Post 4: Freshwater White Spot Disease in Home Aquariums

Home aquariums have become a popular way of having pets and and decorating the home in the 21st century. Due to the costs associated with saltwater aquariums, plenty of people are opting for freshwater.
Unfortunately there are diseases that have evolved to thrive in these conditions that pose risks to freshwater fish.

Ichthyophthirius multifiliis (Freshwater White Spot) is a parasite that exists on the outside of a fish that can cause 100% of mortalities in an aquarium or aquaculture setting (Jiravanichpaisal et al 2004). It gets its name from the 1mm long white cysts that typically grow on the gills and body of the fish (Wu et al 2002), and each spot is a cyst comparable to grains of sugar that encloses a parasite (Nigrelli et al 1976).

I. multifiliis can become introduced into an aquarium usually by introducing contaminated fish, exchanging untreated and contaminated water into the system or using contaminated instruments in the same water body as the fish (Dickerson 2006).
As the cysts grow on the individuals gills and body, respiration becomes increasingly difficult as the cysts block water flow through the gills and because fish excrete excess mucous due to irritation from the cysts (Dickerson 2006). Wounds left by parasites also affect the fishes swimming ability making it harder to feed (Dickerson 2006).

A visual diagnosis of the fish is the fastest way to detect an I. multifiliis infection, with the stand out symptoms being the presence of white cysts, rapid operculum movements as the fish struggles to breath and anorexia due to a lack of feeding (Dickerson 2006).
Treatment is the quarantine of infected individuals into clean water until the symptoms subside-or the individual dies and/or the addition of salt into the system to a maximum of 4 parts per thousand, as freshwater fish can tolerate higher salinity than the parasite (Dickerson 2006).

I. multifiliis targets the gills and body

References:

Dickerson, H 2006, 'Ichthyophthirius multifiliis and Cryptocaryon irritans (Phylum Ciliophora)', 'Fish Diseases and Disorders' pp. 116-118

Jiravanichpaisal, P. Soderhall, K. Soderhall, I 2004, 'Effect of Water Temperature on the Immune Response and Infectivity Pattern of White Spot Syndrome Virus (WSSV) in Freshwater Crayfish', 'Fish and Shellfish Immunology' vo. 17, pp. 265-275

Nigrelli, R. Pokorny, K. Ruggieri, G 1976, 'Notes on Ichthyophthirius multifiliis, a Ciliate Parasitic on Fresh-Water Fishes, with Some Remarks on Possible Physiological Races and Species', 'Transactions of the American Microscopical Society', vol. 95, pp. 607-613

Wu, J. Nishioka, T. Mori, K. Nishizawa, T. Muroga, K 2002, '

A Time-Course Study on the Resistance of Penaeus japonicus Induced by Artificial Infection with White Spot Syndrome Virus', 'Fish and Shellfish Immunology', vol. 13, pp. 391-403

   

Post 3: Streptococcus: the Flesh Eating Bacteria in the Far North & the Evolution of an Epidemic

Between the years 2007 to 2011, over 90 Queensland Grouper (Epinephelus lanceolatus) and a variety of wild fish and estuarine stingrays were found dead in the Cairns inlet in Far North Queensland (Bowater et al 2012). The symptoms were black patches of necrotic tissue and visible signs of both internal and external bleeding. The Department of Northern Fisheries diagnosed the problem as a disease called Streptococcus agalactiae, a flesh eating bacterium, which lead to septicaemia (Presence of bacterium in the blood) in the infected (Bowater et al 2012). This was the first recorded outbreak of S. agalactiae in Australia (Bowater et al 2012) and because it occurred in the wild, there was very little that responders could do besides removing the infected and deceased individuals from the environment. 

In the last 30 years, Streptococcus has been realised as an epidemic, with S. agalactiae being the leading cause of fast spreading infections in new born mammals (Brochet et al 2006). 
Other symptoms aside from skin necrosis and internal bleeding, infected fish can be seen swimming erratically and their eyes appear bulging (Abuseliana et al 2011). 

In an aquaculture or aquarium setting, antibiotics are the only realistic treatment for S. agalactiae when septicaemia is present. S. agalactiae has however evolved a number of resistances to antibiotics with 9 similtaneous antibiotic resistances being seen using PCR tests (Zeng et al 2006).
The first treatment should be a ten day course of the antibiotic Oxy-tetra Cycline (OTC) by either incorporating this into food or dosing the water body. If this treatment doesn't work, it becomes a trial and error process with other antibiotics to see what can irradicate the bacterium from the system.

A deceased Queensland Grouper that died during the Streptococcus outbreak in Cairns

References:

Abuseliana, A. Daud, H. Aziz, S. Bejo, S. Alsaid, M 2011, 'Pathogenicity of Streptococcus agalactiae Isolated from a Fish Farm in Selangor to Juvenile Red Tilapia (Oreochromis sp.)', 'Journal of Animal and Veterinary Advances', vol.10, pp. 914-919

Bowater, R. Forbes-Faulkner, J. Anderson, I. Condon, K. Robinson, B. Kong, F. Gilbert, G. Reynolds, A. Hyland, S. McPherson, G. O'Brien, J. Blyde, D 2012, 'Natural Outbreak of Streptococcus agalactiae (GBS) Infection in Wild Giant Queensland Grouper, Epinephelus lanceolatus (Bloch), and Other Wild Fish in Northern Queensland, Australia', 'Journal of Fish Dieseases', vol. 35, pp. 173-186

Brochet, M. Couve, E. Zouine, M. Vallaeys, T. Rusniok, C. Lamy, M. Buchrieser, C. Trieu-Cuot, P. Kunst, F. Poyart, C. Glaser, P 2006, 'Genomic Diversity and Evolution within the Species Streptococcus agalactiae', 'Microbes and Infection', vol. 8, pp. 1227-1243

Zeng, X. Kong, F. Wang, H. Darbar, A. Gilbert, G 2006, 'Simultaneous Detection of Nine Antibiotic Resistance-Related Genes in Streptococcus agalactiae Using Multiplex PCR and Reverse Line Blot Hybridization Assay', 'Antimicrobial Agents and Chemotherapy', vol. 50, pp. 204-209

Post 2: Bacterial Fin Rot in Aquaculturally Reared Queensland Grouper and Issues Surrounding the Frequent use of Antibiotics

The Queensland Grouper (Epinephelus lanceolatus) is the largest bony fish to reside around coral reefs in the world (Jennings & Lock, 1996). Aqua cultural facilities and aquariums that work in the breeding and rearing of Queensland Grouper for research and/or other purposes sometimes lose fish due to pathogens and parasites. One such pathogen is a disease called Fin Rot, which gets its name from the way it slowly destroys mainly the tail fin (caudal fin) of Grouper and many other fish species and can be caused by either a fungal infection or by a bacterium (Nagasawa & Cruz-Lacierda 2004). In this post, I will be discussing the bacterial fin rot disease which results from a Pseudomonas Fluorescens infection.

Bacterial fin rot affecting the Caudal, Elongated Dorsal and Anal fin

This disease is often associated with poor water quality and dense populations. Poor water quality can increase the stress in cultured grouper which in turn lowers their immune system which makes them more vulnerable to pseodomonas fluorescens (Nagasawa & Cruz-Lacierda, 2004). Queensland Grouper are also cannibalistic and so in dense populations, the larger fish attack the smaller fish and the injuries incurred allow for opportunistic fin rot infections.
Treatment for bacterial fin rot is the simple use of antibiotics, the most commonly used is Oxy-Tetra Cycline (OTC) over a 10 day treatment period (Austin & Austin, 2007). Issues surrounding the frequent use of this however include the bacterium developing an immunity to this. Bacterial resistance for antibiotics has been observed since the 1950's and the two theories surrounding Fin Rot is whether it is the result of bacteria evolving in response to the use of OTC or whether the bacterium already possesses genes which give it immunity (Groisman & Ochman, 1996).
Hopefully with more research, more effective treatments can be found.

References:

Austin, B. Austin, D. 2007, 'Bacterial Fish Pathogens: Disease of Farmed and Wild Fish', 'Springer Science'

Groisman, E. Ochman, H. 1996, 'Pathogenicity Island: Bacterial Evolution in Quantum Leaps', 'Cell', vol. 87, pp. 791-794

Jennings, S. Lock, J. 1996, 'Population and Ecosystem Effects of Reef Fishing', 'Reef Fisheries', vol. 20, pp. 193-218

Nagasawa, K. Cruz-Lacierda, E. 2004, 'Diseases of Cultured Groupers', 'South-East Asian Fisheries Development Centre'

Somga. J, Somga, S. 2002, 'Impacts of Disease on Small-Scale Grouper Culture in the Philippines', 'Primary Aquatic Animal Healthcare', vol. 14, pp. 248-261

Post 1: Betanodavirus-An examination of potential management strategies.

Betanodavirus is a genus of virus that causes a specific strain of a disease called Viral Nervous Necrosis (VNN) in a variety of marine organisms including fin-fish and shellfish (Chi et al, 2008). VNN is a single stranded, RNA virus and is one of the main problems aquaculture facilities face as it can cause mortalities of up to 100% of reared populations and it effects 157 known species worldwide (Chi et al, 2003). VNN is regarded as a very hardy virus, affecting fish in both tropical and temperate environments and  has been known to be able to survive for up to 10 years in soil (Munday et al, 2002).
Because viruses have a high mutation rate and exist within the hosts cells (Gojobori et at, 1990), they are very hard to treat and thus there is no current cure for VNN.
VNN symptoms can be witnessed as the infected organisms exhibit very lethargic behaviour, show a disinterest for food which leads to anorexia and in fin-fish, spiral swimming is a symptom due to a loss of motor function (Arimoto et al, 1996).
VNN outbreaks can be linked to environmental factors such as large salinity and temperature fluctuations and high sediment loads in the water. To reduce outbreaks, especially in an Aquaculture setting, temperature and salinity should be maintained at a level that minimises stress to the fish.
Prevention can also include incorporating ozone into a circulating water system before the water is added into the tank containing fish, as ozone is toxic to pathogens. Also being an unstable molecule, ozone quickly dissipates out of the system and therefore if incorporated in correct doses will not be harmful to the fish.
VNN outbreaks are most common in fish aged between 4-70 days old (Fakuda et al, 2005) and hopefully through further research, Vaccines may be found to prevent this disease when organisms are most susceptible.

References:

Chi, S. Shieh, J. 2003, 'Genetic and Antigenic Analysis of Betanodaviruses Isolated from Aquatic Organisms in Taiwan', 'Diseases of Aquatic Organisms', vol. 7, pp. 238-249

1. Fenner, B. 
2. Thiagarajan, R.
3.  Chua. H, Kwang, J. 2005, '
Betanodavirus B2 Is an RNA Interference Antagonist That Facilitates Intracellular Viral RNA Accumulation', 'Journal of Virology', vol. 80, pp. 85-94

Arimoto, M. Sato, J. Maruyama, K. Mimura, G. Furusawa, I. 1996, 'Effect of Chemical and Physical Treatments on the Inactivation of Striped Jack Nervous Necrosis Virus (SJNNV)', 'Aquaculture', vol 143, pp. 15-22

Chi, C. Lo, B. Lin, S. 2008, 'Characterization of Grouper Nervous Necrosis Virus (GNNV)', 'Fish Diseases', vol. 24, pp. 3-13

Fakuda, Y. Nguyen, H. Furuyashi, M. Nakai, T. 1996, 'Mass Mortality of CUltured Sevenbanded Grouper, Epinephelus Septemifasciatus, Associated with Viral Nervous Necrosis', 'Fish Pathology, vol. 31, pp. 165-170

Munday, B. Kwang, J. Moody, N. 2002, 'Betanodavirus Infections of Teleost Fish', 'Journal of Fish Diseases', vol. 25, pp. 127-142

Gojobori, T. Moriyama, E. Kimura, M. 1990, ' Molecular Clockwork of Viral Evolution and the Neutral Theory', 'Current Issue' vol. 87, pp. 24-32