Aquatics Flashcards
Describe the APVMA, and its purpose ?
APVMA = Australian pesticides and veterinary medicines authority
- no antibiotics are registered for use in Australia
- two are typically used but under minor use permits
- Sates and territories have their own regulations
- many veterinary chemical products are registered for use in companion animals. Most contain products which are banned for use in food producing farmed species
formalin, various antibiotics, anthelmintics and organophosphates
Where would you go to get Veterinary information on how to dispose of dead fish from a nationally significant aquatic disease ?
National investigation and reporting protocols for fish kills.
- fisheries authorities
- Local government council and environmental agencies
-
What is the difference between circling and whirling ?
What is flashing piping in fish ?
Definitions
Circling = controlled blindness ?
Whirling = ‘corkscrew’ uncontrolled neurological disease
Flashing = itchy rubbing against objects / ectoparasites
Pipping = Gulping for air, oxygen poor water, gill disease or anaemia
What can lateral or bilateral exophthalmia suggest in a fish ?
Exophthalmia = protrusion of one or both eyes
It is a common finding of septicaemia, but may also indicate gas disturbances. (high partial pressure of nitrogen).
Discuss how you would take a history for farmed fish ?
Collecting a farmed fish history
Observe before intervening or handling fishthe
1. Affected fish population
2. The cohorts present
3. Environmental conditions
4. The type of containment and the time since establishment
5. Records
- recent introductions
- water and environmental data
- management data
6. Details of specimens submitted and analysis requested
Discuss how you would take the history of a wild fish cull?
Wild fish cull
Sudden death difficult to determine initially whether environmental factors, infectious disease or toxicity is the agent
- history is critical
- submit fish samples and a variety of water samples
- all relevant authorities must be informed
Collect
1. estimate of number
2. Types of fish, one species ?
3. The area covered
4. Range of decomposition
5. water data
6. environmental data
7. weather conditions on the day
Only collect moribund fish - dead fish are far to decomposed
- require many water samples, oxygen, salinity, hardness and PH
- fill water samples to overflowing
Contact the testing laboratory prior to testing sampling methods differ and containers may require pretreatment.
How would you recommend taking algae samples ?
Algal blooms
Algal blooms tend to concentrate at different depths in the water so collect from varying depths
Quantitative = estimate number of algal cells per litre
Qualitative = strain through a net to identify the algal species
Describe how you would calculate the condition factor ?
What is the purpose of the aquatic manual and aquatic code ?
Aquatic code
Aquatic manual
Used in International trade as the main source of standards
- official diagnostic methods
- declaring freedom from disease
What tissues would you target for viral, bacterial or histopathology ?
What tissues to sample
Typically samples from 5-10 clinically diseased fish
Viruses
- appropriate organs are the anterior mid kidney, spleen, liver and heart or encephalon
- fry remove the yolk sac
Bacteria
- kidney, brain or eye
Histopathology
- Formalin migrates about <0.5cm an hour sample may be fixed whole
- fixatives will not penetrate rapidly into larger fish with abdominal diameter >0.5cm
- fish <10cm may be fixed whole with abdominal flap and gill cover removed to ensure penetration
- preferable deflate the swim bladder to ensure penetration of the kidney
- samples should be no thicker than 1cm in two dimension
In
- larger fish it is more practical to select tissue samples
- target visible lesions plus general organs and tissues.
- gills, skin, liver, kidney, brain and eye
1:10 parts tissue : fixative
What bacteriology culture is a good all round media for fresh water / marine sites ?
What notifiable disease would you need to rule out after sighting a red ulcer on the side of a fish ?
epizootic ulcerative syndrome EUS
a reportable fungal disease of International concern
WOAH and Australian notifiable disease
Describe the three kidney in fish and how the different parts function ?
Fish kidney
The fish kidney has both immunological and acts alike to mammalian bone marrow
Head kidney / Pronephros
Corticosteroids and major site of antibody production
- haemopoetic functions and aglomerular
- highest concentration of B lymphoid cells
- principle immune organ responsible for processing and formation of IgM and immune memory through melanomacrophage centres (MMC)/
- also acts as an important endocrine organ
Homologous to mammalian adrenal glands = releasing corticosteroids and other hormones
Capsulcles of Stannius
Posterior kidney
- both renal and immune tissues
- huge variation with some species not having glomeruli
What is the major secondary immune organ in fish ?
What organ produces T lymphocytes in fish ?
The spleen
Major secondary immune organ
- abundant antibody production IgM and mature B cells
The spleen plays a major role in antigen trapping and presentation.
- clearance of blood born antigens and immune complexes
- initiation of the adaptive immune response
The organ which produces T lymphocytes in fish
Thymus
- stimulates phagocytosis and antibody production by B cells
Describe the principles of fish vaccination ?
The principles of fish vaccination
1. Only vaccinate healthy fish
2. No food 24-48 hours prior to the vaccine
3. Disease free environment during the vaccination period
4. The vaccine must precede exposure to the disease
5. Transfer to a disease prone site only after the appropriate time lag phase.
Other aspects to vaccination
1. The smaller the size of the fish - the greater the risk of local reactions
2. higher temp increase risk of local reactions
3. Onset of immunity is temperature dependant
(Poikilothermic = water temperature dictates metabolism)
4. Adjuvants
(Various adjuvants have been tried out but oil based remains the best).
Type and number of antigens - monovalent vrs multivalent.
Only use an injectable vaccine in fish which are over 10g.
Describe the non specific defence mechanisms that fish can utilise ?
Non specific defence mechanisms
Mucous, skin, sacles and melanocytes
Surface barriers - mucous
- the skin, gills and gut are covered by a layer of mucous which is continually sloughed off inhibiting colonisation be pathogens.
- contains some principles which are toxic to micro organsisms IgM
- mucous production will increase in response to inflammation or fin rot
Skin
Integrity is crucial to maintaining osmotic balance and excluding microorganisms
- epidermis is non keratinised and nucleated
- healing is rapid even at low temperatures
- Malpighian cell migration from the periphery of the wound - different from mammalian scab formation
- can provide an almost immediate barrier
MALPIGIAN CELLS ARE AMONG THE FASTEST MOVING CELLS KNOWN.
Scales
Scales are the dermis sitting under the epidermis
- scales on your hand/net means significant damage
Melanocytes
Melanin plays a role in immune functions
- melanocytes respond to cytokines including interferons, interleukins and tumour necrosis factor.
- leukocytes can produce melanin, playing a role in inflammation
in fish
(melanin present in fillet of farmed salmon is a considerable quality problem - affecting up to 20% of fillets.
- fish scars in contrast to mammals chronic inflammation in fish may appear with abundant pigmentation.
Chronic inflammation in fish often presents as hyperpigmented ‘dark’ fish = poor doing
What is a melanomacrophage centre ?
Melanomacrophage centre
A second group of melanin producing cells are called MELANOMACROPHAGE.
- often seen in groups or centres MMCs (melanomacrophage centres)
- ## increased numbers of MMC can indicate stress or disease in fish
Why is haematology of limited use in fish ?
Haematology - study and treatment of blood
Limited use as an indicator of disease in fish
leucocyte response, automation, only small volumes, poikilothermic
- leucocyte responses to disease can be slow
- leucocyte response to stress and handling can be very rapid
Therefore we may be more likely to detect an affect of handling rather than an affect of disease. - nucleated erythrocytes and thrombocytes - blood counts can not be automated, other than total blood cell count.
- can only collect relatively small volumes of blood
- Poikilothermic - blood cell enzymes operate over a larger a temperature range. (mammals temp drop reduces enzyme activity)
- fish blood cells continue to be active (enzymatically and osmotically) may result in huge changes during transport of mean erythrocyte volume (packed cell volume).
Describe the common immune system cell types of fish ?
The common immune system cell types of fish
Macrophages
- widespread mainly kidney, spleen and cardiac atrium
- monocytes (kidney) 1-3 days in blood before entering tissues as macrophages
Neutrophils
- kidney spleen and blood
- phagocytic, chemotactic and bactericidal
- phagocytosis enhanced by opsonins and cytokines
Natural cytotoxic cells
- can kill certain cell types, ie when infected with avirus or bacteria
- without a need for previous exposure
Granulocytes
- Eosinophilic granular cells (EGCs) roughly equivalent to mast cells
- degranulate = serotonin
Some fish eg carp have been demonstrated to have basophils.
Describe inflammation in fish ?
Describe the immune defence of crustaceans ?
The defence mechanisms of crustaceans ( innate immunity)
Defence factors
cuticle/surface, semi closed circulatory system, copper based hemocyanin, hemocytes and (lysozyme and Penaeidin).
Surface = harbours a microflora which inhibits the growth of virulent pathogens
Cuticle = protective layer comparable to fish scales
Semi closed circulation system
- no separation between the circulatory and lymphatic system
- coregulation of circulation/ respiration preventing a ventilation perfusion mismatch.
(hypoxia ventilation down, HR down)
Copper based hemocyanin
- free in the extracellular fluid (not bound to a blood cell)
Hemocytes
- the only immune cell type
- main site of immune function
Lysozyme and Penaeidin
- common antimicrobial peptides (AMPS) which destroy microbial cell wall by hydrolysis.
- commonly expressed by hemocytes
What they lack
- immunoglobulins
- complement factors
Describe the cellular response of shrimp to a pathogen ?
Only one immune cell type Hemocytes
Main site of immune function
Hemocytes carry out the function of both red and white blood cells
- hyaline, semi granular and granular cells
A cellular response hemocytes - is initiated by a cascade of prophenoloxidase (proPO) activating systems leading to
phagocytosis
encapsulation
- several hyaline hemocytes act cooperatively to attack an enormous microbe
nodulation
- several hyaline hemocytes react cooperatively against many small microbes.
coagulation
melanisation of intruding pathogens.
Lysozyme and Penaeidin
- common antimicrobial peptides (AMPS) which destroy microbial cell wall by hydrolysis.
- commonly expressed by hemocytes
Why is apoptosis important to immune function in shrimp?
Apoptosis - killing of infected cells
This process is carried out be cell proteases
- important regulatory approach of prawns and shrimp
- proteases paly an essential role by receiving external signals and initiating apoptosis
By regulating apoptosis the host can eliminate cells infected by pathogens - thus killing and limiting the spread of pathogens.
What is HPS and immune priming why is it important in shrimp?
Shrimp immunity
Heat shock proteins
- proteins produced in response to heat shock play an important role in protecting many organisms from any sudden change in the cellular environment which would damage proteins.
- induced by change in temp, organic molecules, pollutents and oxygen deficiency
- found in all tissues
- HSP have been associated with the inhibition of viral replication
Immune primming
Distinguishes the phenomenon of some memory like properties in hemocytes alike to (macrophages NK cells in the immune system of animals).
Describe the alternative to vaccination that may be utilised in prawns (4) ?
Alternative to vaccinations in prawns
Passive vaccination
- immunization of another animal (bird, animal)
- egg yolk immunoglobulin IgY from hens can be collected as injected into prawns as a passive vaccine
Gene expression
- alter gene expression
- Dscam gene was found to generate many variants with with specific binding affinity and capability.
RNAi vaccines against against essential specific genes from pathogens
- trigger sequence dependant as well as sequence independent immune responses
- supplying target animal with ds RNAs
dose not require immune priming
Immunostimulants
Prawn are constantly grazing on algae major route of entry for pathogens
- Probiotics, competitive exclusion
- Prebiotics, can modify the microbial community of the gastrointestinal tract to immprove non specific immune responses
synbiotics a mixture of pro and pre biotics
Phytobiotics = yeast / herbs to modulate microflora towards a favourable population that outcompetes the pathogens.
Describe the mollusc immunity ?
Describe the epidemiology and transmission of viral encephalopathy and retinopathy (Ver) ?
Ecephalopathy and retinopathy
Cause = Betanodavirus
A endemic and notifiable disease in Australia
Transmission =
Vertical - broodstock (gonads, fertilised eggs and larvae)
Horizontal - water outbreaks due to introduction of infected juveniles
One of the most important diseases in marine fish worldwide.
Present in wild and farmed fish - >70 fish species affected
- WOAH =most important fish health challenge in the Mediterranean region and possible the main factor inhibiting aquaculture development in South East Asia.
Fry and juvenile fish with high economic losses, may also occur at market size in some species.
- no succes yet in breeding for resistance
-
Describe the pathology and clinical signs of Encephalopathy and retinopathy ?
Clinical signs encephalopathy and retinopathy
- 9-28 dph
- 50-100% mortalities in over 48 hours
- larval barramundi affected fish become lighter, some species become darker such as larval grouper
- cease feeding, corkskrew and whirling swimming
- hyper inflated swim bladder
- belly up appearance when resting, blindness, abrasions
Barramundi larval chromatophores become contracted larvae appear transparent
Histopathology
- pathognomonic cell vacuolisation
- necrosis of the central nervous system
- lesions occurring in the retina and spinal cord
Histopathology and PCR to confirm
Describe how you would diagnose and treat a case of encephalopathy and retinopathy?
Encephalopathy and retinopathy
Diagnose
Histology and PCR
No specific treatment, therefore prevent
- importation of SPF animals - sourcing and movement control
- health certificates
- farmed /wild fish ?
Subclinical infections and viral survival in fish products - restrictions on translocation / interstate movement of baramundi.
- Ozone treat eggs and incoming larvae
- Ver - free brood stock SPF
Describe the epidemiology and transmission of Cryptococcus ?
Cryptococcus
Various bacteria result in streptococcus; streptococcus iniae, S.agalactiae
It is common disease of both fresh water and salt water animals.
S.iniae
- invasive disease with outbreaks - humans zoonotic
- globally an economically important bacterial pathogen of warm water aquaculture
- Australian baramundi suffer severe losses due to S.iniae since 1992
- responsible for losses between 8-15 % of production
(severe outbreaks have lost as much as 70% of production)
Transmission
Common within the pond aquaculture in Australia
- could be resident in mud recurrent problem
- food borne infection in yellow tail (known since the 80s)
- low numbers S.inae are able to cause infection in barramundi
Describe the clinical signs of Streptococcus. iniae in fish ?
Clinical signs of streptococcus iniae
Serotype 1 = skin lesions, rarely meningitis
serotype 2 = damage to different organs , crossing of the blood brain barrier (been found in the bone of fish host)
There are two clinical forms of the disease observed subacute and acute.
Subacute
Takes some time to develop signs including exophthalmia, darkened colouration (melanin and inflammation) and erratic swimming
- blood tinged body cavities
- enlarged reddened spleen and pale liver
- if it affects the brain and nervous system erratic swimming often observed
- only responsible for about 1% of losses
Acute
The most devastating form of disease with the majority of losses occurring over night
- limited clinical signs observed in fish dying of the acute form (no time to develop)
- some cases mild corneal opacity
Describe how you would obtain and a diagnosis and control Streptococcus outbreaks ?
Streptococcus
Diagnosis
- history and clinical signs
- necropsy finding
- highly suspected if fish exhibit abnormal swimming, pop eye and haemorrhages.
rapid and severe mortalities
- Acute - isolate S.iniae from the brain and spleen
Gram positive cocci found in the brain and spleen, kidney
- impression smears ( blot sections of fresh tissue onto a slide of brain, spleen, kidney or liver).
- a confirmed diagnosis requires culture of the bacteria from the brain, spleen or kidney
- Blood agar is the medium of choice
Treatment
Vaccination
Difficult poorly defined serotypes and consequent vaccine escape
- autogenous vaccination
- out break strain isolated (state veterinary labs) - produce a custom IP vaccine used on the farm of orgin
occasionally re-emerging strains occur in previously vaccinated stock due to high variability in the capsular polysaccharide CPS structure.
Describe the epidemiology, clinical signs and transmission of columnaris disease ?
Columnaris disease
Cause = flavobacterium columnare - naturally occurs in healthy systems.
Transmission Becomes a problem in poor environmental conditions. (physical injuries, low oxygen =, oeganic content in wtaer high nitrates)
Clinical signs
- can rapidly affect and cause mortalities
- errosive skin lesions (saddle lesions)
- necrosis, fin rot and white patchy skin
Diagnosis
- filamentous bacteria on microscopy
- gliding motility, forms columns if left for a few minutes
Treatment
- Antibiotic (OTC for ten days) if more than 5% body area affected.
Describe the clinical signs you would observe with Iridovirus?
What is the cause of scale drop disease ?
Describe the epidemiology and transmission of infectious salmon anaemia (ISAv) ?
Infectious salmon anaemia
Highly infective, exotic and reportable
- its the ‘foot and mouth’ of aquaculture - very serious economic implications.
Atlantic salmon (Salmo salar) are the only species known to display clinical signs of ISA.
Describe the risk factors associated with ISAv
- movement of juveniles between farms and regions
- discharge of organic waste of fish farms into the sea
- farm located within 5km of another positive site
- multiple sources, more than one hatchery supply the sea site
- stress, rising/falling temp, pathogens, poor water quality
Outbreaks occur
- sea water
- hatcheries where salt water and fresh water are mixed for PH or to enhance smoltification.
Transmission = mainly transmitted horizontally through the water column , but also through vectors (sea lice, asymptomatic wild fish).
What are the recognised forms of salmon anemia ?
The two recognised form of salmon anaemia
- pathogenic highly polymorphic region (HPR) - deleted HPR ISAv
- capable of causing severe disease - NON pathogenic HPRO (non deleted HPR) ISAv
It may be possible for HPR to emerge from HPRO (low risk, but not impossible)
Describe the pathogenesis of salmon anemia ?
Pathogenesis salmon anemia
Infection occurs mainly through the gills
Predisposed - rapid changes in water temperature over the spring (rising 3 to >15 degrees).
Typically there is a low mortality in in salmonids post smolt.
ISAv causes cumulative mortalities 15-100% if nothing is doen to limit disease.
Pathology
The virus is endotheliotropic
- infecting the endothelium, therefore virus replication can occur in any organ
- hepatic paliosis (pools of blood) on histopathology
- also replicates in leukocytes and macrophages in the kidney
Gross pathology
- pale gills
- swollen abdomen
- exophthalmia ocular haemorrhage
- fin rot
- skin ecchymoses
- scale pocket odema
- liver, kidney and spleen = swollen darkened
- dark red intestinal wall mucosa
- ascites
- haemorrhages
Describe the clinical signs of salmon anaemia (ISAv)?
ISA is generalised and lethal condition characterised by severe anaemia and variable haemorrhages with necrosis in several organs.
- cumulative mortality upto 100%
- loss of apetite
Signs associated with anaemia
- fish gasping at surface (low blood oxygen)
- lethargy
- Haemotocrit <10 end stages, (25-30 often seen in less advanced cases.
>35 is normal
Describe how you would go about preventing infection with infectious salmon anaemia (ISAv) ?
Prevention of ISAv
Good biosecurity and husbandry practices reduce the outbreaks of infection
Implementation of legislative measures
- regarding fish movement, husbandry practices, mandatory health control, transport, slaughterhouse regulations
- importing eggs from ISA free zones
- disinfection of eggs iodine
- resistance breeding
Vaccination (Australia will cull instead)
Describe the transmission and epidemiology of Amoebic gill disease (AGD) ?
Amoebic gill disease
Free living amphizoic marine amoeba - Neoparamoeba percurans
Transmission =
The main health issue in atlantic salmon (S.salar) aquaculture industries.
- affects many species of fish including many of those used to control sea lice
AGD risk factors
- changes in salinity in the water body
- increased stocking density
- cage environmnet ( number of times the nets were changed)
- removal of mortalities
Describe the pathology and consequences of amoebic gill disease ?
Pathology Amoebic gill disease
Multifocal gill hyperplasia which requires multiple treatments.
It is one of the main contributors to the recently recognised complex gill disease.
Pathology
raised multifocal to white plaques distributed across the gills
- minor to severe epithelial hyperplasia of the primary and secondary lamellae
- hypertrophy
- oedema
- secondary lamella fusion and interlamellar vesicular fusion
Consequences
- disease, treatments reduce food conversion and cause down grading
- approx 20% of cost in Tasmania salmon production
Clinical signs
- lethargy
- anorexia
- congregating near the surface
- opercular movements and ventilation
N.perurans only infests healthy gill tissue causes grossly proliferative branchitis
Describe the pathology and consequences of amoebic gill disease ?
Pathology Amoebic gill disease
Multifocal gill hyperplasia which requires multiple treatments.
It is one of the main contributors to the recently recognised complex gill disease.
Pathology
raised multifocal to white plaques distributed across the gills
- minor to severe epithelial hyperplasia of the primary and secondary lamellae
- hypertrophy
- oedema
- secondary lamella fusion and interlamellar vesicular fusion
- possible vascular hypotension
Consequences
- disease, treatments reduce food conversion and cause down grading
- approx 20% of cost in Tasmania salmon production
Clinical signs
- lethargy
- anorexia
- congregating near the surface
- opercular movements and ventilation
N.perurans only infests healthy gill tissue causes grossly proliferative branchitis
Describe how you would monitor and treat amoebic gill disease ?
Amoebic gill disease
Monitoring -
Following smolt transfer AGD monitoring should begin after two weeks in regions of known AGD and continue every two weeks.
- monitor mortalities for gill lesions
- frequency of checks may decline in larger fish as water temperatures decline.
Treatment
The most effective treatment for AGD is a two hour fresh water bath
- osmotic difference removes gill mucous and associated amoeba
- promotes rapid healing of gill lesions
- stressful for fish and considerable cost
Amoeba numbers can recover after approximately 10 days - they only infect healthy tissue. (when the gill recovers it can get reinfected)
Describe how you would carry out a gill sample ?
Define complex gill disease ?
Complex gill disease CGD
Complex gill disease is an emerging term (CGD)
used to refer to the varied syndromes of probable multifactorial aetiology and variable histopathology.
a wide range of clinical disease presentations on the gills of farmed salmon
- end of summer to early winter
- AGD is the most significant disease in CGD
Describe the transmission and epidemiology of Furunculosis ?
Epidemiology of Furunculosis
Enterobacteriaceae - Aeromonas Salmonicida subsp Salmonicida
Exotic and notifiable
Only the exotic form is present in Australia
Transmission = horizontal in the water column and direct fish to fish or vectors (birds, invertebrates)
Outbreaks typically occur >10 degrees ( outbreaks may occur in young fish as low as 2-4 degrees)
Predisposing factors / stress
- endogenous smoltification
- exogenous handling temperature and water quality
- hygiene can survive on the surfaces of eggs or for long periods in the environmnet
Survivors = carriers
Describe the pathology of Furunculosis ?
Furunculosis = Aeromonas
The pathogen is intracellular so avoids most of the host immune defences.
produces at least >25 extracellular products/ toxins which play a significant role in the pathogenesis is of the disease.
Pathology
Water temperature, fish age, and the virulence of the agent can affect whether its peracute, acute or chronic
Peracute
- mortality without any clinical signs
- in some cases darkening of the skin
Acute
- lethargy, inappetence and darkening of the skin
- haemorrhages often result in gill palour
Chronic
Liquifactive haemorrhagic furancles (boils), which may rupture releasing many bacteria
Describe how you could go about diagnosing a case of Furunculosis ?
Furunculosis
Diagnosis
Histopathology “almost pathognomic”
- dense aggregates of bacteria in organs such as the heart, kidney, spleen, muscle and gills.
- remarkable little tissue reaction around these aggregates of bacteria (early stages of disease)
- later stages liquefactive necrosis
Treatment
Furanculosis must be controlled on farm through antibiotics or vaccination.
- some farms cull infected on site
Describe the process of tuna ranching in Australia and how it results in disease?
Tuna ranching
Southern blue fin tuna
- ranching season January to July
- caught along the shelf of the Great Australian bight
- Towed back at 1 knot/hour over 8 -10 days / fed sardines opportunistically
- each tow is called a cohort - eventually placed in ranching pontoons
Cohort
- may contain fish from different catches
- grown 3-5 months to about 30-35 kg
RANCHING CAUSES DISEASE
Suffer from sanguinicolid flukes - blood flukes
- infected after stocking into nets 0% at catch - 70% flukes at harvest.
- ranching extremely stressful (lysoszyme humoral response 8-15 higher in wild caught fish
- is the high fat diet to rich ?
The fish will eventually adapt to capture but weekly response is variable.
Describe the pathology and clinical signs of blood flukes Sanguinicolid flukes?
Pathology Sanguinicolid flukes (blood flukes)
Polychaete worms living under the sea cages can act as an intermediate host.
Cardicola forsteri adults live in the heart causing myocarditis
C. orientalis live in the blood vessels causing thrombosis
Clinical signs
- peak mortalities 2-15% after 6-12 weels post transfer
- mortality levels depend on how long they spend in the nets
Since 2012 treated with praziquantel about 4 weeks post transfer
- reduces mortalities to = 2%
- injected into the sardines and bait fish which are used as feed
- some pontoons are kept free of treatment to prevent the build up of resistance
THE EGGS CAUSE HUGE DAMAGE IN THE GILLS
- have been found else where in the body
Describe the epidemiology and transmission of salmon orthomyxoviral necrosis (POMV) in salmon ?
Orthomyxoviral necrosis (POMV)
Usually a disease of salmon
Certovac vaccine available
Transmission = Introduced by feeding pilchards to tuna ranching.
Describe the pathogenesis and clinical signs of skin fluke in yellow tail Kingfish ?
Skin fluke Capsalid monogenes
Current observations from Siuth east Asia indicate Capsalid monogenes infections are the most serious and pathogenic amongst all the parasitic diseases.
Pathogenesis
Capsalid monogenes is commonly found on the skin and occasionally the eyes of marine fishes.
- fluke feeding behaviour may induce hyperplasia which can partly enclose the fluke
- fish can be pruritic flashing, rub bottom or sides of the tank
-heavy gill infestations result in gill disease
- swollen pale gills
- increased respiratory rate
- piping and reduced tolerance of low oxygen conditions
Clinical signs
- if left untreated fish quickly develop skin and tail rot
- mortality rates of 30-40% are common
Describe the pathogenesis and clinical signs of Benedenia?
Yellow tail king fish Benedenia
Pathogenesis
Benedenia usually affects younger fish
- large approximately 3-10mm
Clinical signs
- causes extreme irritation
- a proportion of the young fish will go off their feed and become lethargic
- also irritates the eyes causing opacity and exophthalmia pop eye
- gradually the caudal and pectoral fins will become frayed (white appearance in the water)
- large numbers can kill fish
Infected fish may have capsalids at different stages of maturity.
Describe how you go about diagnosing and treating cases of Benedenia?
Benedenia
Diagnoses
The parasite is easy to spot on farm after the whole fish is submerged in fresh water for some minutes the parasite will turn opaque - die.
Treatment / Prevention
A specific parasite prevention program
with routine fresh water emersion, skin scrapes and gill clips should be considered an integral part of the health management protocols.
Describe what you could do to treat a fluke infestation on farm ?
Treatment of a fluke infestation
Fluke species and populations on the same farm differ in their sensitivity to treatment, so may require multiple treatments.
monogeneans = praziquantel
(not approved for use in food fish).
Formalin
FW and SW baths
Biological control by using cleaner fish
Environmental control - understand the agents pathogens
Mongenes can not survive longer than two weeks off the host - many die within minutes
Benedenia oviparous fluke free swiming larvae can be filtered out using 80mmm pore nylon mesh.
Must also take eggs into account may not hatch for 4-21 days requiring extra treatments.
Describe red spot disease ?
Epizootic ulcerative disease
- ulcerative fungal disease notifiable in Australia
- squash preparations from beneath an ulcer to identify the septae hyphae.
Eradication is required
Describe the epidemiology and biosecurity of white spot disease in Crustacea ?
White spot syndrome in crustacea
Whispovirus
The most important disease limiting production of prawns/shrimp globally.
- all decapod crustaceans are susceptible prawns lobsters and crayfish
- could be catastrophic for wild stock and the ecosystem
Carriers - rotifers, marine molluscs, artemia, polychaetae worms etc
Biosecurity
-Biosecurity extension including movement restriction areas in QLD. (high risk animals such as yabbies, prawns and marine worms) and cleaning routines.
NEVER USE SHOP BROUGHT PRAWNS AS BAIT.
Describe the pathology and clinical signs of white spot disease in crustacea ?
White spot Whispovirus
Pathology
The pathogen may be present in a the absence of any clinical signs.
- rapid onset of mass mortality (80%) in farmed penaeid prawns, during the grow out period.
- productions drops to 40% for two years then continues on at 70% of normal indefinitely
Clinical signs
- white spot (white calcium deposits 0.5 - 3.0 mm in diameter)
- lethargy, cessation of feeding
- aggregations of moribund prawns near the water surface
- lose carapace
- white mid gut line through the abdomen
- delayed clotting reaction of haemolymph
Describe the pathology and clinical signs of white spot disease in crustacea ?
White spot Whispovirus
Pathology
The pathogen may be present in a the absence of any clinical signs.
- rapid onset of mass mortality (80%) in farmed penaeid prawns, during the grow out period.
- productions drops to 40% for two years then continues on at 70% of normal indefinitely
Clinical signs
- white spot (white calcium deposits 0.5 - 3.0 mm in diameter)
- lethargy, cessation of feeding
- aggregations of moribund prawns near the water surface
- lose carapace
- white mid gut line through the abdomen
- delayed clotting reaction of haemolymph
What is the cause and clinical signs of mid crop mortality syndrome in prawns ?
Mid crop mortality -
The most significant viral disease of prawn farming in Australia
A syndrome with multiple aetilogies
- Gill associated virus (GAV) appears to be a prominent virus
- hypodermal and haematopoetic necrosis virus (IHHNV)
- spawner mortality virus (SMV)
More accurately MCMs is the absence of any other identifiable agent.
Large range of clinical signs
- redness
- fouling
- stunting
- nerve necrosis
- eye necrosis
Describe the clinical signs of Gill associated virus YHV-2 and infectious hyperdermal and haematopoietic necrosis virus IHHNV ?
Mid crop mortailty syndrome comprises of
Gill associated virus also know as yellow head virus YHV-2
- outbreaks with high viral loads post stocking combined with stress results in mortalities up- to 80%
- culling recommended
- reddening of the tail fin and biofouling with ectoparasites
- emaciation
- asymptomatic carriers common
- horizontal transfer water, ingestion
Infectious hyperdermal and haematopoietic necrosis virus IHHNN
- worldwide present in QLD and NT its a notifiable disease
- high mortalities animals abruptly stop feeding
- rise slowly roll over and sink = cannibalised
- implications when obtaining brood stock from the wild, causes reduced hatching and survival
- translocated with prawn movents.
A chronic form IHHNN RDS
- L. vannamei infection is chronic runt deformity syndromse RDS.
- high mortalities are usual
- growth suppression and deformities of the cuticle are common
- deformed sixth abdominal segment
- a bend of rostrum45-90 left or right
- pathognomonic for infection with IHHNV
-
Describe what you can do to control for YHV-2, IHHNV and RDS
Control
No success with chemotherapy or immunstimulation has been described
The best way is to prevent disease
- development of SPF shrimp stocks
- PCR pre screening of wild or pond reared broodstock or their spawned eggs nauplii.
Development of resistant lines of stock
- developing lines of L.vannamei which SPF is one approach
Specific pathogen free
Specific pathogen resistant = refractory genetically resistant to disease
Specific pathogen tolerant = lines that do not develop lines of disease when infected with specific pathogens.
Describe the epidemiology of bacterial infections in prawn ponds of Australia ?
Epidemiology of bacteria in prawn ponds
Vibrio sp, and septicaemias
The majority of diseases in ponds is due to bacterial infections
- Vibrio are ubiquitous in the marine environment
- low salinity <20ppt appears to reduce incidence
- possible vector species polychaetae worms
- peak occurrence hot and dry season
High ammonia can lead to damage of the hepatopancreatic tubules - this can lead to bacterial invasion into the haemocoel and resulting in high mortalities.
Transmission = horizontal oral transmission, over feeding, poor seed quality, poor water quality, poor feed quality, algal blooms or crashes and inefficient sweeping of the bottom and paddle wheels.
Describe the cause and clinical signs of Acute hepatopancreatic necrosis disease ?
Hepatopancreatic necrosis disease of prawns
cause = Vibrio parahaemolyticus
Causes rapid death of infected shrimp - sudden mass mortalities up to 100%
There are two distinct phases
1. Hepatopancreas degeneration in the absence of bacterial cells
2. Terminal - hepatopancreas (HP) pallor and atrophy
- soft shells, intestine with discontinuous or no contents.
- Black melanised foci or linear streaks visible within the HP
