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
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
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
4
Q
acute hepatopancreatic necrosis disease: how is the bacteria transmitted
A
- Horizontal oral transmission and co-habitation
5
Q
What reduced acute hepatopancreatic necrosis disease
A
- Low salinity during the hot and dry season from April to July
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
7
Q
What is necrosing hepatopancreatitis
A
- Exotic and notifiable: infection w/ Candidatus Hepatobacter penaei an obligate intracellular bacterium
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
9
Q
Where do NHP persist
A
- Lengthy periods of high water tempertaure and elevated salinity
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
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
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
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
14
Q
Describe runt deformity syndrome
A
- Chronic form of IHHVV disease
- Supressed growth
- Bent or derfoemed rostrum
- Deformed 6th abdominal segment
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
*
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
Good management of IMN
* Disinfection of eggs and lsrvae
26
What is seen with gill-associated virus
* Reddening of the tail fin and biofouling with ectoparasites; emaciation
27
Signs of Yellowhead
* 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
How is YHV transmistted
* Vertical - both male and female
* Horizontally by ingestion of infected tissues or cohabitation with infected shrimp
29
What is the gross pathology signs of YHV
* 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
What is the crayfish plague caused by
Infection with the oomycete Aphanomyces astaci
- Fresh water only
31
When does the crayfish plague usually occur
* Summer
32
What is the primary transmission mechanism of crayfish plague
* Motile zoospores of A. astaci swim actively in the water column and show positive movement towards other crayfish
33
Clinical signs of crayfish plague
* 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
What are the gross pathologies with crayfish plague
* 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
