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Aquaculture > Lecture 10 > Flashcards

Lecture 10 Flashcards

1
Q

What is binamiosis caused by

A

Infection with Bonamia spp - an intrahaemocystic protist classified in the order of Haplosoridia

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2
Q

What does Bonamia. Ostreae affect

A

Oysters

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3
Q

What are signs of Bonamia

A
  • Poor condition
  • Shell gaping
  • Increased mortility
  • Concurrent infections also occur
  • Use light microscope
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4
Q

What sould be sampled for Bonamia

A
  • Gaping or freshly dead induviduals as a priority to increase the chances of finding infected oysters
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5
Q

How to do histology for Bonamia

A

Best preservation is Davidson’s AFA, but 10% buffered formalin or other standard histology fixatives are also acceptable

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6
Q

What are the clinical signs of Bonamia

A
  • Dead or gaping oysters
  • Increased mortality
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7
Q

Gross pathology of Bonamia

A
  • Stunted growth and poor condition
  • Weakened shell closure, leading to slight gaping
  • Pale atrophied digestice gland
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8
Q

Histopathology for Bonamia

A
  • Microcell parasites within haemocytes
  • Individual microcells are basophilic, spherical or ovoid parasites, 2-3 um in diameter
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9
Q

When do the most mortalities happen with Bonamia exitosa

A
  • Mid to late summer in southern hemisphere
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10
Q

What can affect Bonamia exitosa

A
  • Temperature extremes
  • High salinity
  • Handling
  • Heavy coinfection
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11
Q

How is Bonamia exitosa transmitted

A
  • Via infective stages that are carried from one oyster bed to another by water currents
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12
Q

What is Microcytos mackini infected by

A
  • Infection with Microcytos mackini, a intracellular protozoan that causes lethal infection
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13
Q

Where does Microcytos mackini reside in the cell

A
  • Cytoplasm
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14
Q

What are the clinical signs of Microcytos mackini

A
  • Dead or gaping oysters
  • Increased mortality
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15
Q

What is the gross pathology of Microcytos mackini

A
  • Focal yellow or green lesions up to 5mm in diamter within the body wall or on surfaces of the gonad, labial palps, gills or mantle brown scars in the shell adjacent to lesions on the mantle surface gaping oysters due to impaired adductor muscle contraction
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16
Q

What is the histopathology of Microcytos mackini

A
  • Focal intracellular infection, mainly of vesicular CT cells, resulting in haemocyte infiltration and tissue necrosis intracellular and extracellular microcell protozoa, 2 to 3 um in diameter
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17
Q

What is infection with Marteillia also known as

A
  • Marteillosis
  • QX disease
18
Q

What are the diseased signs of Marteillia

A
  • Reduced growth rate
  • Gaping shells
  • High cumulative mortalities of up to 100%
19
Q

What is the gross pathology with Marteillia

A
  • Shrunken, watery body
  • Generally poor condition
  • Death within 60 days
  • Collourless and translucent tissue because gonad is resorbed
  • Disgestive gland becomes pale yellow or brown
20
Q

What is the microscopic pathology signs of Marteillia

A
  • Focal haemocytic inflammation of the gills
  • Hyperplasia of the connective tissue and gill epithelium with fusion of gill filaments
  • Massive infection of the digestive gland tubule epithelium with sporogenic stages
21
Q

What is onset of Marteillia associated with

A

Immunosupression of oysters due to stressors such as flooding or low salinity, high water temperature and excessive sedimentation

22
Q

What is pacific oyster mortality syndrome

A
  • Ostreid herpesvirus-1 microvarient
23
Q

What oysters are susceptible to pacific oyster mortality syndrome

A
  • Pacific oysters and portuguese oysters
24
Q

What are the clincial signs of pacific oyster mortality syndrome

A
  • Rapid and high cumulative mortalities in Pascific oysters, approaching 100% within 8-10 days of infection
  • Although the virus can be detected in all oyster stages, mortality due to microvariants mainly concern is spat and juveniles
25
Q

What is the gross pathologu of pacific oyster mortality syndrome

A
  • Cessation of feeding and swimming by larvae, which exhibit velar lesions
  • Gaping in adults
  • Pale digestive gland in spat and older oysters
26
Q

What is the histopathology of pacific oyster mortality syndrome

A
  • Ulcerative and erosive lesions in the connective tissue of mantle, gills, labial palps and digestive tissue
  • Nuclear hypertrophy, nuclear chromatin margination and pyknosis
  • Inflammatory changes ranging from milk and localised, to severe and extensive
27
Q

What is infection with abalone viral ganglioneuritis known as

A
  • Abalone herpesvirus
  • Infection with haliotid herpesvirus 1
  • Abalone viral mortality
28
Q

Explain the effects of pacific oyster mortality syndrome

A
  • Affects nervous system of abalone and results in curling of the foot, swelling of the mouth, weakness and death
  • Currently, species known to be susceptible to AVG in Australia are the greenlip abalone, backlip abalone
29
Q

What are the signs of affected abalone with pacific oyster mortality syndrome

A
  • Abscence of the marked extension of the foot shown in the righting reflex when healthy abalone are turned onto their backs
  • Tetanic patalysis of the foot and mantle tissue
  • Excessive mucus production
  • Swollen mouth parts
  • Reduced pedal adhesion to surfaces
  • Abscence of marked foot extension sene in the righting reflex
  • Curled mantel edge
  • High mortalities
30
Q

What is the histopathology and diagnosis with pacific oyster mortality syndrome

A
  • Major lesions are confined to nervous tissue, centered on the cerebral, pleuropedal and buccal ganglia, the cerebral commissue and the peripheral nerves arising from the ganglia
  • Lesions have increased cellularity, individual neural cell necorsis and oedema
  • Occassional neurons have marginated chromatin and central pallor, resembling ground glass nuclei, which is morphologicallu suggestive of intranuclear viral inclusions
  • Mouth parts show severe multifocal oedema
31
Q

What is the bacteria Xenohaliotis californiensis also known as

A
  • Withering Syndrome of Abalone
32
Q

What is Withering Syndrome caused by

A

Rickettsia-like intracellular organism Candidatus Xenohaliotis californiensis - obligate intracellular bacterium

33
Q

Where does X.californiensis occur

A

In marine waters and attacks the lining of the digestive tract causing metaplastic cellular changes ans apparently obstructing the production of digestive enzymes

34
Q

What is the result of X.californiensis

A
  • Abalone starve and catabolise their musculature causing withering of the foot, which impairs their ability to adhere to substrates and makes them vulnerable to predation
  • Die from starvation
    *
35
Q

Transmission of X.californiensis

A

Horizontal

36
Q

How to treat X.californiensis

A

ANtibiotics

37
Q

Signs of X.californiensis

A
  • Reduced feeding
  • Inability of individuals to right themselves when upside down
  • Weakness and lethargy
  • Inability to adhere to the substrate
  • Increased mortality
38
Q

What is the gross pathology with X.californiensis

A
  • Wasting of body mass
  • Retraction of mantle
  • Atrophy of the foot muscle
  • Decreased response to tactile stimuli
  • Diminished reproductive output
  • Mottling of digestive gland
39
Q

What is the histopathology of X.californiensis

A
  • Presence of intracellular bacteria in the cells of the digestive epithelua
  • Atrophy of digestive tubules
  • Increase in connective tissue, inflammation and metaplasia of the digestive glands
40
Q

Whare are the responses to X.californiensis

A
  • Eradication
  • Containment and control via zoning/compartmentation
41
Q

Treatment of X.californiensis

A
  • Possible but not praticle
  • Reducing temperatures can reduce bacteria
  • Antibiotics depend on the EAD respinse

Aquaculture (11 decks)

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