Lecture 7 Flashcards

1
Q

What is acute hepatopancreatic necrosis disease

A
  • A notifiable and exotic disease
  • A gram negative bacillus that contains an approximate 70kbp plasmid with genes that encode homologues of the Photohabdus insect-related binary toxins, PirA and PirB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is acute hepatopancreatic necrosis disease characterised by

A
  • Sudden, mass mortalities, ususally within 30-35 days of stocking grow-out ponds with post larvae or juveniles although older juveniles may also be affected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clinical signs of acute hepatopancreatic necrosis disease

A
  • Hepatopancreatic pallor and atrophy, soft sheels, intestine with discontinuous, or no contents, black, melanised foci or linear streaks visible within the HP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

acute hepatopancreatic necrosis disease: how is the bacteria transmitted

A
  • Horizontal oral transmission and co-habitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What reduced acute hepatopancreatic necrosis disease

A
  • Low salinity during the hot and dry season from April to July
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How to control acute hepatopancreatic necrosis disease

A
  • No treatments, vaccination, immunostimulants or resistance-breeding successes to-date
  • As with other infections, establish good sanitary and biosecruity ptactices
  • Good broodstock management, use of high quality port-larvae and good shrimp farm management including strick feeding rate control andappropriate stocking density
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is necrosing hepatopancreatitis

A
  • Exotic and notifiable: infection w/ Candidatus Hepatobacter penaei an obligate intracellular bacterium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the clinical signs of Hepatobacteria penaei

A
  • No CS are pathognomoic
  • Acute disease with v. high mortalities in young juveniles, adults and broodstock
  • Lethargy,reduced food intake
  • Noticable reduced growth and weight gain
  • Soft shells and flaccid bodies
  • Black or darkened gills
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where do NHP persist

A
  • Lengthy periods of high water tempertaure and elevated salinity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When do mortalities with NHP occur

A
  • Midway through the grow-out phase and can be 90-95% within 30 days of outbreak
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is NHP transmitted

A
  • Direct ingestion of carrier prawns and through contaminated water
  • NHP bacteria mayalso be shed in faeces and contribute to disease transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain infectious hypodermal and haematopoietic necrosis virus

A
  • Member of the family Parcoviridae
  • Target tissue is CT, gills, haematopoietic noudles and haemocytes, vental nerve cord and ganglia, antenal gland tubule epithelial cells and lymphoid organ parenchymal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Signs of Infectious hypodermal and haematopoietic necrosis virus

A
  • Not specifc
  • Go off food followed by behavioural chnages and appearance
  • Morbidity and mortality
  • Become motionless, rise to top of tank, turn over and slowly sink
  • White or buff coloured spots
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe runt deformity syndrome

A
  • Chronic form of IHHVV disease
  • Supressed growth
  • Bent or derfoemed rostrum
  • Deformed 6th abdominal segment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How to control runt deformity syndrome

A
  • Replication at high water temps is reduced
  • PCR pre-screening of wild or pond-reared brookstock or thei spaened eggs/napulli
    *
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does white stop syndrome affect

A

Crustaceans

17
Q

Where is white spot a problem

A
  • The disease has mainly been a problem in farmed penaids but all decapod crustaceans are considered susceptiblw to infections
  • Birds can spread the virus
18
Q

What are the signs of white spot syndrome

A
  • Rapid onset of mass mortality in farmed penaeid prawns druing thegrow-out period
  • Letharrgy
  • Cessation of feeding
  • Aggregations of moribund prawns near the water surface at the edgeof the rearing pond or tank
19
Q

Gross pathology of white spot syndrome

A
  • Loose carapace
  • Heavy fouling of the surfsce and gills by external parasites
20
Q

Explain infectious myonecrosis virus

A
  • Follows from stressful events
  • Virus targets the striated muscles,CT, haemocytes and lymphoid organ parenchymal. cells
21
Q

Where does IMNV remain infectious

A

Gut and faeces of seabirds - due to non-enveloped dsRNA virus structure

22
Q

How is IMNV transmitted from shrimp to shrimp

A
  • Cannibalism
  • Water
  • Ventrally from broodstock
23
Q
A
24
Q

Acute stage of IMN

A
  • Focal to extensive white necrotic areas in striated muscles, especially the distal abdominal segments and tail fin
25
Q

Good management of IMN

A
  • Disinfection of eggs and lsrvae
26
Q

What is seen with gill-associated virus

A
  • Reddening of the tail fin and biofouling with ectoparasites; emaciation
27
Q

Signs of Yellowhead

A
  • Aggregations of moribund prawns near the water surface at the edge of the rearing pond or tank
  • Abnormally high feeding rate of infected5g-15g prawns for several days and then cessation of feeding
  • Mass mortality occuring 2-4 days after cessation of feeding
28
Q

How is YHV transmistted

A
  • Vertical - both male and female
  • Horizontally by ingestion of infected tissues or cohabitation with infected shrimp
29
Q

What is the gross pathology signs of YHV

A
  • Yellowing of the cephalothorax and general bleacing of the body
  • White, yellow and brown gills
  • Exceptionally soft digestive gland compared with normal
  • Yellow, swollen digestive gland, making head appear yellow
30
Q

What is the crayfish plague caused by

A

Infection with the oomycete Aphanomyces astaci

  • Fresh water only
31
Q

When does the crayfish plague usually occur

A
  • Summer
32
Q

What is the primary transmission mechanism of crayfish plague

A
  • Motile zoospores of A. astaci swim actively in the water column and show positive movement towards other crayfish
33
Q

Clinical signs of crayfish plague

A
  • High mortality
  • Many dead ot weak floating or lying in water courses or ponts
  • In open water during daylight hours unstrady and raised gait
  • Progressive paralysis
34
Q

What are the gross pathologies with crayfish plague

A
  • Fungal growth on soft, non-calcified parts of the carapace
  • Brown or black spots on the carapace where fungal hyphae proliferation
  • Fine black line on the soft shell underneath the tail melanised shell in chronically affected individuals