World Aquaculture 13 timations. Water exchange was carried out using a continuous bottom water releasing method. Because of production costs and the lack of appropriate aquaculture fertilizers, urea was used as a nitrogen source and super triple phosphate was used as a phosphorus source. During the last quarter of 2003, shrimp production was 2,000 kg/ha after 138 days of culture, with a FCR of 2.1. By that time, some shrimp showed grey discoloration in muscle tissues of the abdominal region. Mortality appeared two months before harvesting when the shrimp reached a size of 6 g. Final survival was 65 percent. When there were hypoxic conditions in the ponds, some shrimp displayed a reddish tail that was associated, in most of the cases, with necrosis. During the molting period, shrimp mortality increased dramatically. Normally, the number of dead shrimp encountered daily in ponds or feed trays were 6-10 individuals. In contrast, this number increased to as many as 200 dead shrimp daily in a large pond during molting periods and the acute phase of IMN. To enhance production, stocking was decreased from 25 to 16 individuals/m2 in ponds with reduced survival. However, this shrimp pond management strategy did not function as expected and the mortality continued to hamper production. The increased mortality persisted until the final cycle. In the final cycle, the maximum mortality registered was approximately 400 individuals per day in a large pond. In general, mean survival was only 53 percent. Light microscopic examination of shrimp guts revealed the presence of an extreme abundance of bacteria and gregarines, especially during the 2004 rainy season (January-May), as well as broken and evacuated guts. Gregarines were represented by different developmental stages (gamonts, gametocysts and trophozoites) and could have also played a critical role in low shrimp production. IMN Macroscopic Clinical Signs The external appearances and features of the affected shrimp showing the different grades of infection generated by the IMNV are as follows: Initial phase (grade 1 infection). This phase is initiated with a minor, light whitish–pink coloration, opacity, or grey discolorations in focal areas, expanded slightly along the muscle of the abdominal segments from the under parts to the upper parts (Figure 1). Moderate phase (grade 2 infection). During this stage of the disease, the opacity increases in size, reaching other areas of the abdominal region and becoming more whitish than the coloration found in the initial phase (Figure 2). Here, the muscular necrosis extends more into the abdominal area. Severe or Pre-Acute phase (grade 3 infection). In this grade of IMN, the focal whitish opacities are more evident and concentrated, mainly on the under parts and sides of all the abdominal segments, including the base of the pleopods (Figures 3 and 4). The extensive opaque white coloration can appear in the cephalothorax. Acute–Chronic phase (grade 4 infection). This transition of the terminal phase is characterized by complete necrosis of the abdominal striated muscles of the segments. Here, a diffuse milky white opacity can be observed through the entire abdominal area, though it is most evident in segments four through six. The myonecrosis extends from the telson and uropods to the cephalothorax. A reddishpink necrotic coloration is clearly evident on the tail fan (telson and uropods; Figures 4 and 5), and even in the last segments. Mortality occurs during this phase. Fig. 1. Individual showing the IMN–initial phase or grade 1. (Credit picture: ®Gustavo Dominguez). Fig. 2. A shrimp reflecting the IMN–moderated phase or grade 2. (Credit picture: ®Gustavo Dominguez). Fig. 3. Specimens presenting IMN–pre-acute phase or grade 3. (Credit picture: ®Gustavo Dominguez).
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