INTRODUCTION

Shrimp culture in Bangladesh has emerged as a big industry over the last three decades although shrimp culture in greater parts of the farming area is done in traditional ways. Bangladesh government has also taken necessary measures along with the private sectors to increase production, upgrading processing industries and to promote export performance. Long supply chain of raw material collection, inadequate infrastructure facilities, poor level of maintaining cool chain and lack of adequate HACCP based training on hygiene and sanitation among the different people involved in field level are the main problems of quality loss of raw materials. Shortage of raw materials resulted poor capacity utilization of the processing plants. The bagda (P. monodon) hatchery sector has expanded rapidly over the last few years mostly concentrated in Cox’s Bazar region is enough to meet the target production. However, there is a shortage of pelleted shrimp feed in Bangladesh.  Bangladesh at the time of its independence in 1971 had only 15 fish processing plants. The number of processing plants had increased to 145 by 2006. The unplanned growth of such plants exceeded the potential of raw materials resources encouraging unhealthy competitions amongst the processors, thus resulting in loss of quality and international marketing good will. Moreover, due to a ban by the European Union (EU) in 1997 many plants went out of operation. So far 72 Processing plants were issued license by Department of Fisheries (DOF) after modernization until 2006, out of which 60 plants are EU approved. About 20-25 (30%) plants are involved in production and export of value added fish and shrimp products and more plants are likely to go for product diversification in near future.

WHY DO WE NEED STUDY ABOUT SHRIMP CULTURE?

As a student of Fisheries and Marine Resource Technology Discipline (FMRT) we must know the proper knowledge about shrimp culture as it is very important resources in our country.

Shrimp culture plays very important role in Bangladesh particularly in the contest of export earning.. Shrimp culture started in the costal district of Satkhira in 1960s.  Gradually its culture expanded to the coastal belts of Khulna, Bagerhat, Cox’s Bazar and Chittagong and now the area under shrimp culture has increased from 52,000 ha in 1982-83 to 141,000 ha in 1999-00. About 75% of this land is located in the Khulna, Bagerhat and Satkhira districts in the south-eastern region of the country. Penaeus monodon and Machrobrachium rosenbergii are the two major species cultured in Bangladesh. There are now approximately 37,397 bagda farms (P. monodon) with an average farm size of 4.5 ha. Bagda production has increased by 20% per annum in the last fifteen years. There are also 30,000 ha of land under galda (M. rosenbergii) culture with an average farm size of 0.28 to 4 ha comprising 105,000 galda farms, located mostly in Khulna division.  An estimate showed that total shrimp production in 2003-04 was 114,660 MT (DOF, 2005) as against the production of 30,000 MT in 1995. It alone contributes more than 70% of the total export earning from all the agro-based products, including tea, raw jute, vegetables, fruit, etc. The shrimp industry also provides direct employment to over 600,000 people who in turn support well over 3.5 million dependents. The export performance in shrimp industries is indeed highly appreciable. In 1973, the export earnings were US$ 3.17 million, which stands at US$ 420million in 2004- 05 financial year by exporting 63,377 MT shrimp and other fishery products, in which shrimp alone contributed 89% of the total export in spite of  having a severe price fluctuation in the international market(BFFEA, 2006). (http://www.bqsp.org/index.php)

Bangladesh is exporting yearly around 32,000 tons of frozen shrimps using block-freezing process. There are many demerits of this current process, like production of inferior quality frozen shrimp, creating hazardous gases and harming human health. If this current process is changed to Liquid Nitrogen Individual Quick Frozen (LN IQF) process then, the country could earn extra $208 millions/year and could add around 0.4% to GDP. This LN IQF process could produce high quality frozen shrimp and would not create any harmful gases to the environment. Although the investment for the new process would be around $34 millions, this investment cost of the LN IQF process could be recovered within two months from the extra earning of the frozen shrimps. The LN IQF would also allow the Bangladesh shrimp producers to access directly into the international shrimp market, since in the current process they have to go through the intermediate buyers to sell the frozen shrimps. This LN IQF would reduce the supply chain of the frozen shrimps from Bangladesh to the final consumers in the international market. Consequently this would add value to our shrimp exports and increase our GDP substantially. (http://orp.aiub.edu/Vol6_2.aspx#a7)

 

Fig.1: Percentage Share of Shrimp in (GDP)

(www.fao.org)

Fig.2: Frozen Shrimp Export from Bangladesh

(www.fao.org)

 

SUITABLE LEVEL OF ENVIRONMENTAL PARAMETERS FOR SHRIMP CULTURE

Salinity:

• Penaeid shrimp are considered to be brackish water shrimp, but they grow up in bay sand estuaries of the world, which are subject to abrupt changes in salinity (and other parameters) due to freshwater or watershed runoff.
  
• These brackish water shrimp actually grow better when the salinities are lower (10-25 ppt) than the normal oceanic seawater (35 ppt).
  
• However, oceanic salinities and stable conditions are necessary for reproduction.
  

Temperature:

• Tropical shrimp tolerate only a small temperature range.
  
• Growth occurs from 23 to 34°C for most tropical shrimp; however, the reproduction temperature ranges are even more narrow (28±2°C for most tropical penaeid shrimp).
  

pH and alkalinity:

• Low pH affects blood affinity for oxygen. pH levels of less than 5 affect growth negatively.
  
• Shrimp can tolerate high levels of pH for a short time.
  
• Phytoplankton often cause the pH in the pond to rise to 9 or 10, sometimes higher, during the day and when there is a heavy bloom in the pond.
  
• A high pH converts more ammonia to the toxic un-ionized form.
  
• A pH level between 6.5-8.0 is recommended for growout and 7.88.2 for maturation.
  

Dissolved oxygen (DO):

• Below 2.0 ppm DO begins to stress shrimp.
  
• 0.1 to 1.5 ppm can be lethal to shrimp depending upon species and other parameters such as salinity, pH, temperature, etc.
  
• A chronic low DO level can cause shrimp to stop eating, cause stress, and subsequently can cause the onset of secondary bacterial infections.
  
• Pond aeration and water movement devices and pumping water are the treatments for low DO.
  

 

 

Turbidity:

• Indication of the phytoplankton bloom in the pond and is maintained with pumping and fertilizing procedures.
  
• It is generally read by using a Secchi disc and is kept at an optimum reading of 8-10 inches.
  

Excretory products:

• Culture systems should be designed and managed so that excretory products do not build up.
  
• In ponds, most excretory products will break down.
  
• In intensive systems, excretory products must be removed. Soluble metabolic by-products such as ammonia and by-products of organic materials breaking down to nitrites are a problem.
  
• Nitrites above 0.1 ppm may cause problems with reproduction. Tolerance levels in growout are not well known but much higher levels have been recorded (.75-2 ppm at 8.3 pH) without mortality.
  
• Some gill damage may occur when the level of un-ionized levels of ammonia go above .5 mg/l and when other stresses are present (low DO, handling, etc.). However, growth can be reduced at these higher levels.
  

(aquanic.org/publicat/govagen/ncae/shrimpd.pdf)

 

 

 

 

 

 

 

 

Table 1:
Classification scheme carried out in the study according to Kapetsky and Nath, 1997.

	1	2	3	4
Environmental Parameters	Very suitable	Moderately	Marginally	Presently
		suitable	Suitable	Unsuitable
Water Parameters Water temperature for	22-300C	18-220C, 30-330C	15-180C, 33-350C	<150C >350C
shrimp and crab
Salinity for shrimp and	8-26ppt	5-8, 26-32ppt	4-5, 32-37ppt	<4 >37ppt
crab
Dissolved oxygen	5-10ppm	4-5, 10-12ppm	3-4, 12-13ppm	<3 >13ppm
Water pH	6.5-8.5	5.5-6.5	4.5-5.5	<4.5 >8.5
Soil parameters
Soil pH	6.5-9	5.5-6.5	4.5-5.5	<4.5 >9
Soil salinity	8-26ppt	5-8, 26-32ppt	4-5, 32-37ppt	<4 >37ppt
Soil texture	>75% fine	>75% medium	50-75% coarse	>75% coarse
		50-75% medium	<50% all

 

(Source: Kapetsky and Nath, 1997)

 

 

 

 

 

 

DISEASE

A disease is an abnormal condition of an organism that impairs bodily functions. In this broader sense, it sometimes includes injuries, disabilities, disorders, syndromes, infections, isolated symptoms, deviant behaviors, and atypical variations of structure and function, while in other contexts and for other purposes these may be considered distinguishable categories. While many diseases are biological processes with observable alterations of organ function or structure, others primarily involve alterations of behavior.

SHRIMP DISEASE

Both infectious and non-infectious disease has continuously plagued the various sectors of the shrimp industry. Although it is generally recognized that intensive culture systems often encounter serious disease problems, more recent experiences have shown that low-density culture systems can also be severely affected. Diseases of both infectious and non-infectious etiology have been described, but their effects on shrimp and impacts on culture activities remain poorly understood. Diseases caused by viruses, bacteria, fungi and parasites are considered very significant to shrimp culture.

PRINCIPLE CAUSES OF DISEASES IN SHRIMP CULTURE

• Degradation of pond bottom and water quality.

• Loss of balance in environment.
  
• High stocking density with limited water exchange facilities. 
  
• Use of excessive artificial feed and chemicals.
  
• Nutritional deficiency/ poor nourishment. 
  
• Accumulation of unutilized feed followed by its purrefaction by the native heterotrophic microorganisms. 
  
• Poor and inadequate management. 
  
• Inadequate aeration.  
  
• Suboptimal or heavy algal blooms in the pond.  
  
• Physical injury.  
  
• Presence of virulent pathogen in high counts.
  

 

BEHAVIOURAL, EXTERNAL AND INTERNAL SIGNS OF SHRIMP DISEASE

• Change of body colour and pigmentation.
  
• Crowding near the aerator, pond edge and water surface.
  
• Stopping or reduced feed intake and growth.
  
• Becoming lethargic or erratic.
  
• Body and shell soft.
  
• Swollen cephalothorax, abdomen and tail.
  
• Spot on shell, muscle, and erosion of shell and appendages.
  
• Abnormality on gills, muscle, hepatopancreas and intestine.
  

TYPES OF SHRIMP DISEASES

We can divide shrimp disease in many ways. Different types of shrimp disease are discussed below:

A. According to pathogen:

1. Viral Shrimp Disease
   
2. Bacterial Shrimp Disease
   
3. Fungal Shrimp Disease
   
4. Parasitic Shrimp Desease
   

B. Non-infectious disease:

1. Chronic Soft Shell Syndrome
   
2. Black Gill Disease
   
3. Red Disease
   
4. Cramped Tail Disease
   
5. Gas-Bubble Disease
   
6. Muscle Necrosis
   

A. According to pathogen:

I. Viral Shrimp Disease

At least 15 viruses are known to infect cultured and wild marine penaeid shrimp. Reported types include parvoviruses, baculoviruses, reoviruses, togaviruses and rhabdoviruses. Three systemic baculoviruses have recently been described for penaeid shrimp: yellowhead virus (YBV) (Boonyaratpalin et al., 1993), hemolymph baculovirus (Owens, 1993) and systemic ectodermal and mesodermal baculovirus (SEMBV) (Wongteerasupaya et al., 1995). YBV and SEMBV infections have caused drastic mortalities resulting in severe economic losses in shrimp culture facilities in Thailand, Indonesia and India. Also described is a rod-shaped nuclear virus of Penaeus japonicus (RV-PJ) (Inouye et al., 1994) which has been implicated in mass mortalities of cultured P.japonicus in Japan in 1993.

White Spot Syndrome Viral Disease (WSSVD) / China virus disease

Disease signs at the farm level

• characterised by high and rapid mass mortality of rapid onset, mainly in farmed penaeid prawns
  
• can occur at any stage of the grow-out period
  

Disease signs at the tank and pond level

• prawns with white spot disease often do not show distinctive clinical signs
  
• lethargy
  
• cessation of feeding
  
• a few days later, moribund prawns near surface at edge of rearing ponds
  

 

 

 

Clinical signs of disease in an infected animal

• loose shell
  
• white calcium deposits embedded in shell, causing white spots 0.5-2.0 mm in diameter for which the disease is named (but white spot disease can occur without these signs)
  
• darkened (red or pink) body surface and appendages
  
• heavy surface and gill fouling by external parasites
  
• white midgut line through abdomen of severely affected larvae and postlarvae
  

The shell lesions range from minute spots to discs several millimetres in diameter, and may coalesce into larger plates. They are most easily observed by removing the cuticle over the cephalothorax, scraping away any attached tissue with the thumbnail and holding the cuticle up to the light.

White spots in the cuticle are unreliable even for preliminary diagnosis of white spot disease, because similar inclusions can be produced by some bacteria, high alkalinity and other infectious or environmental conditions.

 

 

 

 

 

 

Fig.3: White Spot Syndrome Viral Disease.

 

Disease Causing Agent

White spot syndrome baculovirus. The causative agent of white spot disease is white spot virus, a large DNA virus assigned to the new genus Whispovirus (family Nimaviridae). The virus infects only crustaceans and appears not to be related to any other known viruses. It is not involved in the parasitic disease, common in finfish, also known as white spot.

Geographic Distribution

The term white spot is a description of the characteristic white spot appearance that has accompanied outbreaks of this viral disease around the globe. The mere appearance of white spots is not necessarily indicative of the disease that is caused by this virus. Other things can cause white spots. In P. vannamei, though there are white spots, in the disease in the field, they appear late in the infectious cycle and are much smaller than the classic spots noticed in other shrimp species.

The disease was first reported in shrimp in China in 1992-93. In 1995, it was reported in several shrimp farms located in south Texas. The disease was probably transported from its origins in China by infected shrimp that were used as a bait or food for the shrimp in Texas. This is the first report of a natural infection of crawfish in the United States. It is possible that shrimp escaped from those farms and migrated into the Gulf, which may be the source or our present problem in farmed crawfish.

Host Range

All decapod crustaceans (order Decapoda) including prawns, lobsters and crabs from marine, brackish or freshwater environments, are considered susceptible to infection. However, the disease has mainly been a problem in farmed penaeid (family Penaeidae) prawns.

Crustaceans known to be susceptible whitespot disease: black tiger prawn* (Penaeus monodon), Chinese white shrimp* (Penaeus chinensis), Gulf banana prawn* (Penaeus merguiensis), Indian, banana prawn* (Penaeus indicus), Kuruma prawn* (Penaeus japonicus), Pacific white shrimp*, Penaeus vannamei), red claw freshwater crayfish* (Cherax quadricarinatus), blue shrimp (Penaeus stylirostris), green tiger prawn (Penaeus semisulcatus). White spot virus also occurs naturally in many other decapods, including:
mud crabs* (Scylla serrata, Charybdis feriatus, Portunus pelagicus, P. sanguinolentus)
sand shrimp* (Metapenaeus spp) and other arthropods. Currently, three marine prawn species, Penaeus monodon, P. japonicus and P. merguiensis, and one freshwater species, Macrobrachium rosenbergii, are farmed commercially in Australia.

* naturally susceptible (other species have been shown to be experimentally susceptible)

Impact on the Host

Acutely infected shrimp show rapid reduction in food consumption; lethargy; high mortality rates with cumulative mortalities reaching 100 percent within 3 to 10 days of the onset of clinical signs; acutely infected shrimp often have loose cuticle with white spots (which represent abnormal deposits of calcium salts by the cuticular epidermis) of 0.5 – 2.0 mm in diameter that are most apparent on the inside surface of the carapace; in many cases moribund shrimp display a pink to reddish-brown colouration due to expansion of cuticular chromatophores & few if any white spots.

Monodon Baculo virus Disease (MBV)

Disease signs at the farm level

• lethargy
  

Clinical signs of disease in an infected animal

• emaciation
  
• secondary gill and surface fouling by ectoparasites
  

Gross signs of disease in an infected animal

• white hepatopancreas (digestive gland) and midgut
  

Fig.4: Monodon Baculo virus Disease (MBV)

Disease Causing Agent

Penaeus monodon type baculovirus, MBV.

Geographic Distribution

Widely distributed in cultured shrimp in P.R. China, Taiwan, Indonesia, Philippines, Malaysia, Thailand, Sri Lanka, Singapore, Australia, India, Israel, Kuwait, Oman, Italy, Kenya, Gambia and South Africa. Has been introduced into Tahiti, Hawaii, Brazil, Ecuador, Mexico, Puerto Rico and in several southeastern states of the United States.

Host range

Crustaceans known to be susceptible to the virus: banana prawn* (Penaeus merguiensis), brown tiger prawn* (Penaeus esculentus), caramote prawn* (Penaeus kerathurus), eastern king prawn*, (Penaeus plebejus), giant tiger prawn* (Penaeus monodon) – most susceptible, grooved tiger, prawn* (Penaeus semisulcatus), red endeavour prawn* (Metapenaeus ensis), redtail prawn* (Penaeus pencillatis)

* naturally susceptible (other species have been shown to be experimentally susceptible)

 

 

Impact on the Host

Lethargy, anorexia, dark coloured, and with heavy surface fouling. Acute MBV causes loss of hepatopancreatic tubule and midgut epithelia and consequently, dysfunction of these organs, often followed by secondary bacterial infections. MBV has been linked with high mortalities (over 90%) in late postlarvae and juvenile shrimp in many culture facilities. It has caused heavy mortalities (70% of all stages of P. monodon in the Philippines and 90% of postlarval P. monodon in Madras, India), and is considered partially responsible for the collapse of the shrimp culture industry in Taiwan in the late 1980s. Usually juvenile and adult P. monodon are more resistant to MBV than larval shrimp. Although good culture practices may enhance survival of MBV infected stocks, growth, crop value and performance may be significantly reduced and MBV may predispose infected shrimp to infections by other pathogens, with corresponding higher mortality rates.

Yellow Head Disease (YHD)

Disease signs at the farm level

• moribund prawns aggregate near surface at pond edges
  
• infected 5-15 gram prawns begin feeding at abnormally high rate for several days and then cease feeding entirely
  
• mass mortality three days after cessation of feeding
  

Clinical signs of disease in an infected animal

• white, yellow or brown gills
  
• yellowing of the cephalothorax and general bleaching of body
  
• yellow, swollen digestive gland makes head appear yellow
  

Fig.5: Yellow Head Disease (YHD)

Disease agent

The causative agent of yellowhead disease is yellow head virus (YHV), a corona-like RNA virus that has been classified in the genus Okavirus, family Ronaviridae and order Nidovirales.

Host range

YHV is highly infectious for most known species of cultivated penaeid prawns.

Crustaceans known to be susceptible to yellowhead disease: black tiger prawn* (Penaeus monodon) – primarily, Gulf banana prawn* (Penaeus merguiensis), northern white shrimp*, (Penaeus setiferus), prawn* (Palaemon styliferus), red endeavour prawn* (Metapenaeus ensis), tropical krill* (Acetes spp), blue shrimp (Penaeus stylirostris), northern brown shrimp (Penaeus aztecus), northern pink shrimp (Penaeus duorarum), Pacific white shrimp (Penaeus vannamei).Until proven otherwise, it should be assumed that most penaeid prawns worldwide are susceptible to infection with yellowhead disease.

* naturally susceptible (other species have been shown to be experimentally susceptible)

 

 

Impact on the Host

P. monodon suffers acute epizootics with high cumulative mortalities which may reach 100% within 3-5 days after appearance of clinical signs. Infection is horizontally transmitted. Tiger shrimp postlarvae (PL) 15 were found to be resistant to infection but stages PL 20-25 and on growing juveniles through to subadults were found to be highly susceptible.

Geographic Distribution

Diagnosed in Thailand, but distribution may be wider in southeast Asia and the Indo-Pacific region as unconfirmed reports of outbreaks include Malaysia, Sri Lanka, Indonesia, Philippines, China and possibly Taiwan. A morphologically similar virus with similar cytopathology but apparently asymptomatic as for RSP was reported from P. monodon in Australia and called Lymphoid organ virus (LOV, but is distinct from another virus LPV also from the lymphoid organ and from Australian penaeids).

Penaeus monodon, the giant black tiger shrimp, is the species primarily affected. Penaeus merguiensis, Palaemon styliferus, and Metapenaeus ensis were experimentally infected. However, P. merguiensis, that were acquired incidentally as postlarvae in pond source water and co-cultured with P. monodon that suffered high mortalities with YHD, showed no signs of the disease. Palaemon styliferus is a carrier that survives the infection well; Euphausia spp., Krill (Acetes spp.) and other small shrimp species could also carry the disease. Juvenile stages of American penaeids, Penaeus vannamei, Penaeus stylirostris, Penaeus setiferus, Penaeus aztecus, and Penaeus duorarum were experimentally infected but postlarval stages were found to be relatively resistant to challenge.

Infectious Myonecrosis Viral Disease (IMNV)

Disease Causing Agent

Infectious myonecrosis virus (IMNV).

Geographic Distribution

It is found in North-eastern Brazil and South-East Asia.
IMN occurs in Penaeus vannamei farmed in brackish and marine water.

Fig.6: Infectious Myonecrosis Viral Disease

Impact on the Host

Affected shrimp present focal to extensive white necrotic areas in striated (skeletal) muscles, especially in the distal abdominal segments and tail fan, which can become necrotic and reddened in some individual shrimp. These signs may have a sudden onset following stresses (e.g. capture by cast-net, feeding, sudden changes in temperature or salinity). Severely affected shrimp may have been feeding just before the onset of stress and will have a full gut. Such severely affected shrimp become moribund and mortalities can be instantaneously high and continue for several days. Exposing the paired lymphoid organs by simple dissection will show that they are hypertrophied to 3–4 times their normal size.

Haepatopancreatic Parvo Viral Disease (HPV)

Disease Causing Agent

Hepatopancreatic parvovirus disease, HPV.

Geographic Distribution

Enzootic in captive, wild and hatchery-reared penaeids in Korea, Yellow Sea area of P.R. China, Taiwan, Philippines, Indonesia, Malaysia, Singapore, Australia, Kenya, Israel and Kuwait. Introduced into South America with imported and cultured Asian penaeid shrimp and in now found in cultured P. vannamei in North and South America and in cultured and wild penaeid shrimp along the Pacific coast of western Mexico and coastal El Salvador and Brazil. HPV may now have a cosmopolitan distribution.

 

Fig.7: Haepatopancreatic Parvo Viral Disease

Impact on the Host

Typically affects mid-juvenile stages with signs of necrosis and atrophy of the hepatopancreas, poor growth rates, anorexia and reduced preening with a concurrent increase in surface and gill fouling by epicommensal organisms. Increased mortality, particularly under stress or crowding conditions has been noted. Although HPV has been accused of causing serious disease losses on farms, it is seldom observed alone and usually occurs in multiple agent epizootics with opportunistic pathogens like Vibrio sp. Thus, the significance of HPV in causing epizootics and economic losses is not fully understood.

Infectious Hypodermal and Haemtopoitic Necrosis Viral Disease (IHHNV)

Disease signs at the tank and pond level

• reduced food consumption
  
• sometimes prawns repeatedly float slowly to water surface, roll over and then sink to bottom
  
• increasing morbidity/mortality
  

Clinical signs of disease in an infected animal

• reduced and irregular growth in juveniles and subadults (runt-deformity syndrome)
  
• white to buff mottling of shell, especially at the junction of shell plates of the abdomen
  
• giant black tiger prawn (Penaeus monodon) may appear blue
  
• deformed rostrums grow to one side .
  

 

 

 

    

Fig.8: Runt deformity syndrome (RDS) caused by IHHNV in Penaeus vannamei. Two shrimp specimens showing deformed rostra– one curved down and the other up and both shorter than normal.

 

Disease agent

Infectious hypodermal and haematopoietic necrosis (IHHN), or runt-deformity syndrome, is caused by a parvovirus.

Host range

Crustaceans known to be susceptible to IHHN: blue shrimp* (Penaeus stylirostris), giant black tiger prawn* (Penaeus monodon), grooved tiger prawn* (Penaeus semisulcatus), Kuruma prawn* (Penaeus japonicus), Pacific white shrimp* (Penaeus vannamei)
southern white shrimp* (Penaeus schmitti), western white shrimp* (Penaeus occidentalis), yellow-leg shrimp* (Penaeus californiensis), Chinese white shrimp (Penaeus chinensis), Gulf banana prawn (Penaeus merguiensis), Indian banana prawn (Penaeus indicus), northern brown, shrimp (Penaeus aztecus), northern pink shrimp (Penaeus duorarum), northern white shrimp (Penaeus setiferus).

* naturally susceptible (other species have been shown to be experimentally susceptible)

Impact on the Host

Reduced food consumption, cannibalism, increased mortality. In some cases, shrimp repeatedly rise slowly to surface, roll over and sink to bottom. Disease particularly severe among juveniles in high density tank and raceway cultures. Some members of the population which survive IHHNV infection and/or epizootics apparently carry the virus for life and pass it onto their progeny and other populations by vertical and horizontal transmission. Although IHHNV may cause 80-90% cumulative mortalities in postlarvae and juveniles, the aetiological and economic significance in Asia remains unclear.

Geographic Distribution

Enzootic in Taiwan, Singapore, Malaysia, Thailand, Indonesia, Australia and Philippines and possibly also enzootic in Ecuador, Peru, and Central America. Thought to have been introduced and now widely distributed in cultured penaeids in the southeast United States, Caribbean, Brazil, Hawaii, Guam, Tahiti, New Caledonia and Israel.

Taura Syndrome Disease (TSV)

Disease signs at the farm level

• lethargy
  
• cessation of feeding
  
• animals gather at pond edge when moribund
  

Clinical signs of disease in an infected animal

• pale red body surface and appendages
  
• tail fan and pleiopods particularly red
  
• shell soft and gut empty
  
• death usually at moulting
  
• multiple irregularly shaped and randomly distributed melanised cuticular lesions
  

Fig.9: Taura Syndrome Disease (TSV) in white shrimp.

Disease agent

Taura syndrome is caused by Taura syndrome virus (TSV), a small picorna-like RNA virus that has been classified in the new family Dicistroviridae.

Host range

Crustaceans known to be susceptible to Taura syndrome: blue shrimp* (Penaeus stylirostrus), Pacific white shrimp* (Penaeus vannamei), Chinese white shrimp (Penaeus chinensis), giant black tiger prawn (Penaeus monodon), Kuruma prawn (Penaeus japonicus), northern brown, shrimp (Penaeus aztecus), northern pink shrimp (Penaeus duorarum), northern white shrimp (Penaeus setiferus), southern white shrimp (Penaeus schmitti).

* naturally susceptible (other species have been shown to be experimentally susceptible)

Impact on the Host

The disease has three distinct but overlapping phases, namely acute, transition and chronic. The disease cycle has been characterized in detail in Litopenaeus vannamei. L. vannamei is particularly susceptible to this disease. After infection either by cannibalism or water-borne exposure, the acute phase develops. Clinical signs can occur as early as seven hours after infection in some individuals. Infected shrimp display anorexia, lethargy, erratic swimming behavior, opacification of the tail musculature, soft cuticle and, in naturally occurring infection, chromatophore expansion (red tail). Histologically, this phase is characterized by nuclear
pyknosis/karyorrhexis and numerous cytoplasmic inclusion bodies in the subcutis and cuticular epithelium within the appendages, foregut, hindgut, general body cuticle and the gills. The inclusions give a buckshot appearance to the tissue and are considered pathognomonic for the disease. The acute phase can last up to 7 days and mortality rates up to 95% can occur. Shrimp that survive this first phase move into a transitional phase (roughly day 5 to 8 post-exposure). Characteristic of this phase are variably shaped and sized melanized lesions that can be seen on the head and the tail of the shrimp. If the shrimp undergoes another successful molt following this phase it will cast off the melanized lesions and enter the chronic phase. The chronic phase is characterized histologically by the absence of acute lesions and the presence of lymphoid organ spheroids (LOS) of successive morphogeny. Lymphoid spheroids are not by themselves characteristic of Taura syndrome infection and can be seen in other viral disease of shrimp such as infection with white spot syndrome virus. The chronic phase is first seen 6 days post infection and can persist for an undetermined period of time, at least 8 months under experimental conditions. Diagnosis of the disease during this phase is problematic as shrimp do not display any outward signs of the disease. Shrimp surviving outbreak of TSV seem to be refractory to reinfection while remaining infectious.

Geographic Distribution

Taura syndrome is one of the more devastating diseases affecting the shrimp farming industry worldwide. Since its first description in Ecuador, it has spread to all shrimp-growing countries of the Americas and outbreaks have been described in many South-East Asian regions. It was first thought that the disease had a toxic etiology and was caused by pesticides used on nearby banana plantations. The infectious cause of the disease is now widely accepted.

Baculoviral midgut gland necrosis

Disease signs at the tank and pond level

• larvae float inactively on the surface
  

Clinical signs of disease in an infected animal

• midgut gland (hepatopancreas) suddenly turns white in larvae and postlarvae
  
• high mortality
  
• white midgut line seen through abdomen
  

Disease agent

Baculoviral midgut gland necrosis virus is currently an unassigned virus of the family Baculoviridae. It was known as Penaeus japonicus nonoccluded baculovirus (PjNOB) before it was removed from the classification structure by the International Committee on Taxonomy of Viruses in 1995.

Host range

Crustaceans known to be susceptible to baculoviral midgut gland necrosis: eastern king prawn* (Penaeus plebejus), Kuruma prawn* (Penaeus japonicus), Chinese white shrimp (Penaeus chinensis), giant black tiger prawn (Penaeus monodon), grooved tiger prawn (Penaeus semisulcatus).

* naturally susceptible (other species have been shown to be experimentally susceptible)

Epidemiology

• Baculoviral midgut gland necrosis strikes suddenly and high mortalities follow quickly.
  
• Infection in hatcheries is believed to arise from wild-caught female spawners.
  
• The virus causes high mortality of larvae; late postlarvae tend to be more resistant.
  
• The virus can persist and retain infectivity for up to 20 days in water averaging 15°C.
  
• Transmission is horizontal, through faeces shed during spawning.
  
• The disease affects larvae and up to 20 days of postlarval development (PL-20).
  
• Mortalities are highest (up to 98%) at 9-10 days of postlarval development (PL-9-10).)
  
• There is typically a decrease in mortality rates as the postlarvae reach PL-20.
  

 

 

Gill-associated virus disease

Disease signs at the tank and pond level

• high mortality
  
• moribund prawns aggregate near surface at pond edges
  
• cessation of feeding
  

Clinical signs of disease in an infected animal

• reddening
  
• biofouling with exoparasites
  
• emaciation
  

 

Fig.10: Penaeus monodon infected with gill-associated virus.

 

Disease agent

The causative agent is gill-associated virus (GAV), a corona-like RNA virus that has been classified with yellow head virus in the genus Okavirus, family Ronaviridae and order Nidovirales. Comparison of DNA sequences indicates that GAV and yellow head virus are closely related, but distinctly different viral strains or species.

 

Host range

Crustaceans known to be susceptible to GAV disease: black tiger prawn* (Penaeus monodon), brown tiger prawn (Penaeus esculentus), Gulf banana prawn (Penaeus merguiensis), Kuruma prawn (Penaeus japonicus).

* naturally susceptible (other species have been shown to be experimentally susceptible)

Epidemiology

The epidemiology of GAV is thought to be very similar to that of yellow head virus:

• Transmission may be horizontal, direct from the water column and through ingestion of infected material.
  
• Vertical transmission also occurs from infected broodstock, causing chronic infection in postlarvae.
  
• Viral multiplication and disease appear to be induced by environmental stress.
  
• Massive mortality usually occurs among early to late juvenile stages in rearing ponds.
  
• Vectors may include asymptomatic carrier crustaceans.
  
• GAV occurs commonly as a chronic infection in healthy broodstock and farmed black tiger prawns in eastern Australia. It has also been associated with acute infections and disease outbreaks in ponds, causing high mortality, but produces gross signs and patterns of tissue tropism different from those for yellow head virus. In its chronic form, GAV has also been called lymphoid organ virus.
  

Spawner-isolated mortality virus disease

Signs of disease

Important: animals with disease may show one or more of the signs below, but disease may still be present in the absence of any signs.

Disease signs at the farm level

• lethargy
  
• moribund prawns aggregate at water surface and pond edges
  
• slow and sometimes erratic swimming
  

Clinical signs of disease in an infected animal

• general discolouration
  
• biofouling with exoparasites
  
• emaciation
  

Disease agent

Spawner-isolated mortality virus (SMV), a parvovirus, is one of several viruses associated with mid-crop mortality syndrome, which caused significant mortalities among cultured juvenile and subadult giant black tiger prawns cultured in Australia from 1994 to 1996.

Fig.11: Small runt has spawner-isolated mortality virus disease; larger prawn is a control

Host range

Crustaceans known to be susceptible to SMV: giant black tiger prawn* (Penaeus monodon) – adult red claw freshwater crayfish* (Cherax quadricarinatus). Until proven otherwise it is reasonable to assume that many cultured crustaceans would be susceptible to infection.

 

Epidemiology

• Outbreaks most commonly occur in 12-15 gram prawns (midway through the reproductive stages). However, they can occur at any stage and at any time of the year.
  
• Transmission is horizontal, via the water and cannibalising of weak or moribund prawns.
  
• Shedding of the virus via faeces is a likely source of transmission, as are infected transport and intake water, and nets and other equipment.
  
• A major source of infection in ponds is via apparently healthy carrier fry that have acquired the virus from spawners in infected hatcheries.
  
• Mortalities have been known to occur in broodstock.
  
• Although vertical transmission has not been demonstrated, the virus is found in the reproductive organs of male and female prawns.
  

Tetrahedral baculovirosis

Signs of diseases

Important: animals with disease may show one or more of the signs below, but disease may still be present in the absence of any signs.

Disease signs at the farm level

• reduced feeding
  

Clinical signs of disease in an infected animal

• high mortality in larval, postlarval and juvenile prawns
  
• reduced growth rates in surviving juveniles and adults
  
• increased fouling with exoparasites
  

 

 

Gross signs of disease in an infected animal

• milky-white midgut
  

There are few visible signs indicating infection with this disease other than rapid high mortality of hatchery prawns in the early life stages. Therefore, diagnosis is usually based on microscopic and histological examination.

Disease agent

The causative agent is Baculovirus penaei.

Host range

Crustaceans known to be susceptible to tetrahedral baculovirosis: aloha prawn* (Penaeus marginatus), blue shrimp* (Penaeus stylirostrus), giant black tiger prawn* (Penaeus monodon), northern brown shrimp* (Penaeus aztecus), northern pink shrimp* (Penaeus duorarum), northern white shrimp* (Penaeus setiferus), Pacific white shrimp* (Penaeus vannamei), Pomada prawn* (Protrachypene precipua), red-spotted shrimp* (Penaeus brasiliensis), redtail prawn* (Penaeus pencillatus), roughback shrimp* (Trachypenaeus similis), San Paulo shrimp* (Penaeus paulensis), southern brown shrimp* (Penaeus subtilis)
southern white shrimp* (Penaeus schmitti).

* naturally susceptible (other species have been shown to be experimentally susceptible)

Epidemiology

• Transmission is horizontal, directly from the water column or through cannibalism.
  
• Eggs and newly hatched nauplii may be exposed to the virus through faeces of infected adult spawners taken from the wild.
  
• Infection is restricted to the hepatopancreas and anterior midgut.
  
• Tetrahedral baculovirosis does not occur in wild populations infected with Baculovirus penaei.
  
• Crowding, chemical stress or environmental stress may increase pathogenicity and the prevalence of disease.
  
• Transmission typically occurs via the oral route, with cannibalism and faecal-oral contamination the principal mechanisms.
  

Monodon Slow Growth syndrome (MSGs)

General

• From 2000, economic losses from this disease became apparent and more attention was given to this by the industry.
  
• It affects only black tiger shrimp and the most drastic consequence to the farmer is the uncertainty of final harvest output and value.
  
• In a typical case, after 3–4 months of culture, the farmer sees size variations from 80 pcs/kg to 300 pcs/kg in a single pond.
  

Prevention

• One way to overcome MSGs is to use good quality PL.
  

 

 

 

 

 

 

Fig.12: Extreme size variation in black tiger shrimp infected with MSGs

II. Bacterial Shrimp Disease

The bacteria causing diseases of penaeid shrimp constitute part of the natural microbial flora of seawater. Accumulation of un-utilized feed and metabolites of shrimp in the culture tanks/ ponds enrich the water with organic matter that supports the growth and multiplication of bacteria and other microorganisms. Bacterial infections of shrimp are primarily stress related. Adverse environmental conditions or mechanical injuries are important predisposing factors of bacterial infections and disease. The most common shrimp pathogenic bacteria belong to the genus Vibrio. Other Gram-negative bacteria such as Aeromonas spp., Pseudomonas spp., and Flavobacterium spp., are also occasionally implicated in shrimp diseases.

Bacterial Septocaemia (Vibrio Disease)

Signs and symptoms  

This is one of the severe systemic diseases caused by bacteria. The affected shrimps are lethargic and show abnormal swimming behaviour. The pereopods are pleopods may appear reddish due to expansion of chromatophores and the shrimps may show slight fexure of the abdominal musculature. In severly affected shrimp, the gill covers appear flared up and eroded. In more severe cases, extensively melanised black blisters can be seen on the carapace/abdomen.  

Fig.13: Bacterial Septocaemia (Vibrio Disease)

Causes  

Bacteria such as Vibrio alginolyticus, V. anguillarum, or V. parahaemolyticus.  

Diagnosis  

Based on gross signs and symptoms and confirmed by isolation of pathogen from haemolymph by standard microbiological methods and histopathology.  

Prevention  

Maintain good water quality and reduce the organic load by increased water exchange.  

 

Control  

Increase water exchange with good quality seawater. Feed shrimps with antibiotic fortified fees 9only after ascertaining in-vitro sensitivity of the pathogen), e.g. feeds containing oxytetracycline @ 1.5g/Kg, fed at 2-10% of body weight for 10-14 days along with proper water and pond management. Sufficient withdrawl period (about 25-30 days) should be allowed for the antibiotic to become inactive or harmless. 

Luminescent Bacterial Disease

Signs and symptoms  

The infected larvae appear luminescent in darkness and suffer heavy mortality.  

Cause  

Luminescent bacteria such as Vibrio harveyi.  

Fig.14: Luminescent Bacterial Disease

Diagnosis  

Based on gross signs and symptoms and microscopically demonstrating swarming bacteria within the haemocoel of moribund prawn larvae. The luminiscent bacteria can be isolated on Zobell’s marine agar or a selective medium for luminous bacteria and identified based on their morphological and biochemical characteristics.  

 

Prevention  

Use chlorinated (calcium hydrochlorite 200 ppm for 1 hour) and ultraviolet irradicated water. Clean bottom debris in rearing tanks daily.  

Control  

Exchange water upto 80%daily with sand filltered /UV sterlizes seawater. 

Filamentous Bacterial Disease

Signs and symptoms  

The affected shrimp larvae show fouling of gills, setae, appendages and body surface. Moulting is impaired and the larval shrimp may die due to hypoxia.  

Cause  

Filamentous bacteria such as Leucothrix mucor  

Diagnosis  

Based on gross signs and symptoms and by microscopically demonstrating filamentous bacterial fouling of body surface and appendages of shrimp larvae.  

Prevention  

Maintain good water quality with optimal physico-chemical conditions.  

Control  

0.25-1 ppm copper sulphate bath treatment for 4-6 hours.

Brown Spot Disease (Shell Disease or Rust Disease)

Signs and symptoms  

The affected animals show presence of brown to black eroded areas on the body surface and appendages.  

Causes  

Bacteria such as Vibrio spp., Aeromonas spp., and Flavobacterium spp., with chitinolytic activity. 

Fig.15: Brown Spot Disease (Shell Disease or Rust Disease)

 

Diagnosis  

Based on gross signs and symptoms and confirmed by isolation and identification of bacteria from the site of infection by standard microbiological methods.  

Prevention  

Reduce organic load in water by increased water exchange. Avoid unnecessary handling and overcrowding to minimise chances of injury and infection.  

Control  

Induce moulting by applying 5-10 ppm teaseed cake. Improve water quality by increasing water exchange. If there is no improvement, shrimps may be fed with antibiotic (after ascertaining in-vitro sensitivity of the pathogen) fortified feeds (e.g., 1.5g oxytetracycline /Kg of feed) at 2-10% of the biomass for 10-14 days. 

 

 

Necrosis of Appendages

Signs and symptoms  

The tips of walking legs, swimmerets and uropods undergo necrosis and become brownish black. The setae, antennae and appendages may be broken and melanized.  

Cause  

The epibiotic bacteria such as Vibrio spp., Pseudomonas spp., Aeromonas spp. and Flavobacterium spp.  

Fig.16: Necrosis of Appendages

Diagnossis  

Based on gross signs and symptoms  

Prevention  

Maintain good water qaulity. Stock at optimum density. Avoid unnecessary handling of the shrimps, which may lead to injuries and necrosis.  

Control  

Induce moulting by applying 5-10 ppm teaseed cake. 

 

 

III. Fungal Shrimp Disease

Fungi such as Fusarium spp. cause infections in nauplii, protozoea, juveniles and adults. Black gill disease is often caused by this fungus. Fusarium infects dead or damaged tissue caused by wounds or other infections resulting in locomotory difficulties due to mycelial growth. High mortality in susceptible populations. Fouling of the gills by these organisms probably results from poor husbandry. The fungus can be identified by microscopic examination of its characteristic canoe shaped micro-conidia. Other oomycetous fungi such as Saprolegnia spp. and Leptolegnia spp. are also known to affect shell of shrimp and produce dark necrotic lesions causing gradual mortality.

Larval Mycosis

Signs and symptoms  

Affected shrimp larvae appear qpaque. The protozoeal and mysis stages are highly susceptible. Within 1-2 days, whole stock of shrimp larvae may suffer mortality.  

Cause  

Oomycetous fungi such as Lagenidium spp., Sirolpidium spp., and Halipthoros spp.  

Diagnosis  

Microscopic demonstration of presence of extensively branched non-septate, fungal hyphae within the body cavity of the hrimp larvae.  

Prevention  

Clean tank bottom periodically. Disinfect the tanks and other equipment in the hatchery from time to time. Treat spawners with 5 ppm treflan bath for one hour.  

Control  

Treflan (Trifluralin) 0.1-0.2 ppm bath for one day.

 

IV. Parasitic Shrimp Disease

Among the disease causing organisms of shrimp, parasites, especially protozoan parasites form an important group. Although, several diseases caused by parasites have been noticed in shrimp, often, chronic conditions caused by protozoans play a crucial role in shrimp production. The protozoa, affecting shrimp can be grouped as parasites and commensals.

Fig.17: Parasitic disease

Bopyrid Parasitic Infestation

Signs and symptoms

These parasites can be found lodged in the brachial cavity, which is clearly evident on inspection of the animals. Affected shrimps suffer from impaired respiration  

Cause

Bopyrid parasite, Epipenaeon spp.  

Fig.18: Bopyrid Parasitic Infestation

Diagnosis

Based on gross signs and symptoms and identification of the parasite by gill biosy.  

Prevention

Not known  

Control

Affected shrimps may be separated and given formalin (150-250 ppm for 1 hour bath) treatment

Protozoan Fouling

Signs and symptoms  

Affected shrimps are restless and their locomotion and respiratory functions are hampered. In heavily infected juvenile and adult shrimps, one can observe fuzzy mat-like appearance due to ciliate fouling.  

Cause  

The protozoans such as Vorticella, Zoothamnium, Epistylis, Acineta and Ephelota.  

Fig.19: Protozoan Fouling

Diagnosis  

Based on gross signs and symptoms and microscopic demonstration of ciliates.  

Prevention  

Maintain good water quality. Reduce organic load and silt in water exchange with good quality water.  

Control  

15 to 20 ppm formalin (single treatment) for ponds or dip treatment of affected individuals in 50-100 ppm formalin for 30 min. Maintain good aeration during treatment. 

Cotton Shrimp Disease or Milk Shrimp Disease

Signs and symptos  

Muscle of affected shrimps appears cooked. In severely affected shrimps, the exoskeleton appears bluish black, and white tumor-like swellings may be found on gills and subcuticle.  

Cause  

Microsporadia such as Agmosoma, Ameson and Pleistophora.  

Fig.20: Cotton Shrimp Disease or Milk Shrimp Disease

Diagnosis  

Based on gross signs and symptoms and microscopic demonstration of developmental stages of microsporadia in the affected tiisues.  

Prevention  

Affected animals should be destroyed and buried with lime away from the farms. After harvesting, the pond bottom should be throughly dried to kill the spores of the microsporadia.  

Control  

Not known 

Enterozoic Cephaline Gregarine Infection

Signs and symptoms  

Affected shrimps are anorexic, lethargic and weak. Low levels of mortalities.  

Cause  

Cephaline gregarines (protozoan) such as Cephelolonus sp.  

Fig.21: Enterozoic Cephaline Gregarine Infection

Diagnosis  

Microscopic demonstration of developmental stages of the parasite in the digestive system.  

Prevention  

Avoid wild seeds.  

Control  

Not known. 

B. Non-Infectious Diseases

Non-infectious disease are common in the grow-out farms, as influences of nutritional factors, environmental factors such as temperature extremes and oxygen depletion, toxicity from biotic and abiotic origins, become critical during the lengthy culture period.

Chronic Soft Shell Syndrome

Signs and symptoms  

Shell of the prawn is persistently soft, loose and papery for several weeks. In acutely affected shrimp, lesions/blisters may develop and the body becomes very soft. The shrimps become weak and susceptible to cannibalism. It is very common in traditional, extensive, seasonal as well as perennial ponds. Severely affected P. indicus show undulating gut in the first three abdominal segments.  

Cause  

This disease is found to occur during adverse environmental conditions like sudden increase or decrease of temperature and salinity of ware, high soil pH, highly reducing conditions in soil, low organic matter content in soil, low phosphate content and pesticide pollution in water, nutritional deficiency in insufficient water exchange.  

Diagnosis  

Based on gross signs and symptoms  

Prevention  

Feed adequately with balanced diets. Maintain good water quality by increased water exchange.  

Control  

Restore good water quality by increased water exchange. Feed shrimps adequately with feeds such as fresh clam meat @14% of body weight for 2-4 weeks daily or formulated feeds fortified with calcium and phosporus.

Black Gill Disease

Signs and symptoms 

The affected prawns show brown to black spots on the gills. In acute cases gills may completely become brown or black with atrophy and necrosis. 

Cause 

A number of causes have been assigned to this disease. Presence of excessive levels of toxic substances like nitrate, ammonia, acids, crude oils, potassium premanganate, copper, cadmium, ozone, etc. in the culture water may lead to black gill disease. Presence of 2-3 ppm nitrite leads to black gill condition resulting in low levels of mortalities. High organic matter content and highly reducing conditions in soil also cause black gills. Infection with infectious hydrothermal and haematopoietic necrosis (IHHN) virus, bacteria (Vibrio, Cytophaga, Flexibacter) and fungi (Fusarium and Halithoros) also leads to black gill syndrome. 

Fig.22: Black Gill Disease

Diagnosis 

Based on the signs and symptoms and histopathology. Black gill condition due to microbial etiology may be confirmed by standard microbiological methods. 

Prevention 

Maintain good water quality and avoid overfeeding. 

Control 

Treatment of this disease depends upon cause of the disease. When the disease is due to pollution of pond water with toxic substances, the water quality must be improved by sufficient water exchange and aeration. If the disease is due to microbial infection, antibiotic treatment may be given after knowing the in-vitro sensitivity of the pathogen. 

 

 

 

Red Disease

Signs and symptoms

The disease starts as yellowish dicolouration of the body, subsequently, the appendages turn red and finally the whole shrimp becomes red. In the cephalothorax region, excessive fluid with foul odour may be found 

Cause

Definite causative agent of this disease is not known. Presence of toxins in feed, prolonged high pH and low salinity of water lead to red disease. 

Diagnosis

Based on gross signs and symptoms and confirmed by demonstration of massive necrosis of hepatopancreas in histological sections. 

Prevention

Use fresh and properly stored feeds. Reduce organic matter content in water by increased water exchange. Do not use high doses of lime during ound preparation since it increases pH of water during culture 

Control

Not known. Avoid using old and rancid feed.

Cramped Tail Disease

Signs and symptoms  

Affected prawns have very rigid flexed abdomen. These prawns lie on their sides at the bottom of the pond and are susceptible to cannibalism.  

Cause  

Exact cause for this disease is not known. The disease may be due to adversse environmental conditions.  

 

Diagnosis  

Based on gross signs and symptoms.  

Prevention  

Avoid handling shrimps during hot humid climate.  

Control  

Not known. 

Gas-Bubble Disease

Super saturation of atmospheric gases and oxygen in the pond can result in the gas-bubble disease, which affects the shrimps of all sizes. Presence of gas bubble in the gills or under the cuticle is the characteristic of this disease. Gas bubble disease due to oxygen is not lethal, while that of nitrogen can be lethal. The threshold saturation level to cause the gas-bubble, in the case of nitrogen is 118 % while that of oxygen is 250 % of normal saturation. The severely affected or dead shrimp due to this disease may float near the water surface. Super saturation of the gases must be avoided to prevent the disease.

Muscle Necrosis

Shrimps of all life stages are affected with muscle necrosis. Affected shrimps are characterized by the presence of white opaque areas in body musculature, usually in the lower abdomen or some times in the appendages. The condition is reversible in the early stages if the corrective measures are taken, but in severe cases sloughing of the affected areas occurs due to secondary bacterial infection leading to death. This disease is associated with poor environmental conditions such as low oxygen levels, and salinity or temperature shock. Overcrowding and poor handling also can cause muscle necrosis. Avoidance of overcrowding, proper handling and maintenance of favorable environmental factors may help to contain the disease.

 

 

OVERCOME THE DISEASE PROBLEM IN SHRIMP CULTURE

Probably the biggest single problem faced by shrimp farmers is sudden environmental fluctuations that accompany the rainy season. Sudden changes in salinity and temperature have been implicated in many outbreaks. As the disease moves from one area to another the viral load in the environment will increase to the point where the virus will be ever present. Ideally shrimp should be destroyed once they are ill to prevent high loads of the virus from entering the environment. Unfortunately this is usually not practical. Harvesting shrimp is and should be encouraged even if shrimp are too small to sell. Cutting losses and minimizing the spread of the virus are to the farmer’s advantage. It is believed that one of the major methods for the movement of virus (and others) has been the movement of infected PL’s. If this can be stopped, it should lessen the rate of spread of the virus. Many countries have taken steps to ensure this though how successful they will be will only be apparent with time. Once the virus gains a foothold it appears that it is there to stay. Fortunately viral diseases such as BP, IHHN, TSV, and MBV, the impact of the disease lessen with time. Pesticides can be used to kill the vectors before stocking in the ponds. Usually a very potent pesticide is added to the water to kill any crustaceans and other vectors that might be present in the pond carrying the virus. But the problem is the costs would be quite high and the huge amounts of pesticides that would have to be dumped into the ecosystem are not desirable. This should be discouraged and only considered as a very last resort. Filtering intake water into the pond is one viable approach to eliminating some vectors. Conventional filters may be problematic due to the large demands for water. Though this demand can be moderated and relatively small amounts of water added to the system. Filters that use plant fibers to trap everything in conjunction with serial mesh filtration might be useful. Using 250 micron or smaller mesh filters including small mesh bags can be helpful as well. Another recommendation is to avoid the exchange of water. There appears to be some merit in this in that recent outbreaks of WSSV in S. Carolina in the USA have been associated with the addition of water to ponds. Whether this stressed the shrimp and set off an epizootic or introduced vectors and virus into the ponds is not known. In intensive systems, aeration is used while it is not in semi-intensive systems. The ability to aerate the water mechanically without resorting water exchange might be very useful in those ponds where oxygen levels can not be managed without water exchange. Animals that are positive for the virus by PCR are not purchased. In some cases it has been reported that screening stocked animals for the presence of the virus has been found to be a useful tool to follow the status of the disease in the population. This can be used to time harvests and to minimize the potential spread of problems to other ponds and/or neighbors. By avoiding nauplii or PL’s from a source that could be or is infected with the virus. It is likely that iodine and water washes remove and destroy the virus when used on eggs, nauplii and PLs. It is essential that this process be consistent. Hatcheries must maintain good biosecurity measures and examine each batch of animal. The hatchery needs to be constructed to prevent the introduction of the virus from the ocean. There are some ways that we can do this and many that you can not. Some of the things that you can do are:

• Increase acclimation times before stocking
  
• By using non-specific immune stimulants (NSIS) and fortified mineral and vitamin diets to increase stress tolerance
  
• Consider must be taken during stocking times of the year that we know there will not be experiencing severe stresses from sudden changes in temperature and salinity. It has been reported that these types of stresses can precipitate an epizootic in a population that carries the virus.
  
• By using good quality diets and continue the use of NSIS through out the life cycle
  
• By stocking at lower densities
  
• Monitoring for the presence of vectors carrying WSSV in the ponds and control them.
  

All of the data to date suggests that shrimp have relatively primitive immune systems that can not respond to vaccination. In fact it appears that we can not vaccinate shrimp in any sense of the word. Their immune response is short lived, non-specific in nature and provides a modest level of immunity. Though it is possible to exploit this with a variety of polysaccharides, there are very few reports of success using these compounds in the field. The compound with the most field data is a bacterial based material. Lab and field studies have shown a wide range of potential benefits, though like all other tools, these require that they be used as part of on overall management strategy geared towards minimizing the impact of the pathogen.

 

Disease Prevention in Hatcheries

Location of hatchery  

The hatchery should be located in place where good quality water is ensured for maintenance of broodstock, spawning, larval rearing, phytoplankton culture and all other hatchery activities  

Water treatment  

Disinfect the seawater with calcium hypochlorite (20-30 ppm) or sodium hypochlorite (150 ppm) for 1-2 days ensuring thorough mixing to eliminate pathogenic microorganisms. Remove excess chlorine from the seawater by neutralising with sodium thiosulphate. Filter the seawater and preferably sterilize by UV treatment.  

Cleanliness of hatchery facilities  

The tanks used for broodstock, spawning, larval rearing, etc. should be kept thoroughly clean by scrubbing, disinfecting and thorough rinsing.  

Treatment of broodstock  

The brood shrimps should be treated with 2ml/100 l formalin (20 ppm) and oxytetracycline (10 ppm) for 30 minutes before stocking in broodstock tanks to reduce the population of epibiotic microflora  

Care at the time of spawning  

 Remove the scum formed after spawning.  

Stocking of nauplii  

Stock only healthy nauplii at an optimal stocking density. The nauplii may be disinfected by dip treatment in 20-30 ml formalin/100 l (200-300 ppm) or 0.1 ppm iodophore.  

 

Care during larval rearing  

Remove the unused feed, sediments, debris, algal growth and wastes accumulated at the bottom or sides of the tank routinely by siphoning and scrubbing as these waste encourage bacterial proliferation.  

Feeding

Feed the larvae with optimal amount of good quality balanced feed as the defence mechanism of the larvae depends upon their nutritional status.  

Use of chemicals and antibiotics  

The antibiotics should be used carefully at right doses, only after ascertaining in-vitro sensitivity of the pathogens. Low dose of antibiotics leads to development of antibiotics resistant mutants of bacteria and higher doses may be toxic to the shrimp larvae.  

Monitoring of larval health and water quality  

 Examine the larvae every morning before changing water for any visual abnormality, and microscopically for fouling protozoa, filamentous bacteria, fungal infection, and presence of swarming bacteria within the haemocoel. Wet mount preparations of hepatopancreas should be examined from time to time for viral infections. Observe rearing water and shrimp larvae in dark for bioluminescence. This help in understanding the status of health of the shrimp larvae and thereby take appropriate remedial measures as needed. Monitor the water quality to maintain important parameters at optimal levels (Temp 27-30 C, Salinity 27-31 ppt, DO > 5 ppm, pH 7.8 – 8.5; Ammonia N: <0.5 ppm, Nitrite-N: <0.02 ppm)  

Since treatment of viral diseases of shrimps in not known, disease outbreak due to viral infection may be avoided by quarantine measures and destroying carriers and contaminated animals. Once viral infection is detected in hatchery, all activities should be stopped and all the contaminated facilities should be thoroughly disinfected before restarting hatchery activities

 

Disease Prevention in Grow-Out Ponds

Location of the shrimp farms  

The shrimp farms should be located in areas free form industrial, agricultural or domestic pollution  

Pond preparation  

Before stocking, the pond should be thoroughly drained, sun dried, black layer of soil formed during the previous crop be removed and the pond tilled. Lime should be applied at the rate of 200 – 600 kg/ha depending on the pH of the soil.  

Stocking  

Stock only healthy postlarvae after achieving optimum algal bloom in the ponds. Maintain optimum density of shrimp larvae.  

Water management  

Always maintain good wate quality in the pond. Visual examination of pond water is known to be ideal. Very clear water and high turbidity are known to be stressful for the shrimps. Presence of bubbles or foam on the surface of water is also undesirable. Monitor routinely the pond environment for optimum colour (light green), transparency (30-40 cm) DO (4-6 ppm), pH (7.5-8.5), unionized ammonia : <0.1 ppm content in the pond water. Upon cnsiderable fluctuations in these parameters; water exchange becomes necessary. The incoming water must be ensured for optimum quality especially with respect to pH, salinity and turbidity.  

Feeding  

The shrimp should be fed with balanced diets at optimum quantities. Care should be taken to avoid accumulation of unutilized feed, otherwise it may lead to spoilage of the pond bottom. Do not use old, rancid and mouldy feed.  

 

 

Health check up  

A routine examination should be carried out on the status of health of the shrimps. Examine shrimps routinely for their swimming behaviour. Infected shrimps often show poor escape reflex. Frequent microscopic examination of gills, hepatopancreas and haemolymph for microbial infections or any disease symptoms should be done to ensure the health of the shrimps. Diseased and infected shrimp should be destroyed by burning or burying with lime into the soil away from the shrimp farms, in order to avoid spreading of infection.

DISEASE CONTROL

The disease control programmes in aquaculture must include examination of diseases and mortalities in holistic manner and consider various factors such as stocking densities, environment (turbidity, temperature, pH, salinity, dissolved oxygen of water and redox potential of soil), rate of water exchange, presence of bottom dwelling algae, the type of feed and its rate of consumption by the shrimps, phytoplankton bloom, physiological status of shrimps, etc. Thesse factors considered together go on long way in management of disease problems. Most of the disease control methods are based on preventive measures. They are : 

• Quarantine measures  
  
• Use of genetically resistant stock for culture purpose  
  
• Use of prophylactic vaccines  
  
• Use of drugs 
  

Quarantine measures  

The seed and brood shrimps may sometimes harbour pathogenic microbes particularly viruses without showing external clinical manifestations. Transport of such seed and broodstock to other geographic regions for culture purposes may lead to disease outbreaks. Hence, it is important to screen the seed and broodstock for pathogenic microorganisms before they are transported to different geographic regions for aquaculture purposes.  

Use of genetically resistant stock for culture purpose

Susceptibility of shrimps to various infectious agents appears to be species specific and is probably genetically aquired trait, eg. the yellow head disease has been reported to be specific to Penaeus monodon. Hence, in the shrimp farming areas endemic to yellow head disease culture of other penaeid species such as Penaeus indicus which is known to be resistant to this disease may be helpful in the prevention of yellow head disease. Similar possibilities may be explored to prevent other such epizootics.

Use of prophylactic vaccines  

Prophylactic vaccines may be used for controlling specific diseases. Certain commercial vaccine preparations against vibriosis of shrimps are available for use. Various factors, such as method of administration of vaccines, disposal of spent vaccine suspensions that may create environmental problems have to be considered carefully.

Use of drugs 

In spite of best management practice adopted in the hatcheries and grow-out ponds, disease outbreak may occur, and we may have to use drugs for controlling these diseases. Although some drug have been advocated for treatment of diseases, drugs should be employed only as a last option, since the art of disease control in aquaculture is in the early phase of development. various aspects of using drugs for disease control such as their dosages, intervals of drug administration, duration of exposure of shrimps to drugs, their effect on shrimps, their efficiancy in controlling the disease, withdrawal period from the tissues, their impact on the environment, etc. are yet to be clearly understood. The disease control measures using drugs would be useful only if they are applied during the early phase of the disease. Hence, right diagnosis of diseases at an early stage is a very important aspect that will aid in taking measures to control the disease.

 

 

 

 

 

 

 

 

 

 

Table 2: Drugs useful in aquaculture

 

(Source: www.nio.org/prawn)

 

 

RECOMMENDATIONS FOR THE FUTURE

It is important for research to come up with information to secure the stability, sustainability and profitability of the shrimp industry. This could be done through:

• Developing rapid and sensitive methods to detect pathogens within the animal and in its environment;
  
• Increasing the availability and accessibility of disease diagnosis, prevention, and treatment services;
  
• Increasing the availability of quality fry for stocking (fry which are disease resistant, fast growing, tolerant to sub-optimum environmental conditions etc.);
  
• Developing a reliable method to assess fry quality;
  
• Increasing the availability of environmentally sound and cost-effective culture methods (determination of pond carrying capacity, fine tuning of feeding strategies, waste recycling methods, polyculture etc.);
  
• Undertaking studies on pond dynamics and its influence on shrimp health, and
  
• Developing or verifying technologies for the use of probiotics, bioaugmentation and bioremediation products for shrimp aquaculture.
  

Sufficient resources to develop and transfer technologies to support an industry faced with huge problems should be made available. Government funds, as well as contributions from international funding agencies, have initially funded research. Closer interaction with industry representatives should be made in order to come up with schemes to help finance expensive research.

 

 

 

 

 

 

 

CONCLUSION

Due to reclusive nature of shrimp and the difficulty of observing dead shrimp in ponds, little is known about the importance of disease and parasites in pond culture. However, heavy mortalities from disease occur frequently in more intensive types of shrimp culture, such as hatcheries, raceways and tanks. Since unexplained mortalities do occur in ponds, a close watch should be kept for signs of disease or parasites. Unfortunately, dead or diseased shrimp are not easily observed in a pond. Frequently, a farmer does not learn that his shrimp have died until he harvests a pond and finds there are only a few shrimp left. For this reason, it is important that the shrimp in a pond be sampled regularly, at least weekly, and examined for disease. From this very important report we can get proper knowledge about different shrimp diseases and prevent those diseases.

 

 

 

 

 

 

 

 

 

 

 

 

REFERENCES

http://www.disease-watch.com

http://www.nio.org/prawns

http://www.fao.org

http://www.bqsp.org/index.php

http://orp.aiub.edu/Vol6_2.aspx#a7

Magazine- ‘Aquaculture Asia pacific’; Vol- Jan/Feb, 2006.

Foster, J.R.M. and T.W. Beard. 1974. Experiment to assess the suitability of nine species of prawn to intensive culture. Aquaculture 3:355–368.

Kungvankij, P. 1976. On the monoculture of jumbo tiger shrimp Penaeus monodon Fabricius. Phuket Marine Fisheries Station Contribution No. 7. 14 pp.

Kubo, I. 1949. Studies on the penaeids of Japan and its adjacent waters. J. Tokyo University Fish., 20(10). 870–872.

Kungvankij, P. 1973. A survey of the distribution and abundance of economically important shrimp along the Indian Ocean coast of Thailand. Phuket Marine Fisheries Station, Fisheries Cont. No. 3. 1–9.

 

 

 

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