Veterinary · Para-clinical · also MSVE VPP-322, Fish and Shrimp Health
Diseases of fish and crustaceans, the role of water quality, aquaculture biosecurity, and the residue rules for therapeutants used in food fish.
In the exams: NAVLE aquatics 1%; China runs a separate aquatic-animal category of its national exam
Aquatic animal health is the veterinary medicine of farmed and wild fish, crustaceans (mainly shrimp, prawns and crayfish) and molluscs. Aquaculture now supplies a large share of the fish and shellfish people eat, and most of it comes from Asia: carps and tilapia in ponds, catfish, pangasius, penaeid shrimp, and salmon and trout in cages and tanks. The patient is almost never a single animal. It is a population of thousands or millions living in water that the animals share, breathe, drink or absorb, and excrete into. Most disease on a fish or shrimp farm starts with the water, the stocking density or the handling, and a pathogen finishes the job.
This manual follows the curriculum units: how fish and shrimp bodies work, water quality and the diseases it causes, the viral, bacterial, fungal and parasitic diseases of farmed fish and shrimp, the diseases listed by the World Organisation for Animal Health (WOAH), diagnosis, biosecurity, therapeutants and residues, and the degree-day system used to set withdrawal periods in fish. Welfare and the basic production numbers (stocking density, feed conversion, growth rate) are included because a practitioner is judged on them. Diseases are described at the clinical and diagnostic level. WOAH listing is stated only for diseases whose listed status is certain; the list is revised, so check the current Aquatic Animal Health Code, chapter 1.3, before relying on it.
Worldwide the subject is examined lightly in general licensing exams and heavily in specialist ones. NAVLE gives aquatic species about 1% of its items. China runs a separate aquatic-animal category of its national veterinary exam. In India it is a BVSc course (MSVE VPP-322) and appears in ICAR postgraduate and ASRB papers. No drug doses are given in this manual. Where a calculation needs a concentration, the concentration is the one the prescriber chose, and every real use must be checked against the product label and your national formulary.
Fish are poikilotherms (ectotherms): their body temperature follows the water. Metabolic rate, oxygen demand, immune response, the speed of a pathogen's life cycle and the rate at which drugs are eliminated all rise with temperature, roughly doubling for each 10 °C rise within the tolerated range. This one fact explains seasonal disease patterns, why treatments are repeated at intervals that depend on temperature, and why withdrawal periods in fish are counted in degree-days.
The gill is the main organ of gas exchange, of nitrogen excretion and of ion regulation. Each gill arch carries filaments, and each filament carries thin secondary lamellae where blood and water flow in opposite directions (counter-current exchange), which makes oxygen uptake efficient. Most nitrogenous waste in teleosts leaves as ammonia across the gill, not as urea in the urine. Because the gill epithelium is only a cell or two thick and is in direct contact with the water, it is the first tissue damaged by poor water, irritant chemicals and parasites. Its common response is epithelial hyperplasia and fusion of lamellae, which thickens the diffusion barrier and causes hypoxia even when the water has enough oxygen.
A freshwater teleost is hyperosmotic to its environment. It gains water by osmosis and loses ions, so it drinks little, produces large volumes of dilute urine and actively takes up sodium and chloride through gill ionocytes (chloride cells). A marine teleost is hypo-osmotic to sea water. It loses water, so it drinks sea water, excretes excess sodium and chloride through gill ionocytes, and produces small volumes of urine that carry divalent ions such as magnesium and sulphate. Any skin or gill damage therefore becomes an osmotic crisis: freshwater fish with ulcers lose salts and take on water, which is why a small rise in salinity is used as supportive care in freshwater species. Fish skin is living epithelium with mucus-secreting goblet cells; there is no dead keratinised layer. Handling that removes mucus or scales opens a route for bacteria and oomycetes.
The teleost heart is a single-circuit pump: sinus venosus, atrium, ventricle and an elastic bulbus arteriosus; blood passes the gills before reaching the body. Fish have no bone marrow and no lymph nodes. The anterior (head) kidney is the main haematopoietic and lymphoid organ and also contains interrenal (adrenocortical) and chromaffin tissue, so it is where stress hormones are made. The posterior kidney is mainly excretory. The spleen and thymus complete the lymphoid organs. The head kidney and spleen are the organs sampled for bacteriology and virology in most fish diseases.
The swim bladder (gas bladder) controls buoyancy. In physostomous fish such as salmonids and carp it stays connected to the gut by a pneumatic duct, so the fish gulps or releases air. In physoclistous fish such as many marine perciform species the duct closes, and gas is secreted and resorbed through a gas gland with a counter-current rete mirabile.
Fish immunity has innate and adaptive arms. The main serum antibody of teleosts is a tetrameric IgM, and a mucosal immunoglobulin (IgT, called IgZ in some species) protects skin, gill and gut. Antibody responses are slower and weaker at low temperature, and there is no class switching of the mammalian kind. These facts shape vaccination: fish are vaccinated by injection into the body cavity (often with oil adjuvant, which can cause adhesions and pigmentation), by immersion, or orally, and they are vaccinated when the water is warm enough for a response.
Penaeid shrimp are decapod crustaceans. The body has a cephalothorax covered by a carapace and an abdomen, the part eaten. The exoskeleton of chitin and protein must be shed to grow (moulting, or ecdysis). Just after moulting the new shell is soft, the animal is vulnerable to cannibalism and handling injury, and it needs calcium and other minerals from the water, which is one reason water hardness and alkalinity matter in shrimp ponds. Gills sit in a branchial chamber under the carapace.
Crustaceans have an open circulatory system: the heart pumps haemolymph into sinuses, not a closed set of vessels. The oxygen-carrying pigment is haemocyanin, a copper protein dissolved in the haemolymph, not haemoglobin in red cells. The hepatopancreas (midgut gland) digests, absorbs and stores food and is the target of many shrimp diseases, including acute hepatopancreatic necrosis disease, necrotising hepatopancreatitis and microsporidiosis. Penaeid shrimp have a lymphoid organ that filters haemolymph. Excretion is through the antennal gland. The defence system is entirely innate: haemocytes, clotting, the prophenoloxidase cascade that produces melanin (the black spots seen at wounds), and antimicrobial peptides. Shrimp make no antibodies, so conventional vaccination does not work; disease control rests on pathogen-free stock, exclusion and environment.
Bivalve molluscs filter large volumes of water and concentrate microbes and algal toxins; a few of their parasites, such as Bonamia, Marteilia and Perkinsus, are internationally regulated.
Dissolved oxygen (DO) is the first thing to measure on any farm visit. The amount of oxygen water can hold at saturation falls as temperature and salinity rise. Fresh water at sea-level pressure holds about 9.1 mg/L at 20 °C, 8.3 mg/L at 25 °C and 7.6 mg/L at 30 °C, so warm water holds less oxygen at exactly the time fish need more. Percent saturation is measured DO divided by the saturation value at that temperature and salinity, times 100. Safe minimums depend on species and are quoted differently across texts; cold-water salmonids need more oxygen than warm-water carps, tilapia or catfish, and many texts advise keeping warm-water ponds above about 5 mg/L and treating values below about 3 mg/L as a crisis. Use the species guidance in your region.
In a pond, algae produce oxygen by photosynthesis during the day and every organism in the pond consumes it all the time. DO therefore rises through the day and falls through the night, and is lowest just before dawn. Low DO is most likely at dawn after a hot, still, cloudy day, after an algal bloom collapses (a die-off), after heavy feeding, and when a thermally stratified pond turns over. Signs are fish gasping at the surface (piping), gathering at inflows, and deaths of the largest fish first, because they have the highest total oxygen demand. Response is aeration, water exchange and stopping feeding.
The opposite problem is gas supersaturation. When the total dissolved gas pressure exceeds atmospheric pressure, usually from nitrogen, gas comes out of solution in the fish's blood and tissues. This is gas bubble disease: bubbles in fins, gills and skin, exophthalmia, and emboli. Causes include a leaking pump intake that draws air under pressure, water heated without degassing, groundwater, and water plunging below dams. Treatment is degassing: packed columns, splash aeration, or letting water stand.
Fish excrete ammonia across their gills, and uneaten feed and faeces release more as they decompose. Total ammonia nitrogen (TAN) exists in water as two forms in equilibrium: the un-ionised ammonia molecule NH3, which is lipid-soluble, crosses the gill and is the toxic form, and the ammonium ion NH4+, which is far less toxic. The un-ionised fraction depends mainly on pH and, less strongly, on temperature: fraction = 1 / (1 + 10^(pKa - pH)), where pKa = 0.09018 + 2729.92 / T, with T in kelvin (the Emerson equation). At 25 °C, pKa is about 9.25, and the un-ionised fraction is about 0.56% at pH 7, 5.4% at pH 8 and 36% at pH 9. Each unit of pH rise increases the toxic fraction almost tenfold. That is why a pond with moderate TAN becomes dangerous in the afternoon, when algal photosynthesis removes carbon dioxide and pushes the pH up. Laboratories report either NH3-N (as nitrogen) or NH3; to convert NH3-N to NH3 multiply by 17/14, about 1.22. Always check which basis a limit is written on.
Chronic ammonia exposure causes gill hyperplasia, poor growth and greater susceptibility to infection; acute toxicity causes hyperexcitability, convulsions and death. Nitrifying bacteria in biofilters and pond sediment oxidise ammonia to nitrite (ammonia-oxidising bacteria such as Nitrosomonas) and nitrite to nitrate (nitrite-oxidising bacteria such as Nitrobacter and Nitrospira). A new biofilter takes weeks to establish, so new recirculating systems show an ammonia peak followed by a nitrite peak (new tank syndrome).
Nitrite is actively taken up across the gill by the chloride uptake pathway and oxidises haemoglobin to methaemoglobin, which cannot carry oxygen. The blood turns chocolate brown, the disease called brown blood disease. Because chloride competes with nitrite for uptake, adding salt to raise chloride protects freshwater fish. Nitrate is much less toxic and becomes a concern mainly in recirculation systems with little water exchange.
Carbon dioxide builds up where many fish breathe in little water: transport tanks, intensive recirculating systems and ponds at night. High CO2 lowers blood pH and reduces the blood's ability to load oxygen (the Bohr and Root effects), and chronic exposure is associated with nephrocalcinosis (calcium deposits in the kidney). pH extremes damage gills directly; most farmed fish do best in roughly neutral to mildly alkaline water, and acid water from acid rain or acid-sulphate soils also mobilises aluminium, which precipitates on gills. Alkalinity (mainly bicarbonate and carbonate) buffers pH swings, and hardness (calcium and magnesium) matters for moulting crustaceans. Agricultural lime is used to raise both in acid ponds. Metals such as copper and zinc are far more toxic in soft, low-alkalinity water.
Hydrogen sulphide forms in anaerobic pond bottoms and sediment under cages. Opposite to ammonia, its toxic un-ionised form (H2S) increases as pH falls. Chlorine and chloramine in tap water are lethal to fish and must be removed. Pesticides washed in from farmland are highly toxic to fish and crustaceans.
The diagnostic lesson is simple. When many species or all ages die at once, especially at dawn or after a weather change, suspect the water before a pathogen. Measure DO, temperature, pH, TAN, nitrite and, where relevant, salinity, alkalinity and CO2 at the site and at the time of the problem. A sample carried to a laboratory the next day tells you little about DO or pH.
Diagnosis on a fish or shrimp farm is an investigation of a population and its environment. Take a history: species, source and health status of the stock, date of stocking, recent movements, handling, grading or transport, feed and feeding response, water source, recent weather, treatments given, and the pattern of deaths by day, by pond or tank, and by size. Record water quality at the time of the problem. Then watch the animals before handling them. Flashing (fish rubbing on surfaces), rapid opercular movement, piping at the surface, crowding at the inflow, lethargy at the edges, spiral or whirling swimming, loss of appetite and colour change are all useful signs. In shrimp, look at feeding trays, animals swimming weakly at the pond edge, soft shells, gut fullness and colour of the hepatopancreas.
Sample live, clinically affected animals, not the dead. Dead fish autolyse within hours and secondary bacteria overgrow the primary pathogen. Send water samples with them.
On the farm, the most useful test costs almost nothing: a wet mount. Skin mucus scraped from the flank and fin and a clipped piece of gill filament are placed on a slide with a drop of the animal's own water and examined at low and medium power within minutes. This finds most external parasites (ciliates such as Ichthyophthirius and Trichodina, flagellates such as Ichthyobodo, monogeneans, and crustacean parasites) and shows gill hyperplasia and oomycete hyphae. In shrimp, a squash of the hepatopancreas under the microscope shows tubule condition, lipid droplets and some pathogens.
A systematic necropsy examines the external surface, fins, eyes and gills, then the body cavity, the organs in place, and the organs removed. Record haemorrhage, ulceration, exophthalmia, ascites, pale or swollen kidney and spleen, nodules, and gut content. For bacteriology, sample the posterior or anterior kidney aseptically through the body wall or cavity, because the kidney is heavily vascular and bacteraemia shows there. General media such as tryptone soya agar and blood agar grow most fish pathogens, incubated at about 20 to 25 °C rather than at mammalian body temperature. Some pathogens need special media: Renibacterium salmoninarum grows slowly (weeks) on kidney disease medium, Flavobacterium species need low-nutrient cytophaga-type media, and marine vibrios grow on media with added salt (thiosulphate-citrate-bile salts-sucrose agar is used for Vibrio). Antimicrobial susceptibility testing matters because resistance is common in aquaculture and results change treatment.
For histology, fix small pieces of tissue promptly in 10% neutral buffered formalin, at least ten volumes of fixative to one of tissue. Shrimp are usually fixed whole or in large pieces in Davidson's fixative, injected into the hepatopancreas and body, because the hepatopancreas autolyses in minutes. Histology shows gill lesions, granulomas, the inclusion bodies of shrimp viruses, myxozoan spores and microsporidia, and the tissue response that tells a primary from a secondary pathogen.
Fish viruses are isolated in fish cell lines incubated at temperatures suited to fish, commonly around 15 °C for cold-water viruses. Standard lines include EPC and FHM for spring viraemia of carp and IHN viruses, BF-2 for VHS virus, CHSE-214 for birnaviruses, and ASK cells for infectious salmon anaemia virus. The cytopathic effect is then confirmed by a specific test. Shrimp viruses cannot be grown in any routine continuous cell line, so their diagnosis relies on histology, molecular tests and, rarely, bioassay in susceptible shrimp.
The polymerase chain reaction (PCR), including real-time quantitative PCR, is now the main diagnostic and screening tool for most listed aquatic diseases and for screening broodstock and postlarvae. A positive PCR shows the pathogen's nucleic acid, not disease; interpret it with clinical signs and histology, and remember that a sample may be positive at low level in carriers. Antigen-detection tests (fluorescent antibody tests, ELISA) are used for some bacteria, notably Renibacterium. Serology is used less than in terrestrial animals: fish antibody responses depend on temperature, and shrimp make no antibodies.
The WOAH Manual of Diagnostic Tests for Aquatic Animals sets out the recommended methods for each listed disease and distinguishes tests for surveillance, for presumptive diagnosis and for confirmation. Sample size for surveillance follows the same probability as for terrestrial herds. To be 95% confident of detecting at least one infected animal when prevalence is p, in a large population, n = ln(0.05) / ln(1 - p); for 2% prevalence n is about 149, often rounded to 150 fish, and for 5% about 59.
Viral haemorrhagic septicaemia (VHS) is caused by a novirhabdovirus (family Rhabdoviridae). It is best known in farmed rainbow trout in Europe and occurs at low water temperatures. Clinical forms range from acute, with darkening, exophthalmia, pale gills with petechiae, haemorrhages in muscle and viscera and high mortality, to chronic and nervous forms with abnormal swimming. Genotypes also circulate in many wild marine fish. Infectious haematopoietic necrosis (IHN), also a novirhabdovirus, affects salmonids, especially young fish, originally in western North America and later in Europe and Asia; signs include darkening, abdominal swelling, haemorrhage at fin bases and necrosis of the haematopoietic tissue of the kidney and spleen. Both are listed by WOAH.
Spring viraemia of carp (SVC) is caused by a sprivirus of the Rhabdoviridae. It affects common carp and some other cyprinids in spring, when water warms after winter and the fish's immunity lags behind. Signs are lethargy, darkening, exophthalmia, a swollen abdomen with ascites, petechiae on skin and gills, and a protruding vent. SVC is listed by WOAH.
The lesson common to these diseases is that no treatment exists. Control is by sourcing stock from free zones or compartments, egg disinfection, clean water supply, and eradication by slaughter, disinfection and fallowing where the disease is notifiable.
Koi herpesvirus disease is caused by cyprinid herpesvirus 3 (family Alloherpesviridae). It affects common carp and koi at water temperatures of about 18 to 28 °C and can kill most of a population. The hallmark is severe gill necrosis with patchy white and red gills, together with sunken eyes, pale irregular skin patches and excess or reduced mucus. Survivors can carry the virus latently. It is listed by WOAH. Diagnosis is by PCR, because isolation in carp cell lines is insensitive.
Infectious salmon anaemia (ISA) is caused by an isavirus of the family Orthomyxoviridae. It affects farmed Atlantic salmon in sea water. Affected fish are lethargic with pale gills from severe anaemia; internally there is ascites, a dark congested liver with haemorrhagic necrosis, and a dark swollen spleen. Variants are described by their haemagglutinin-esterase gene: HPR-deleted strains cause disease, and HPR0 strains are found in healthy fish; WOAH lists infection with both. Control relies on single-year-class sites, fallowing, movement controls and, in some countries, vaccination.
Other fish viruses listed by WOAH include salmonid alphavirus, which causes pancreas disease in sea-farmed Atlantic salmon and sleeping disease in rainbow trout, with lesions in the exocrine pancreas, heart and skeletal muscle; red sea bream iridoviral disease, caused by a megalocytivirus in many marine species in Asia; and epizootic haematopoietic necrosis, caused by a ranavirus in redfin perch and rainbow trout in Australia.
The following viruses are important, but their listed status is not stated here; check the current WOAH list. Infectious pancreatic necrosis is caused by an aquabirnavirus (family Birnaviridae). It kills salmonid fry and first-feeding fingerlings and post-smolts shortly after transfer to sea; affected fish spin, darken and have a distended abdomen, and the gut contains a clear or whitish mucus. Survivors can become lifelong carriers, and the virus can be transmitted with eggs.
Viral nervous necrosis (viral encephalopathy and retinopathy) is caused by betanodaviruses (family Nodaviridae) and kills larvae and juveniles of many marine species, including sea bass and groupers. The fish swim abnormally, spinning or floating belly-up, because the virus causes vacuolation of the brain and retina. Tilapia lake virus, an orthomyxo-like virus first described in the 2010s, causes high mortality in farmed tilapia in several continents.
White spot disease is caused by white spot syndrome virus (WSSV), a large enveloped double-stranded DNA virus of the family Nimaviridae. It has an unusually wide host range among decapod crustaceans, including all farmed penaeids, crabs, crayfish and lobsters, and it is carried by many wild crustaceans. It is the most economically damaging shrimp disease worldwide. In farmed penaeids, a pond can go from first signs to near total mortality in three to ten days. Affected shrimp stop feeding, gather at the pond edge, and may show white spots, about 0.5 to 2 mm across, on the inner surface of the carapace, together with a pink or reddish discoloration. White spots are not specific: bacterial infection and high alkalinity can cause similar deposits, so confirmation is by PCR and by histology, which shows large intranuclear inclusion bodies in tissues of ectodermal and mesodermal origin. Outbreaks are linked to sudden changes in water temperature and to stress. It is listed by WOAH.
Yellow head disease is caused by yellow head virus genotype 1, an okavirus (family Roniviridae), a positive-sense RNA virus. It affects Penaeus monodon and other penaeids, mainly in Asia. Shrimp feed heavily and then stop, and the cephalothorax becomes yellowish because the hepatopancreas and gills are pale-yellow. Deaths follow within days. It is listed by WOAH, as infection with yellow head virus genotype 1.
Taura syndrome, caused by Taura syndrome virus (family Dicistroviridae), was first seen in Pacific white shrimp (Penaeus vannamei) in Ecuador. Acute cases have a reddish tail fan and soft shell and die during moulting; survivors show multiple irregular melanised (black) lesions in the cuticle, the healing stage. Infectious hypodermal and haematopoietic necrosis virus (IHHNV) causes high mortality in P. stylirostris and, in P. vannamei, runt-deformity syndrome: a bent or deformed rostrum, wrinkled antennae, and very uneven size in a pond, which cuts value more than it kills. Infectious myonecrosis, caused by a totivirus-like virus, produces white, opaque necrotic areas in the skeletal muscle of the abdomen and tail of P. vannamei, with a prolonged moderate mortality. White tail disease of the giant freshwater prawn Macrobrachium rosenbergii is caused by Macrobrachium rosenbergii nodavirus (with an associated extra small virus); larvae and postlarvae turn milky-white in the tail and die. Taura syndrome, IHHNV, infectious myonecrosis and white tail disease (as infection with Macrobrachium rosenbergii nodavirus) are all WOAH-listed.
These diseases changed the industry. They drove the move from wild-caught broodstock to domesticated lines certified as specific-pathogen-free (SPF), meaning free of named pathogens under a defined surveillance programme, and to lines selected as specific-pathogen-resistant (SPR). SPF is a statement about pathogen status, not resistance: an SPF shrimp can still become infected if it meets the pathogen in the pond.
Because shrimp have no adaptive immunity and no antiviral drugs exist, control is by exclusion and by keeping the environment within the animal's tolerance. The key steps are well established. Buy postlarvae from SPF broodstock and screen batches by PCR before stocking. Prepare ponds by drying and liming, and filter or disinfect intake water to remove crustacean carriers; many farms settle and chlorinate water in reservoir ponds and let the chlorine dissipate before use. Build crab fences and bird netting, because crabs and birds move WSSV between ponds. Avoid sudden changes of temperature and salinity, keep stocking densities matched to aeration and water exchange, and do not share equipment between ponds.
Recall the families for examinations: WSSV, Nimaviridae; yellow head virus, Roniviridae; Taura syndrome virus, Dicistroviridae; IHHNV, Parvoviridae (a densovirus); Macrobrachium rosenbergii nodavirus, Nodaviridae.
Furunculosis is caused by Aeromonas salmonicida subsp. salmonicida, a Gram-negative, non-motile rod. It is a classical disease of salmonids in fresh and sea water. The acute form is a septicaemia with haemorrhage at fin bases and in viscera; the subacute and chronic forms produce furuncles, raised swellings in the muscle that burst to leave deep ulcers. Carrier fish are a major source. Oil-adjuvanted injectable vaccines transformed antimicrobial use in salmon farming. Motile aeromonads, especially Aeromonas hydrophila, are opportunists present in almost all fresh water. They cause motile aeromonad septicaemia, with haemorrhage, ulcers and dropsy, when fish are stressed by handling, crowding, poor water or high temperature, so the environment must be corrected along with any treatment.
Enteric redmouth disease, caused by Yersinia ruckeri (Enterobacteriaceae), is a septicaemia of salmonids, especially rainbow trout, with subcutaneous haemorrhage around the mouth and throat. Immersion vaccination has been used against it for decades.
Flavobacteria are Gram-negative, long, thin rods that move by gliding. Flavobacterium columnare causes columnaris disease in warm fresh water: greyish-white patches on skin, often a saddle-shaped lesion across the back, fin erosion, and gill necrosis. On a wet mount the bacteria gather into columns or haystacks. Flavobacterium psychrophilum causes bacterial cold-water disease and rainbow trout fry syndrome, with erosion of the caudal peduncle and anaemia in young salmonids. Flavobacterium branchiophilum causes bacterial gill disease, where bacteria cover the gill surface in crowded hatcheries with poor water. In sea water, Tenacibaculum maritimum produces similar erosive lesions.
Vibriosis is caused by halophilic Gram-negative curved rods. Vibrio anguillarum (also named Listonella anguillarum) causes haemorrhagic septicaemia in many marine and brackish species. Aliivibrio salmonicida causes cold-water vibriosis (Hitra disease) of Atlantic salmon. Photobacterium damselae subsp. piscicida causes photobacteriosis (formerly pasteurellosis or pseudotuberculosis), with small white nodules in the spleen and kidney of marine fish.
Bacterial kidney disease (BKD), caused by Renibacterium salmoninarum, a small Gram-positive rod often seen in pairs, is a chronic granulomatous disease of salmonids. The kidney is swollen with greyish-white nodules; deaths are slow and persistent. It is transmitted horizontally and also vertically, inside the egg, so egg surface disinfection cannot stop it; control relies on screening broodstock (by ELISA or fluorescent antibody test and PCR) and culling positive females' eggs. The organism grows very slowly in culture.
Streptococcus iniae and Streptococcus agalactiae are Gram-positive cocci that cause meningoencephalitis and septicaemia in warm-water fish, notably tilapia: erratic spiral swimming, exophthalmia and corneal opacity. S. iniae has caused infections in people handling fresh fish. Edwardsiella ictaluri causes enteric septicaemia of catfish, including a chronic 'hole-in-the-head' lesion on the frontal bone; Edwardsiella tarda affects many species. Piscirickettsia salmonis is an intracellular bacterium causing piscirickettsiosis, a major disease of farmed salmon in Chile. Mycobacterium marinum and related species cause chronic granulomas in many fish and a skin granuloma ('fish tank granuloma') in people who handle fish or aquaria; it is an important zoonosis.
Acute hepatopancreatic necrosis disease (AHPND), earlier called early mortality syndrome, is caused by strains of Vibrio parahaemolyticus, and some other vibrios, that carry a plasmid encoding the binary toxins PirA and PirB. It strikes P. vannamei and P. monodon within the first weeks after stocking, commonly in the first 35 days. The hepatopancreas becomes pale and shrunken, and histology shows massive sloughing of tubule epithelial cells without bacteria in the early phase, followed by heavy bacterial colonisation. Diagnosis is by histology and PCR for the toxin genes. It is WOAH-listed.
Necrotising hepatopancreatitis is caused by Hepatobacter penaei, an intracellular alpha-proteobacterium. It causes chronic disease in P. vannamei, with a pale, atrophied hepatopancreas, soft shell and poor growth, often in water that is warm and saline. It is WOAH-listed.
Luminous vibriosis, caused mainly by Vibrio harveyi and related species, kills larvae in hatcheries; affected larvae glow in the dark. Many other vibrio infections are secondary to poor water, injury and stress.
Most of the 'fungal' diseases of fish are caused by oomycetes, the water moulds. Oomycetes look like fungi, with branching aseptate hyphae, but they are not true fungi: they belong to the Stramenopiles, their cell walls contain cellulose rather than chitin, and they respond differently to some drugs. Saprolegnia and related genera are everywhere in fresh water. They are mainly opportunists that colonise damaged skin, dead eggs, or fish whose immunity is suppressed by low temperature, spawning or handling. The lesion is a cotton-wool-like white, grey or brown mat on skin, fins, gills or eggs; underneath, hyphae invade the epidermis and dermis, and death follows from osmotic failure. In hatcheries Saprolegnia spreads from dead eggs to healthy ones, so dead eggs are removed and eggs are treated during incubation with a chemical authorised for that purpose in the country.
Malachite green was once the standard treatment for oomycetes and external parasites. It is no longer permitted for food fish in the European Union, the United States, India and many other countries, because it and its metabolite leucomalachite green persist in tissue and are considered carcinogenic and genotoxic; residue monitoring still finds it. Prevention of saprolegniasis is careful handling, good water quality, removal of dead eggs and fish, and avoiding crowding.
Epizootic ulcerative syndrome (EUS), also called red spot disease or mycotic granulomatosis, is caused by the oomycete Aphanomyces invadans. It affects many freshwater and estuarine species, particularly snakeheads, barbs, gouramis and mullets, across South and Southeast Asia, Australia, parts of Africa and North America. Common carp, tilapia and milkfish are regarded as resistant. Outbreaks typically follow a fall in water temperature and heavy rain. Early lesions are red spots; later, deep ulcers expose the muscle. Histology shows invasive hyphae surrounded by granulomas, the diagnostic lesion, and the pathogen can be confirmed by PCR. The disease is listed by WOAH as infection with Aphanomyces invadans. A related oomycete, Aphanomyces astaci, causes crayfish plague, which has devastated native European crayfish after introduction with resistant North American crayfish; it too is WOAH-listed.
Branchiomycosis, gill rot, is caused by Branchiomyces species (true fungi) in warm water rich in organic matter, typically ponds with algal blooms and high feeding. The hyphae grow inside gill blood vessels and cause thrombosis and ischaemic necrosis, so the gills look marbled with red and white areas. Correcting the water is the main measure.
Ichthyophonus hoferi is a mesomycetozoean, a protist related to fungi and animals. It infects many marine and some freshwater fish, often through eating infected fish, and produces white nodules and granulomas in heart, kidney, liver, spleen and muscle; heavily infected skin feels rough like sandpaper. There is no treatment. Feeding raw marine fish products is a recognised route in farmed fish.
In shrimp hatcheries, oomycetes such as Lagenidium and Haliphthoros cause larval mycosis, with hyphae filling the larvae and rapid death; hygiene of broodstock, eggs and water is the control. In grow-out, Fusarium species (true fungi) invade damaged cuticle and gills and cause black gill lesions and melanised nodules in penaeids and lobsters.
Ichthyophthirius multifiliis, the cause of white spot disease (ich), is a large ciliate of freshwater fish worldwide. Its life cycle explains its treatment. The feeding stage, the trophont, lives under the skin and gill epithelium and appears as white spots up to about 1 mm; there it is protected from chemicals in the water. The mature trophont leaves the fish, settles and encysts as a tomont, which divides into hundreds of tomites. These are released as free-swimming infective theronts that must find a fish within a short time. Only the free-swimming stages can be killed by bath treatments. The cycle is faster in warm water and slower in cold, so treatments must be repeated at intervals that cover the whole period during which theronts emerge, and the interval depends on temperature. Heavy gill infection kills by asphyxia and osmotic failure. The marine counterpart is Cryptocaryon irritans, with a similar cycle.
Other ciliates include Trichodina, a saucer-shaped ciliate with a ring of denticles that is common in small numbers and harmful in large numbers on stressed fish, and Chilodonella, which damages gills and skin. The flagellate Ichthyobodo (formerly Costia) is tiny and hard to see; it causes a bluish-grey film on skin. Amyloodinium ocellatum, a dinoflagellate, causes marine velvet disease with rapid mortality from gill damage; Piscinoodinium is the freshwater equivalent. Sessile ciliates such as Epistylis and, in shrimp, Zoothamnium attach to the surface; in shrimp, heavy fouling on gills indicates high organic load and causes hypoxia at moult.
Monogeneans are flatworms with a direct life cycle and a posterior attachment organ (haptor) armed with hooks. Dactylogyrus lives mainly on gills, lays eggs and has eyespots; Gyrodactylus lives mainly on skin and fins, has no eyespots and gives birth to live young that already contain an embryo (it is viviparous, the 'Russian doll' arrangement), so numbers can build up very quickly. Gyrodactylus salaris killed large numbers of wild Atlantic salmon parr in Norwegian rivers after introduction and is WOAH-listed.
Digeneans have indirect life cycles with a snail as the first intermediate host. Fish usually carry the metacercariae. Diplostomum species, the eye flukes, lodge in the lens and cause cataract and blindness; the final hosts are fish-eating birds. Black spot disease is caused by metacercariae surrounded by melanin in the skin. Several fish-borne trematodes are zoonotic: Clonorchis sinensis and Opisthorchis species in freshwater cyprinids in Asia infect people who eat raw or undercooked fish and cause bile-duct disease and cholangiocarcinoma.
Cestodes include Ligula intestinalis, whose plerocercoids fill the body cavity, and Diphyllobothrium species, whose plerocercoids in fish muscle infect people. Among nematodes, the larvae of Anisakis and related genera in marine fish cause anisakiasis in people who eat raw fish; freezing kills them, and national rules on freezing temperature and time differ between the EU and the USA.
Myxozoans are microscopic cnidarian parasites with spores bearing polar capsules. Many need an invertebrate host. Myxobolus cerebralis causes whirling disease in young salmonids: the parasite damages cartilage of the skull and spine, so fish swim in circles, have black tails and develop skeletal deformity. Its alternate host is the oligochaete worm Tubifex tubifex, which releases triactinomyxon spores that infect fish. Tetracapsuloides bryosalmonae causes proliferative kidney disease (PKD) in salmonids, with a swollen grey kidney, anaemia and mortality in warm summers; its invertebrate host is a freshwater bryozoan.
Parasitic crustaceans include Argulus, the fish louse, a flattened branchiuran that moves freely over the skin and feeds with a preoral stylet, causing wounds; Lernaea, the anchor worm, a copepod whose females embed their heads in the muscle; Ergasilus, a gill copepod; and the sea lice of salmon farming, Lepeophtheirus salmonis and Caligus species. Sea lice feed on skin, mucus and blood and cause erosions, osmotic stress and secondary infection. They are controlled by fallowing and single-year-class stocking, medicines (with widespread resistance), non-medicinal methods such as warm-water or mechanical delousing, and cleaner fish such as wrasse and lumpfish, each of which raises welfare concerns. Amoebic gill disease, caused by Neoparamoeba perurans, produces white mucoid gill patches in sea-farmed salmon and is managed with freshwater baths.
In shrimp, the microsporidian Enterocytozoon hepatopenaei (EHP) infects the hepatopancreas and causes hepatopancreatic microsporidiosis: shrimp do not die in large numbers but grow slowly and unevenly. It is spread by cannibalism and in pond sediment, and spores are hard to kill, so pond preparation and screening of broodstock matter.
The World Organisation for Animal Health publishes the Aquatic Animal Health Code, which sets standards for safe international trade in aquatic animals and their products, and the Manual of Diagnostic Tests for Aquatic Animals. Chapter 1.3 of the Code lists diseases of fish, molluscs, crustaceans and amphibians. A disease is listed when it meets criteria about international spread, significant impact on production or wild populations or human health, a defined cause and a reliable diagnostic test. Member countries must notify WOAH, through the World Animal Health Information System (WAHIS), of the first occurrence or reoccurrence of a listed disease in a country, zone or compartment, and report its status regularly. Listing does not mean the disease is zoonotic; almost none of the listed aquatic diseases are.
Listed diseases of fish include epizootic haematopoietic necrosis, infection with Aphanomyces invadans (epizootic ulcerative syndrome), infection with Gyrodactylus salaris, infection with infectious salmon anaemia virus, infection with salmonid alphavirus, infectious haematopoietic necrosis, koi herpesvirus disease, red sea bream iridoviral disease, spring viraemia of carp and viral haemorrhagic septicaemia. Listed diseases of crustaceans include acute hepatopancreatic necrosis disease, infection with Aphanomyces astaci (crayfish plague), infection with Hepatobacter penaei (necrotising hepatopancreatitis), infection with infectious hypodermal and haematopoietic necrosis virus, infection with infectious myonecrosis virus, infection with Macrobrachium rosenbergii nodavirus (white tail disease), infection with Taura syndrome virus, infection with white spot syndrome virus and infection with yellow head virus genotype 1. Mollusc diseases on the list include infection with Bonamia ostreae, Marteilia refringens and Perkinsus marinus. The list is revised by the World Assembly of Delegates, and diseases are added and removed, so this is not a complete or permanent list. National lists add diseases of local concern; India's schedule under its 2009 animal diseases act, for example, includes fish, mollusc and crustacean diseases.
Biosecurity is the set of measures that keep pathogens out of a farm (bio-exclusion), stop their spread within it, and stop them leaving it (bio-containment). The main routes of entry are live animals and eggs, water, equipment and vehicles, people, feed (especially fresh or raw fish feed), wild animals and birds, and dead animals.
The most important single measure is the health status of what you stock. Buy eggs, fry, postlarvae or broodstock from sources with documented freedom from listed and locally important pathogens, preferably from a free country, zone or compartment as defined in the WOAH Code, or SPF stock for shrimp. Quarantine new animals away from the main stock and test them. Disinfect the surface of fish eggs, usually with an iodophor, while remembering that surface disinfection does not remove pathogens carried inside the egg, such as Renibacterium.
Water can be protected by using groundwater or treated water: settling reservoirs, screening and filtration to remove intermediate hosts and carriers, and ultraviolet light or ozone to kill pathogens. Within the farm, work from the youngest and cleanest stock to the oldest, keep separate equipment and footbaths for each unit, remove dead animals every day and dispose of them safely by ensiling, rendering or burial according to local rules, and keep records. All-in, all-out stocking with a fallow period between cycles breaks the cycle of pathogens and parasites; in salmon farming, single-year-class sites and synchronised fallowing across an area are standard tools against ISA and sea lice.
Vaccination is also a biosecurity tool: injectable and immersion vaccines against furunculosis, vibriosis, enteric redmouth and several viral diseases have sharply reduced antimicrobial use where applied.
The WOAH Code allows a country to declare freedom from a listed disease for the whole country, for a zone (an area defined geographically, such as a river catchment) or for a compartment (one or more establishments under a common biosecurity management system, independent of geography). Freedom is based on surveillance of defined design and sample size, historical absence with basic biosecurity conditions, or absence of susceptible species. Trading partners may require that live aquatic animals come from free countries, zones or compartments, backed by an international aquatic animal health certificate.
When a listed disease is suspected on a farm, the veterinarian's duty is to restrict movement of animals, water and equipment, collect the right samples for the national reference laboratory, and notify the competent authority as national law requires. Control options depend on the disease and the policy: stamping out with disinfection and fallowing, containment and vaccination, or living with an endemic disease through management.
A therapeutant is any chemical used to treat or prevent disease in aquatic animals: antimicrobials, antiparasitic drugs, disinfectants, anaesthetics and some general chemicals. Few medicines are authorised for aquatic species, and the list differs greatly between countries. Many countries allow veterinarians to use unauthorised medicines under strict rules (the 'cascade' in the EU and UK, extra-label drug use in the USA, where extra-label use in medicated feed is not permitted). Before treating, answer four questions: what is the diagnosis, is the cause environmental and correctable, is there a legal product for this species and use, and what will the treatment do to residues, the environment and resistance?
Routes of administration are oral (in medicated feed), bath (immersion), injection and topical. Oral medication is the only practical route for systemic antimicrobial treatment of a large population, but sick fish eat little, so the fish that most need treatment take in the least drug; treat early, and check feeding response. Bath treatments suit external parasites and some external bacterial infections. The kinds of bath are the dip (a high concentration for seconds to minutes), the short bath (up to about an hour), the prolonged or indefinite bath (low concentration left in the system) and the flush (a dose added at the inflow of a raceway and allowed to pass through).
The arithmetic of a bath is simple and errors kill fish. The mass of active ingredient needed is the concentration multiplied by the volume: 1 mg/L equals 1 g per cubic metre (1,000 L). A 10 m3 tank to be treated at a prescribed 25 mg/L of active ingredient needs 250 g of active ingredient. If the product is 20% active, divide by 0.2. Measure the volume; a circular tank holds pi × radius² × depth. Aerate during bath treatment, watch the fish throughout, and have fresh water ready to flush. The concentration itself must come from the product label or a formulary valid in your country — confirm against the product label and your national formulary. Toxicity of many chemicals changes with water chemistry: copper is more toxic in soft, low-alkalinity water, formalin removes dissolved oxygen from the water and is more dangerous in warm water, and potassium permanganate is consumed by organic matter, so its effective dose depends on the water.
Fish and shrimp are food, so drugs used in them are regulated by maximum residue limits (MRLs) set nationally and internationally (Codex Alimentarius). In the EU, the MRL for finfish applies to muscle and skin in natural proportions. Some substances are prohibited in food-producing animals in many countries because no safe residue level can be set: chloramphenicol and nitrofurans are prohibited in the EU and the USA and appear on India's list of substances prohibited in food-animal production, and malachite green is not permitted for food fish in these jurisdictions. Border residue checks by importing countries regularly detect these substances in farmed shrimp and fish, so residues are also a trade problem.
Antimicrobial resistance is a particular concern in aquaculture. Medicated feed that is not eaten falls to the sediment, where drug residues persist and select for resistant bacteria; resistance genes on plasmids move between aquatic bacteria and can reach human pathogens. Colistin has been banned for use in food animals and aquaculture in India. The international direction is prudent use: diagnosis before treatment, susceptibility testing, the narrowest effective drug, correct dose and duration, no routine prophylaxis, and investment in vaccines, stock quality and husbandry instead.
Fish anaesthetics include tricaine methanesulfonate, benzocaine and eugenol-based products; availability and withdrawal rules vary by country. Tricaine methanesulfonate acidifies soft water and is usually buffered with sodium bicarbonate.
Because fish and crustaceans are poikilotherms, they metabolise and excrete drugs faster in warm water and slower in cold water. A withdrawal period fixed in days would be too short in winter and wasteful in summer. Withdrawal periods for fish are therefore commonly expressed in degree-days: the sum of the mean daily water temperatures, in °C, over the withdrawal period. A withdrawal of 500 degree-days is met in 50 days at a constant 10 °C, in 40 days at 12.5 °C, and in 62.5 days (in practice 63 days) at 8 °C. When temperature varies, add up the daily mean temperatures until the total reaches the requirement.
When a veterinarian prescribes a medicine off-label for fish under the European Union's rules (Regulation (EU) 2019/6, Article 115), the minimum withdrawal period is set by formula unless the product already states one for the species. The main rules are: if the product is authorised for any aquatic species, the longest withdrawal for an aquatic species on the product information multiplied by 1.5, expressed in degree-days; if it is authorised only for food-producing terrestrial animals, the longest withdrawal period in days for any food-producing species multiplied by 50, expressed as degree-days, but not exceeding 500 degree-days; if it is not authorised for any food-producing species, 500 degree-days; and if the highest withdrawal for any species is zero, 25 degree-days. The UK cascade uses a similar scheme; check the current national guidance. Other countries use different systems, and in some the rule is set by the regulator case by case.
Worked example: a product authorised only for cattle and sheep has a longest meat withdrawal of 7 days. Under the EU rule the fish withdrawal is 7 × 50 = 350 degree-days, below the 500 cap. At a mean water temperature of 14 °C the fish may not be harvested for food for 350 / 14 = 25 days. If the longest terrestrial withdrawal were 28 days, 28 × 50 = 1,400 degree-days would be capped at 500 degree-days.
There is now broad scientific agreement that fish can experience pain and stress, and that decapod crustaceans may do so as well; the United Kingdom, for example, recognised decapod crustaceans as sentient in law in 2022. The WOAH Aquatic Code includes welfare standards for farmed fish covering transport, stunning and killing for human consumption, and killing for disease control. Welfare is judged at farm level by operational welfare indicators: mortality, behaviour (swimming, appetite, response to people), body condition, fin damage and fin erosion, skin lesions, eye damage, gill condition, deformities, and water quality.
The main welfare risks come from husbandry. Crowding, poor water, handling, grading, transport, delousing and slaughter all stress fish. Feed is usually withheld for a period before handling, transport and slaughter so the gut is empty and oxygen demand is lower; the period depends on species and temperature. At slaughter, a humane method makes the fish unconscious immediately or without avoidable suffering, and keeps it unconscious until death. Correctly applied percussive and electrical stunning meet this aim. Methods such as asphyxiation in air, live chilling on ice or in ice slurry for many species, and carbon dioxide stunning are widely regarded as causing poor welfare and are being phased out in several countries. In shrimp broodstock, unilateral eyestalk ablation to induce maturation is a recognised welfare concern, and hatcheries are moving to alternatives. Cleaner fish used against sea lice also need welfare provision, including shelter and feed.
Stocking density in tanks and cages is expressed as biomass per volume, in kilograms per cubic metre; in ponds it is usually expressed as number or biomass per unit area, for example postlarvae per square metre in shrimp farming. Density = total weight of fish ÷ volume of water. A circular tank 6 m in diameter and 1.2 m deep holds pi × 3² × 1.2, about 33.9 m3; 2,500 fish of 0.4 kg (1,000 kg) in it are stocked at about 29.5 kg/m3. Stocking a 1-hectare pond (10,000 m2) at 40 postlarvae per m2 needs 400,000 postlarvae. Density alone is a poor welfare indicator: the same density may be acceptable with good water flow and oxygen and harmful without them, and species differ. Water exchange rate is the flow divided by the volume: a 30 m3 tank supplied with 10 L/s (0.01 m3/s) exchanges its volume every 3,000 s, or 50 minutes, about 29 times a day.
Feed conversion ratio (FCR) is the weight of feed given divided by the weight gained. If 1,500 kg of feed raises the biomass of a cage from 200 kg to 1,400 kg, the FCR is 1,500 / 1,200 = 1.25. An economic FCR uses the harvested gain; a biological FCR adds back the weight of fish that died, so it is lower. A rising FCR is an early sign of disease, poor water, overfeeding or loss of stock. Specific growth rate (SGR), percent per day, is 100 × (ln final weight − ln initial weight) ÷ days: fish growing from 50 g to 250 g in 100 days have an SGR of about 1.61% per day. Survival is the number harvested divided by the number stocked: 280,000 shrimp from 400,000 postlarvae is 70% survival.
These numbers are also biosecurity and health numbers. Density, feeding rate and biomass determine oxygen demand and ammonia production, so a farm that pushes density beyond what its aeration and water exchange support will have water-quality disease, and then infectious disease, whatever medicines it uses.
Learn the water chemistry first; it answers a large share of exam questions and most real cases. Be able to calculate the un-ionised ammonia fraction, percent oxygen saturation, a bath treatment mass and a degree-day withdrawal without a formula sheet. Memorise the WOAH-listed fish and crustacean diseases with their agents and families, the ich life cycle, the monogenean differences, the oomycete-versus-fungus distinction, and the banned residues. In practical classes, make wet mounts of skin and gill until you can recognise Ichthyophthirius, Trichodina, Ichthyobodo, Dactylogyrus and Gyrodactylus quickly.
A five-year practitioner on fish or shrimp farms is judged on speed and on getting the order right. Carry a DO meter, pH and ammonia kits, a thermometer and a microscope. On a mortality call, measure water, then wet-mount, then sample moribund animals into the right fixatives. Decide quickly whether the problem is environmental. Know which diseases are notifiable in your country and when to stop movements. Before any treatment, check the legal status of the product for that species, calculate volume and biomass from measurements, confirm the concentration against the product label and your national formulary, and record the degree-day withdrawal.
A senior veterinarian with 25 years' experience designs health programmes for companies and regions: stock sourcing and SPF certification, vaccination plans, area-based fallowing, sea lice or white spot strategies, biosecurity audits, surveillance with defensible sample sizes, and residue monitoring for export markets. They advise regulators on zoning and compartments, write contingency plans for listed diseases, represent industry in trade disputes over residues, and set company policy on antimicrobial use and welfare at slaughter. They also mentor field staff to recognise when a water problem is being mistaken for an infection.
A PhD scientist with 25 years' experience works on the open questions: host-pathogen interaction in poikilotherms, mucosal immunity and vaccine design for fish, the absence of adaptive immunity in shrimp and what can replace vaccination, the ecology of pathogen spread between farms and wild stocks, resistance of sea lice and bacteria to treatments, residue kinetics as a function of temperature, genetic selection for disease resistance, and welfare science including sentience and humane slaughter. They contribute to WOAH expert groups and to reference laboratories that validate diagnostic tests.
Drug doses, bath concentrations and treatment durations are deliberately not given; every concentration used in a calculation is the prescriber's, and must be confirmed against the product label and your national formulary. The WOAH list is given only for diseases whose listed status the writer is certain of; some recently added or reviewed diseases (for example tilapia lake virus, decapod iridescent virus 1 and hepatopancreatic microsporidiosis caused by EHP) are described without a statement of listed status, and infectious pancreatic necrosis and viral nervous necrosis are described without claiming they are listed. Safe limits for dissolved oxygen, ammonia, nitrite and CO2 are species-specific and are quoted only as commonly taught ranges. Mollusc diseases, amphibian diseases (chytrids, ranaviruses), ornamental fish medicine, fish nutrition diseases, harmful algal species, the full list of national notifiable diseases and country-by-country authorised product lists are covered only in outline or not at all. The UK and other non-EU withdrawal rules for fish are described only as similar to the EU rule; check current national guidance.
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