllum scalare), revealed that some of these chemicals may be responsible for a swim bladder disorder in developing fish. In fish suffering from this type of disorder, the swim bladder can not inflate properly and the fry fails to develop into a fully free-swimming adult. Among aquarists, such fish are commonly known as “belly sliders” due to their peculiar way of moving around the fish tank.
Methylene blue
Eggs hatched in the presence of 1, 2 and 5 ppm methylene blue exhibited significant increases in swim bladder non-inflation (11%, 9% and 33%, respectively; none in controls).
Time of exposure to methylene blue was a key factor. Exposure for up to 1 day post-hatch did not affect swim bladder non-inflation, but exposure from 2 days onwards significantly increased swim bladder non-inflation.
Hydrogen peroxide
Hydrogen peroxide at 250 ppm significantly increased swim bladder non-inflation (65% comparing to 27% in the control). Higher concentrations resulted in 100% mortality.
Acriflavin
Exposure to acriflavin at 2.25 ppm, but not 1.25 ppm, significantly increased swim bladder non-inflation (75% and 52% respectively; 20% in controls).
Chloramin-T
Chloramine-T did not significantly affect swim bladder non-inflation.
For more information, see the paper “C. Sanabriaa, A. Diamantb and D. Zilberga (2009) – Effects of commonly used disinfectants and temperature on swim bladder non-inflation in freshwater angelfish, Pterophyllum scalare (Lichtenstein)”. The paper has been published in the journal Aquaculture.
Scientists from the U.S. Geological Survey (USGS) have revealed that largemouth bass injected with oestrogen produces less hepcidin than normally. Hepcidin is an important iron-regulating hormone in fish, amphibians and mammals, and researchers also suspect that hepcidin may act as an antimicrobial peptide. In vertebrate animals, antimicrobial peptides are the body’s first line of defence against unwelcome bacteria and some fungi and viruses, so if there’re right, a lowered amount of these compounds is certainly not good news.
“Our research suggests that estrogen-mimicking compounds may make fish more susceptible to disease by blocking production of hepcidin and other immune-related proteins that help protect fish against disease-causing bacteria,” says lead author Dr. Laura Robertson.
You can find more info in the study “Identification of centrarchid hepcidins and evidence that 17β-estradiol disrupts constitutive expression of hepcidin-1 and inducible expression of hepcidin-2 in largemouth bass (Micropterus salmoides)” by Laura Robertson, Luke Iwanowicz and Jamie Marie Marranca in the latest issue of the journal Fish & Shellfish Immunology. It is the first published study demonstrating control of hepcidin by estrogen in any animal.
For the first time in history, scientists* have succeeded in measuring the physiology of marine phytoplankton through satellite measurements of its fluorescence. With this new tool, it will become possible for researchers to continuously keep an eye on the ocean’s health and productivity. Since it is based on satellite images the method works all over the world.
“Until now we’ve really struggled to make this technology work and give us the information we need,” says Michael Behrenfeld, an Oregon State University professor of botany. “The fluorescence measurements allow us to see from outer space the faint red glow of tiny marine plants, all over the world, and tell whether or not they are healthy. That’s pretty cool.”
Knowing how the world’s phytoplankton populations are doing doesn’t only tell us about the plankton it self; it also provides us with valuable clues that can help us assess a long row of other processes on the planet. By studying phytoplankton, it is for instance possible to learn about climate change and desertification.
* The break through is the result of the successful collaboration of Oregon State University, the NASA Ocean Biology and Biogeochemistry Program, the NASA Goddard Space Flight Center, University of Maine/Orono, University of California/Santa Barbara, University of Southern Mississippi, Woods Hole Oceanographic Institution, Cornell University, and the University of California/Irvine.
Filtered cigarette butts should have new requirements for disposal, says Public Health Professor Tom Novotny after a San Diego State University (SDSU) study revealed filter-tipped cigarette butts to be toxic to marine and fresh-water fish.
According to Novotny and other members of the Cigarette Butt Advisory Group, used cigarette filters ought to be classified as hazardous waste since toxins present in them harm wildlife.
“It is toxic at rather low concentrations,” Novotny explains. “Even one butt in a liter of water can kill the fish in a period of 96 hours.”
Novotny says one way of reducing the amount of cigarette filters in our environment is stronger enforcement of anti-litter laws and non-smoking areas. Fines, waste fees or special taxes are other options, if the money is used to pay for cigarette butt recycling. A third alternative is to force manufacturers to pick up the bill for clean-up costs incurred by their products.
A thrown away cigarette butt is a combination of the original plastic filter and the compounds caught by the filter while the cigarette was being smoked. The plastic makes the filter non-biodegradable and the trapped compounds are toxic until they eventually biodegrades into the environment.
According to Novotny, cigarette butts are the number one littered substance in the world and have been the number one single item picked up on beach cleanup days in San Diego for several years.
“When they unconsciously throw their butts onto the ground, it’s not just litter, it’s a toxic hazardous waste product,” Novotny says. “And that’s what we’re trying to say. So that may be regulated at the local or state level. And we hope people will be more conscious about what they do with these cigarette butts.”
The study was carried out by SDSU Public Health Professor Rick Gersberg.
Picture by: Chris Sanderson, in Peterborough, Ontario, Canada.
A Taiwan research team has successfully extracted a brain-boosting nutrient from squid skin, according to an announcement made by the Council of Agriculture’s Fisheries Research Institute.
The nutrient in question is phospholipid docosahexaenoic acid, commonly known as PL-DHA, a substance known to improve a persons memory and enhance learning ability.
According to the institute official, PL-DHA is superior to TG-DHA another form of docosahexaenoic acid commonly found in deep-sea fish oil — when it comes to inhibiting degradation of the intellect since PL-DHA can cross the blood brain barrier and be absorbed directly by the brain.
Researchers at the institute have also showed that PL-DHA is effective in reviving neural cells and enhancing the content of three oxidation-resistant enzymes — GSH, CAT and SOD. In addition to this, the fatty acid will moderate the oxidative damage to neural cells that can be induced by free radicals in the body, which means that it will decrease the pace of plaque and tangle accumulation in brain cells.
Quoting medical reports, the institute official stressed that Alzheimer’s and other forms of senile dementia is known to be associated with the accumulation of plaque and tangles in the brain.