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Aquaculture > Lecture 8 > Flashcards

Lecture 8 Flashcards

1
Q

What is the foot and mouth of fish

A

Infectious salmon anaemia

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2
Q

Characterisitcs of Infectious salmon anaemia

A
  • Severe anaemia
  • Variable haemorrhages
  • Necrosis of several organs
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3
Q

What are the two recognised forms of Infectious salmon anaemia

A
  • Pathogenic highly polymorphic region (HPR)-delete infectious salmon anaemia virus (ISAV), or non-pathogenic HPR0 (non-deleted HPR) ISAV
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4
Q

What are the only known species to show clinical signs of Infectious salmon anaemia

A
  • Atlantic salmon
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5
Q

Where does Infectious salmon anaemia mainly occur

A
  • Gills in Northern Hemisphere in connection with rapid changes in temperature during the spring
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6
Q

Why is the disease course of Infectious salmon anaemia prolonged

A
  • Low daily mortality
    *
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7
Q

How is Infectious salmon anaemia transmitted

A
  • Horizontally
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8
Q

Where do outbreaks occur with Infectious salmon anaemia

A

Sea water or hatcheries where sea water is mixed with fresh water for pHor adjustment to enhance smoltification

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9
Q

How is Infectious salmon anaemia spread

A
  • With movement of live juvenile salminids between fish farms and regions via well boats
  • With the discharge of organic waste
  • Farm located winthin 5km of another positive site
  • With increased number of hatcheries supplying the sea site
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10
Q

When do majority of outbreaks of Infectious salmon anaemia occur

A
  • Salmonid post-smolts
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11
Q

What part does Infectious salmon anaemia infect

A

Epithelium

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12
Q

Where does replication of Infectious salmon anaemia occur

A
  • Leukocytes and sinusoidal macrophages
  • Endothelial cells so virus replication can occur in any organ
    *
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13
Q

Clinical signs of Infectious salmon anaemia

A
  • 100% mortality
  • Fish congregating near surface
  • Fish gasping at the surface
  • Lethargy
  • Loss of appetite
  • Haematocrit <10 in end stages
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14
Q

What is the gross pathology of Infectious salmon anaemia

A
  • Pale gills and heart
  • Swollen abdomen
  • Exophtalmia, ocular haemorrhage
  • Fin not
  • Skin ecchymoses
  • Scale-pocket oedema
  • Swollen and dark liver, kdney and spleeb
  • Dark red intestinal wall mucosa
  • Ascites
  • Haemorrhages + thin fibrin layer on liver surface and splenomegally
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15
Q

Histopathology of Infectious salmon anaemia

A
  • Renal interstitial haemorrhage and tubular necrosis
  • Branchial lamellar and filamental congestion
  • Congestion of the intestine and pyloric caecae
  • Perivascular inflammation and focal necorsis in liver
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16
Q

Prevention of Infectious salmon anaemia

A
  • Vaccination
  • Biosecruity
  • Movement of fish
  • Slaughterhouse regulations
  • Disinfect eggs
17
Q

Clinical signs with salmonid alphavirus

A
  • Occurs during first year at sea
  • Inappetance
  • Cachectic appearance
  • Lethargy
  • Increased mortality
  • Necropsy shows an empty gyt and petechual haemorrhage around depleted fat
18
Q

How to diagnose

salmonid alphavirus

A
  • Histopathological ecaminations
  • Virus cultures
  • PCR
  • Heart tissue samples
19
Q

How many species has amoebic gill disease affected

A
  • at least 15
20
Q

What does amoebic gill disease affected cause

A
  • Visible multifocal gill hyperplasia
21
Q

Why is amoebic gill disease affected a problem

A

Reduced food conversion and downgrading

22
Q

What is amoebic gill disease affected part of

A

Complex gill disease

23
Q

What are signs of amoebic gill disease affected

A
  • Letharrgy, anorexia, congregation near the surface and increased opercular movements and ventilation
  • N.perurans only colonises healthy gill tissue and causes a grossly visible proliferative branchitis
24
Q

How to diagnose amoebic gill disease affected

A
  • Histopathology
    • Required for definitive diagnosis
    • Reveals severe epithelial hyperasia of the primary and secondary lamellae, hypertrophy,oedema and secondary lamellar fusion and interlamellar vesicle formation
    • Gill damage in turn can lead to compromised respiration, osmoregulation,nitrogenous waste excretion and acid/base balance
25
Q

4 risk factors of amoebic gill disease affected

A
  1. Changes in salinity
  2. Increased stocking density
  3. Cage environement
  4. Removal of mortalitles

Severely affected fish may also suffer from hyperatremia and it is possible that vascular hypertension caused by AGD may elict cardiac changes including ventricular hypertrophy and hyperplasia

26
Q

How to treat amoebic gill disease affected

A
  • Freshwater bathing for min 2 hours
    • The osmotic differences during bathing removes gill mucus and associated amoeba and promotes rapid healing of lesions
    • Amoeba numbers can recover after aprox, 10 days
    • Amoeba can only infect healthy tissue
27
Q

How to manage amoebic gill disease affected

A
  • Regular prophylactic freshwater baths
  • Utilising low salinity sites
  • Sngle-age group sites
  • Reducing stocking density
28
Q

How to gill score

A
  • Main population ( not from the edge)
  • Raise the seine to ‘mix’ the fish, subsample from this
  • Transfer fish to anaesthetic with aeration or circulation
  • Avoid direct oxygenation
  • Examine in bright natural light
  • Open gills anf fully so you can look into the corners between gill arches
  • Change the orientation of the fish to study the 3D structure of lesions
  • Test lesion consistency with finger - AGD with ‘thin’ and ‘move’ when rubbed
  • Regular cross check your score with other experienced operators
  • Return fish to an oxygenated recovery bin/recovery net
29
Q

Explain monitoring frequency

A
  • Devise and adapt strategy acording to the likely risk
  • All cages checked regulary
  • Following smolt transfer, ADG monitoring should begin after 14 days of known AGD
  • Continue to check on 14 day cycle
  • If necessary increase frequency as fish approach treatment threshold
  • Assessment of the population gill socore at treatment is useful
  • for 10-14 days post treatment, scarring and mucus may be present
  • Check mortalities for gill lesions
  • Frequency of checks can be reduced in larger fish as water temperatures decline
30
Q

How to confirm amoebic gill disease affected

A
  • Histology of damaged gills
  • PCR to test for the presence of P.perurans
  • ADG lesions change when rubbed with your finger
31
Q

What in black kidney disease

A
  • Gram positive Rennibacterium salmoninarum
  • Chronic, granulomatous disease affecting freshwater and marine salmonids
  • Diagnosisis usually made in fish older than a year
32
Q

What are the signs of black kidney disease

A
  • External lesions
  • Loss of balance
  • Darkening and mottled appearacne of the skin, ascites
  • Bilateral exophalmia
  • Petechiae and haemorrhaging around the base of the pectoral fins anf the lateral line
  • Cystic cavities, vesicular lesions and haemorrhage appear in the musculature and skin
33
Q

What does histopathology reveal with black kidney disease

A
  • Renal and hepatic granuloma with large numbers of bacteria
  • Granulomatous peritonitis occurs in pancreatic area with numerous bacteria accompanied by focal infiltration of leucocytes
34
Q

How to treat black kidney disease

A
  • No vaccination
  • Fish are too far affected to treat effectively
35
Q

What causes Piscirickettsiosis

A
  • Caused by Rickettsia-like organisms including Piscirikettsia salmonis
36
Q

When is it introduced hat will cause outbreak piscirickettsiosis

A
  • Salt water pens a water temp 12-18 degrees warm
37
Q

How to diagnose piscirickettsiosis

A
  • Clinical sigbs
  • Histopathology
  • Isolation and identification of the lacteria
38
Q

What are the clinical signs of piscirickettsiosis

A
  • Lethargy, swimming near the surface with erratic movements and dark skin solouration
  • Raised scales with associated haemorrhagic skin lesions can be observed
  • At necropsy, gills show anaemia and interally, ascites, splenomegaly, cream coloured, focal sub capsulat nodules in the liver, fibeinous epicarditis and swollen grey kidney are reported
39
Q

What is the histopathology with piscirickettsiosis

A
  • Necrosis of the haematopoietic with tissue and oedema and increase in inflammatory cells, glomerulonephritis
  • Granulomas: liver and spleen and focal to diffuse necrotizing heptatitis
  • Meningitis, peri-, epi-, and endocarditis, peritonitis, pancreatitis and branchitis may be seen with accompanying chronic inflammatory vascular changes, similar to those in the liver
  • Perechiae
  • Neutrophilia is associated with severely anaemic fish

Aquaculture (11 decks)

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