A synthetic antibacterial peptide from Mytilus galloprovincialis reduces mortality due to white spot syndrome virus in palaemonid shrimp

White spot syndrome virus (WSSV) isolated from Penaeus monodon was found to be highly infective for the western Mediterranean shrimp, Palaemon sp. Using polymerase chain reaction (PCR), it was demonstrated that such shrimp are not naturally carriers of WSSV. Following challenge with virus, mortality reached 100% 3.5-4 days after injection at 22 degrees C. Incubation of infected shrimp at 10 degrees C totally suppressed the mortality which rapidly developed when shrimp were returned to 18 or 22 degrees C. Preincubation of WSSV with mature synthetic mytilin significantly reduced shrimp mortality with a 50% efficient dose of about 5 microM. Survival of shrimp was not due to the development of an active mechanism of defence as re-injection of WSSV produced the same mortality pattern. Mortality was probably due to WSSV replication as dot blot failed to detect viral DNA in the injection sample but was positive 1 day post-injection. Protection by mytilin was by interaction at the virus level, preventing replication as no WSSV nucleic acid was detected by PCR even after 7 days in shrimp injected with WSSV preincubated with 10 or 50 microM mytilin.     

Per os challenge of Litopenaeus vannamei postlarvae and Farfantepenaeus duorarum juveniles with six geographic isolates of white spot syndrome virus

White spot syndrome virus (WSSV) is one of the most important pathogens of penaeid shrimp. It is widely distributed in most Asian countries where penaeid shrimp are cultured, as well as in the Gulf of Mexico and SE USA. The virulence of six geographic isolates of WSSV was compared using Litopenaeus vannamei postlarvae and Farfantepenaeus duorarum juveniles. The six geographic isolates of WSSV originated from China, India, Thailand, Texas, South Carolina, as well as from crayfish maintained at the USA National Zoo. For challenge studies, virus infected tissues were given per os to L. vannamei postlarvae and Fa. duorarum juveniles. Resultant WSSV infections were confirmed by histological examination. The cumulative mortality of L. vannamei postlarvae reached 100% after challenge with each of the six geographic isolates of WSSV. However, the Texas isolate caused mortalities more rapidly than did the other shrimp isolates; the crayfish WSSV isolate was the slowest. In marked contrast, cumulative mortalities of juvenile Fa. duorarum reached only 35–60%, and varied among the geographic isolates of WSSV. Interestingly, in Fa. duorarum, the Texas WSSV isolate was also the most virulent, while the crayfish WSSV was the least virulent. The findings suggest that slight differences in virulence exist among geographic isolates of WSSV, and that susceptibility may vary with species and lifestages of the host.     

Effect of high water temperature (33 °C) on the clinical and virological outcome of experimental infections with white spot syndrome virus (WSSV) in specific pathogen-free (SPF) Litopenaeus vannamei

White spot syndrome virus (WSSV) is the most lethal pathogen of cultured shrimp. Previous studies done with undefined WSSV titers showed that high water temperature (32-33 °C) reduced/delayed mortality of WSSV-infected shrimp. This study evaluated the effect of high water temperature on the clinical and virological outcome of a WSSV infection under standardized conditions. Groups of specific pathogen-free Litopenaeus vannamei were challenged either by intramuscular or oral routes with a low (30 SID₅₀) or a high (10,000 SID₅₀) virus titer. Shrimp were kept (i) continuously at 27 °C, (ii) 30 °C or (iii) 33 °C; (iv) maintained at 33 °C before challenge and 27 °C afterwards, or (v) kept at 27 °C before challenge and 33 °C afterwards. Shrimp were maintained at the respective temperatures for 120 h before challenge and 120-144 h post challenge (hpc). Gross signs and mortality were monitored every 12 h until the end of the experiment. Dead and surviving shrimp were screened for WSSV infection (VP28-positive cells) by indirect immunofluorescence (IIF). Shrimp kept continuously at 27 °C or 30 °C, or switched to 27 °C post challenge developed gross signs within 24 hpc, first mortalities at 36-60 hpc and 100% cumulative mortality between 60 and 144 hpc depending on the virus titer. All dead shrimp were WSSV-positive. In contrast, shrimp kept at 33 °C continuously or after WSSV challenge showed no signs of disease and low mortalities (0-30%) regardless of the virus titer. Dead and surviving shrimp were WSSV-negative. Further, early virus replication was studied in two groups of shrimp: one maintained at 27 °C before and after challenge and one switched from 27 °C to 33 °C after challenge with 10,000 SID₅₀. Immunohistochemistry (IHC) analysis showed that WSSV-positive cells were first displayed at 12 hpc in shrimp kept at 27 °C and by 24 hpc the infection became systemic. In contrast, shrimp kept at 33 °C did not display WSSV-positive cells at 12 or 24 hpc. This work confirms previous reports that high water temperature prevents the onset of disease and significantly reduces mortality of WSSV-inoculated shrimp regardless of the route of inoculation or virus titer used. This strategy may have practical applications to control WSSV in tropical shrimp farming countries.     

Pre-exposure to infectious hypodermal and haematopoietic necrosis virus or to inactivated white spot syndrome virus (WSSV) confers protection against WSSV in Penaeus vannamei (Boone) post-larvae

Larvae and post-larvae of Penaeus vannamei (Boone) were submitted to primary challenge with infectious hypodermal and haematopoietic necrosis virus (IHHNV) or formalin-inactivated white spot syndrome virus (WSSV). Survival rate and viral load were evaluated after secondary per os challenge with WSSV at post-larval stage 45 (PL45). Only shrimp treated with inactivated WSSV at PL35 or with IHHNV infection at nauplius 5, zoea 1 and PL22 were alive (4.7% and 4%, respectively) at 10 days post-infection (p.i.). Moreover, at 9 days p.i. there was 100% mortality in all remaining treatments, while there was 94% mortality in shrimp treated with inactivated WSSV at PL35 and 95% mortality in shrimp previously treated with IHHNV at N5, Z1 and PL22. Based on viral genome copy quantification by real-time PCR, surviving shrimp previously challenged with IHHNV at PL22 contained the lowest load of WSSV (0-1x10(3) copies microg-1 of DNA). In addition, surviving shrimp previously exposed to inactivated WSSV at PL35 also contained few WSSV (0-2x10(3) copies microg-1 of DNA). Consequently, pre-exposure to either IHHNV or inactivated WSSV resulted in slower WSSV replication and delayed mortality. This evidence suggests a protective role of IHHNV as an interfering virus, while protection obtained by inactivated WSSV might result from non-specific antiviral immune response.     

Silencing Pacific white shrimp Litopenaeus vannamei LvRab7 reduces mortality in brooders challenged with white spot syndrome virus

White spot syndrome virus (WSSV) is a major threat for farmed shrimp worldwide. RNA interference (RNAi) is the most recent tool against viral diseases. Rab7 silencing effectively inhibited virus infections in juvenile shrimp, but the antiviral effect in brooders remains unknown. This study found a homologue Penaeus monodon Rab7 gene in Litopenaeus vannamei brooders from Mexico. Sequence identity was >99% to a Thai LvRab7 sequence and >94% to Rab7 sequences from P. monodon or Marsupenaeus japonicus. Animals treated with a partial (494 bp) or a complete (618 bp) LvRab7 dsRNA sequences and challenged 48 h post treatment (hpt) with a high WSSV dose showed 80–88% mortality respectively. Shrimp treated with 4 or 20 μg LvRab7 dsRNA and challenged with a WSSV high dose had 80% mortality each, but it was reduced to 33% and 40%, respectively, with a low dose. Efficacy of dsRNA to reduce shrimp mortality was dependent on virus dose used regardless of dsRNA concentration. A significant reduction in LvRab7 mRNA levels was observed at 120 hpt. In conclusion, silencing LvRab7 in brooders showed a mild antiviral effect against a WSSV challenge at 48 hpt.     

Effects of total ammonia,temperature and salinity on the mortality and viral replication of WSSV‐infected Chinese shrimp (Fenneropenaeus chinensis)

In this study, we evaluated the effects of three factors, total ammonia, temperature and salinity, on the mortality of and viral proliferation in white spot syndrome virus (WSSV)‐infected Chinese shrimp. Shrimp maintained in 30‰ seawater at 25°C with 0.34 mg L^?1 total ammonia (control group) were injected with approximately 20 WSSV particles per shrimp and subsequently subjected to the following conditions: 30‰ seawater at 25°C, with 6 mg L^?1 (N1 group) or 14 mg L^?1 (N2 group) total ammonia; 30‰ seawater at 18°C (T1 group) or 30°C (T2 group), with 0.34 mg L^?1 total ammonia and 20‰ (S1 group) or 40‰ (S2 group) seawater at 25°C, with 0.34 mg L^?1 total ammonia. An anova analysis revealed that the cumulative mortality of WSSV‐infected Chinese shrimp was significantly lower when reared in the T1 group compared to that of the T2 and control group. Similarly, the mortality of the shrimp in the S1 group was also significantly lower than that of the S2 and control group. No significant differences were detected among the N1, N2 and control groups. Accordingly, the WSSV level in the T1 and S1 groups was significantly lower than those in the control, T2 or S2 groups respectively. No significant differences in viral loads were detected among the control, N1 and N2 groups. The transfer of Chinese shrimp to lower temperature and lower salinity enhanced their resistance to WSSV infection, whereas a change in the concentration of total ammonia had no significant effect on the mortalities and viral loads of WSSV‐infected shrimp.     

自然养殖水体投喂CpG ODN和表面展示VP28的解脂耶罗维亚酵母对凡纳滨对虾(Litopenaeus vannamei)抗WSSV的免疫保护作用

用添加CpG寡聚核苷酸(CpG ODN)和表面展示VP28的解脂耶罗维亚酵母(VP28-yl)的饵料投喂凡纳滨对虾,进行田间中试实验。投喂30 d后进行WSSV感染实验,评估其对凡纳滨对虾的免疫保护作用。投喂实验结束后,CpG ODN投喂组对虾的相对增重率达到(65.8±7.8)% (P<0.05),这暗示CpG ODN可能具有促生长作用。WSSV攻毒后,CpG ODN和VP28-yl投喂组对虾中WSSV拷贝数与对照组相比均显著降低(P<0.05),相对免疫保护率分别可达到26.7%和36.7%。在投喂结束和WSSV刺激后,CpG ODN组对虾中的呼吸爆发水平均显著升高(P<0.05)。而在VP28-yl投喂组,WSSV引起的细胞凋亡则显著受到抑制(P<0.05)。此外,WSSV刺激后,STAT基因在CpG ODN组和VP28-yl组对虾中的表达水平均显著上调(P<0.05),分别在第5天和第3天达到最大值,而对照组中则显著下调。研究结果表明,CpG ODN和VP28-yl增强了凡纳滨对虾抗病毒免疫力,对养殖对虾病毒性疫病的防控具有显著作用,可以作为免疫增强剂添加在饵料中,具有在养殖生产中推广使用的前景。     

饲料中添加复合芽孢杆菌对凡纳滨对虾抗病毒感染能力及抗病基因表达的影响

自健康凡纳滨对虾(Litopenaeus vannamei)分离到枯草芽孢杆菌(Bacillus subtilis)、地衣芽孢杆菌(B. licheniformis)和短小芽孢杆菌(B. pumilus),将上述芽孢杆菌以单一和3株复合的方式包裹在基础饲料表面,制成益生菌饲料;每日投喂对虾,3周后进行白斑综合征病毒(WSSV)人工感染。统计实验组和对照组的累积死亡率,测定对虾鳃组织内WSSV拷贝数,分析对虾肠道组织含半胱氨酸的天冬氨酸蛋白酶基因(Caspase)和硫氧还原蛋白基因(Trx)的相对表达量。结果显示,感染实验结束时,A组(枯草芽孢杆菌)、B组(地衣芽孢杆菌)、C组(短小芽孢杆菌)和D组(枯草芽孢杆菌+地衣芽孢杆菌+短小芽孢杆菌复合益生菌)的对虾累积死亡率分别为(73.3±7.0)%、(63.3±5.5)%、(75.0±7.9)%和(50.0±5.3)%,显著低于对照组(PBS组)(100%);在整个感染阶段,各实验组的病毒拷贝数呈先上升后下降的趋势,但对照组呈现一直上升趋势,且显著高于实验组。抗病基因表达结果显示,WSSV感染后,各组对虾肠道Caspase相对表达量随感染时间的延长呈先上调再下调的趋势,且在18 h各组对虾肠道Caspase表达量达到最大值;益生菌摄取和WSSV感染都能刺激Trx的表达,益生菌的刺激相对平缓,且各实验组对虾肠道Trx相对表达量在WSSV感染后的18 h时陡升到最大值,极显著高于对照组,且以D组的激活能力最强。研究证实,枯草芽孢杆菌、地衣芽孢杆菌和短小芽孢杆菌均可提高对虾抗WSSV感染能力,复合芽孢杆菌抗病毒能力最突出。对虾抗病力的提高可能与芽孢杆菌减缓了病毒在靶组织的增殖速率、提高了Caspase和Trx基因表达水平相关。     

Quantitative real time PCR for the measurement of white spot syndrome virus in shrimp

Quantitative real time PCR, recently developed in molecular biology, is applied in this paper to quantify the white spot syndrome virus (WSSV) in infected shrimp tissue. The WSSV content in moribund shrimp of all species tested ( Penaeus stylirostris, P. monodon, P. vannamei ) ranged from 2.0 × 10⁴ to 9.0 × 10¹⁰ WSSV copies μg^–1 of total DNA ( n =26). In whole moribund post-larvae, 4.3 × 10⁹ WSSV copies μg^–1 of DNA were detected which is equivalent to 5.7 × 10¹⁰ WSSV copies g^–1 of post-larvae. The comparison of WSSV content between different tissues showed that muscle and hepatopancreas tissues contained 10 times less virus than gills, pleopods and haemolymph. With inocula of known virus content, bioassays by immersion challenge showed that a minimum of five logs of WSSV copies was necessary to establish disease in the challenged shrimp. In contrast, five logs of WSSV copies injected into shrimp muscle produced a LT-50 of 52 h. This real time polymerase chain reaction (PCR) technique is sensitive (four copies), specific (negative with DNA from shrimp baculoviruses and parvoviruses), dynamic (seven logs) and easy to perform (96 tests in <4 h).     

A Profound Effect of Hyperthermia on Survival of Litopenaeus vannamei Juveniles Infected with White Spot Syndrome Virus

This study was conducted to examine the effect of increasing seawater temperature on White Spot Syndrome Virus (WSSV) infection in juvenile Pacific White shrimp ( Litopenaeus vannamei ). Infection by WSSV was achieved using two methods, intramuscular injection and per os (oral) administration. Forty injected and 20 per os infected animals were kept in heated tanks at 32.3 ± 0.8 C, and the same number of WSSV infected animals were maintained in tanks at ambient temperature (25.8 ± 0.7 C). Despite the route of exposure, there were no survivors among the animals kept at ambient temperature; whereas, in heated tanks the survival of the WSSV infected juvenile shrimp was always above 80%, suggesting the existence of a beneficial effect from hyperthermia that mitigated the progression of WSSV disease. Moreover, this beneficial effect was not attributable to viral inactivation. Infected animals kept at 32 C had histologically detectable lymphoid organ spheroids suggestive of a chronic viral infection but were PCR negative (hemolymph) for WSSV. These findings might be related to low viral replication in WSSV-infected shrimp held at the higher environmental temperature. When the WSSV-infected shrimp were transferred from 32 C to ambient temperature, the mortality from WSSV ensued and was always 100%. Although the mechanism related to the beneficial effect of heating was not determined, our results indicate that increasing the water temperature modifies dramatically the natural history of the WSSV disease and the survival curves of WSSV-infected juvenile Pacific White shrimp.     

Protection of crayfish, Cambarus clarkii, from white spot syndrome virus by polyclonal antibodies against a viral envelope fusion protein

White spot syndrome virus (WSSV) is a large double-stranded DNA virus, causing considerable mortality in penaeid shrimp and other crustaceans. WSSV produces five major structural proteins, including two major envelope proteins, VP28 and VP19. To produce VP28 and VP19 as a single protein for antibody production, DNA sequences encoding both open reading frames were fused together and cloned into pET-22b(+) expression vector. The fusion protein, VP(19+28), was expressed in Escherichia coli, purified using Ni2+ His affinity chromatography and injected into a rabbit. Antiserum collected from the immunized rabbit was tested in vivo for ability to protect crayfish, Cambarus clarkii, from disease caused by WSSV. Fifteen days after challenge with WSSV, treatment with VP(19+28) antiserum gave 100% protection against disease in the ambient temperature range of 15-22 degrees C and 65% protection at a constant temperature of 26 degrees C. These results demonstrated VP(19+28) antiserum is effective in protection of crayfish from WSSV and confirmed that VP19 and VP28 play an important role in WSSV host infection. Targeting both VP19 and VP28 may be effective for the design of both immunotherapeutic medicines and reagents to detect WSSV.     

Oral vaccination trials with crayfish, Procambarus clarkii, to induce resistance to the white spot syndrome virus

The potential of oral vaccination against white spot syndrome virus (WSSV) in crayfish Procambarus clarkii was investigated. The protective effect of binary ethylenimine (BEI)-inactivated WSSV was tested by oral vaccination, followed by an oral challenge with WSSV. The crayfish fed with feed pellets coated with BEI-inactivated WSSV showed a resistance to WSSV on the seventh day post vaccination (dpv). The relative percentage survival values were 60%, 70% and 75% for the vaccinated once, twice and thrice with inactivated WSSV. Following an intramuscular injection experiment, no mortality was recorded in the inactivated WSSV group and the negative control at 17 days post challenge. The cumulative mortalities in the heated WSSV group and WSSV group were 100%. Shrimp that survived the WSSV challenge on the seventh day after cessation of oral vaccination were positive for the presence of WSSV by a polymerase chain reaction assay specific for WSSV. This result indicated that inactivated WSSV could protect crayfish against WSSV by oral delivery.     

Antiviral Effect of Fucoidan Extracted from the Brown Seaweed,Sargassum wightii,on Shrimp Penaeus monodon Postlarvae against White Spot Syndrome Virus

This study was carried out to determine the effect of seaweed polysaccharide, fucoidan from brown seaweed, Sargassum wightii, on Penaeus monodon postlarvae (PL) against white spot syndrome virus (WSSV). The fucoidan was extracted from S. wightii, and the yield was observed as 2.832 ± 0.204%. Artemia franciscana nauplii were enriched with extracted fucoidan at four different concentrations (100, 200, 300, and 400 mg/L) and fed to shrimp P. monodon PL for 20 d. After feeding experiment, the P. monodon PL were challenged with WSSV, and the mortality percentage was recorded daily up to 21 d. During the challenge test, the control PL showed 100% cumulative mortality within 9 d, but the fucoidan‐enriched Artemia nauplii fed groups of PL exhibited 60–94% cumulative mortality within 21 d. The reduction in mortality percentage of experimental groups of PL over control PL was ranged between 33.71 and 61.65%. The polymerase chain reaction analysis confirmed the concentration‐dependent variation in WSSV infection.     

Effects of Dietary Administration of Probiotic Halomonas sp. B12 on the Intestinal Microflora,Immunological Parameters,and Midgut Histological Structure of Shrimp,Fenneropenaeus chinensis

The experiment was conducted to investigate the effects of oral administration of probiotic Halomonas sp. B12 (previously isolated from the intestine of Fenneropenaeus chinensis) on the intestinal microflora, immunological parameters, and midgut histological structure of F. chinensis. Shrimp (initial weight: 4.00 ± 0.10 g) were fed diets containing Halomonas sp. B12 at 0 (control), 3.68 × 10⁷ (T1), and 7.18 × 10¹⁰ (T2) colony‐forming units per gram for 6 wk, respectively. The results showed that the total bacterial counts significantly increased (P < 0.05) with supplementation of dietary probiotic B12. However, Vibrio spp. counts significantly decreased (P < 0.05) in the intestine of shrimp with increasing dietary probiotic B12. Hemocyte counts in the shrimp fed the diets supplemented with probiotic B12 were significantly higher (P < 0.05) than the control group. Both phenoloxidase (PO) activity in plasma and hemocyte lysate supernatant were higher in the shrimp fed diets supplemented with probiotic B12 compared with the control group. No significant difference was found in PO activity in plasma between the T1 and the control (P > 0.05). PO activity in plasma was higher in T2 than that in T1. Cumulative shrimp mortality after 10‐d white spot syndrome virus (WSSV) challenge test significantly decreased with increasing dietary probiotic B12 (P < 0.05). No significant difference was found between T1 and control in cumulative shrimp mortality after challenge test (P > 0.05). The oral administration of probiotic B12 to F. chinensis was beneficial to protect the integrity of shrimp intestinal mucosal layer. In summary, even though the low dose (T1) had some effects on bacterial counts and immunological parameters, only the high dose (T2) significantly increased the resistance of the shrimp to WSSV.     

Experimental host range and histopathology of white spot syndrome virus (WSSV) infection in shrimp, prawns, crabs and lobsters from India

Experimental studies were conducted by injecting or feeding white spot syndrome virus (WSSV) derived from infected shrimp, Penaeus monodon (Fabricius), collected from the south-east coast of India, to five species of shrimp, two species of freshwater prawns, four species of crabs and three species of lobsters. All species examined were susceptible to the virus. Experimental infections in the shrimp had the same clinical symptoms and histopathological characteristics as in naturally infected P. monodon . A cumulative mortality of 100% was observed within 5–7 days in shrimp injected with WSSV and 7–9 days in shrimp fed with infected tissue. Two species of mud crab, Scylla sp., survived the infection for 30 days without any clinical symptoms. All three species of lobsters, Panulirus sp., and the freshwater prawn, Macrobrachium rosenbergii (De Man), survived the infection for 70 days without clinical symptoms. However, bioassay and histology using healthy P. monodon revealed that crabs, prawns and lobsters may act as asymptomatic carriers/reservoir hosts of WSSV. This is the first report to suggest the carrier/reservoir capacity of these hosts through histological and bioassay evidences. Ultrastructural details of the virus in experimentally infected shrimp, P. vannamei , (Boone), were also studied.     

Light and electron microscopic evidence of white spot disease in the giant tiger shrimp, Penaeus monodon (Fabricius), and the kuruma shrimp, Penaeus japonicus (Bate), cultured in Taiwan

Since 1992, mass mortalities among cultured giant tiger shrimp, Penaeus monodon (Fabricius), and kuruma shrimp, Penaeus japonicus (Bate), have been observed in Taiwan. The condition is known as 'white spot disease' (WSD), based on the characteristic white spots on the cuticle of diseased shrimp. With the scanning electron microscope, two sizes of white spots were observed. Each spot represented a protrusion on the inside surface of the carapace. The composition of white spots was similar to that of the cuticule, most calcium, as determined with an energy dispersive spectrometer. Histological studies of moribund, infected specimens revealed degenerated cells, characterized by hypertrophied nuclei, in various meso- and ectodermal tissues. Infected tissues included cuticular epidermis, connective tissue, lymphoid organ, antennal gland, and haematopoietic, gill and nervous tissue. Nuclei were Feulgen-positive and no occlusion body was found in the necrotic tissue. Transmission electron microscopy revealed the presence of rod-shaped and enveloped virions in the hypertrophied nuclei. The virions measured 298 ± 21 × 107 ± 8 nm in the giant tiger shrimp and 248 ± 12 × 104 ± 8 nm in the kuruma shrimp. In an experimental infection trial, cumulative mortality was 40% within 14 days under stress conditions. No mortality was observed in controls or in non-stressed infected shrimp. Experimental infections show that environmental stressors such as ammonia may enhance the severity of WSD virus infections in cultured shrimp.     

Virulence and genotypes of white spot syndrome virus infecting Pacific white shrimp Litopenaeus vannamei in north‐western Mexico

White spot syndrome virus (WSSV) has caused substantial global economic impact on aquaculture, and it has been determined that strains can vary in virulence. In this study, the effect of viral load was evaluated by infecting Litopenaeus vannamei with 10‐fold serial dilution of tissue infected with strain WSSV Mx‐H, and the virulence of four WSSV strains from north‐western Mexico was assessed along with their variable number of tandem repeat (VNTR) genotypes in ORF75, ORF94 and ORF125. The LD₅₀ of the Mx‐H strain was a dilution dose of 10^?7.5; the mortality titre was 10^9.2 LD₅₀ per gram. In shrimp injected with 10^2.5 to 10^6.5 LD₅₀, no significant virulence differences were evident. Using mortality data, the four WSSV strains grouped into three virulence levels. The Mx‐F strain (intermediate virulence) and the Mx‐C strain (high virulence) showed more genetic differences than those observed between the Mx‐G (low‐virulence) and Mx‐H (high‐virulence) strains, in ORF94 and ORF125. The application of high‐viral‐load inocula proved useful in determining the different virulence phenotypes of the WSSV strains from the Eastern Pacific.     

Effect of hot water extracts of brown seaweeds Sargassum spp. on growth and resistance to white spot syndrome virus in shrimp Penaeus monodon postlarvae

An experiment was conducted to evaluate the effect of a hot water extract of brown seaweeds Sargassum duplicatum and Sargassum wightii on the growth and white spot syndrome virus (WSSV) resistance in shrimp Penaeus monodon postlarvae (PL). Artemia nauplii (instar II) were enriched with both seaweed extracts at various concentrations (250, 500 and 750 mg L^?1) and fed to the respective P. monodon (PL15–35) group for 20 days. A control group was also maintained without seaweed extract supplementation. The weight gain of the experimental groups was significantly higher (0.274–0.323 g) than the control group (0.261 g). Similarly, the specific growth rate was also significantly higher (16.27–17.06%) in the experimental groups than in the control group (16.03%). After 20 days of the feeding experiment, the shrimp PL were challenged with WSSV for 21 days. During the challenge test, the control shrimp displayed 100% mortality within 8 days. In contrast, the mortality percentage of the highest concentration (750 mg L^?1) of seaweed extract enriched Artemia nauplii fed shrimp was 54–79%. Comparatively, low mortality was observed in S. wightii extract‐enriched Artemia nauplii fed shrimp. The polymerase chain reaction analysis indicated the concentration‐dependent infection of WSSV in P. monodon PL.