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One hundred fifty samples of shrimp feed were collected from the eastern and southern regions of Thailand, and aflatoxins B1, B2, G1, and G2 (AFB1, AFB2, AFG1, and AFG2) in them were analyzed. AFB1 contamination ranged from a nondetectable level (< 0.003 ppb) to 0.651 ppb. Metabolites of AFB1 were less abundant than AFB1. To study the effects of aflatoxin in feed on shrimp production, black tiger shrimp were divided into four groups of 30 shrimp per group, tested in triplicate, and fed diets containing 0 (control), 5, 10, or 20 ppb of AFB1 for 10 consecutive days. After 7 or 10 days of consumption on each diet, the shrimp were weighed and sacrificed for laboratory examination. AFB1 and its metabolites were not detected in shrimp muscle. The mortality rate was slightly higher in the AFB1-treated groups than in the control group. The body weight of the surviving shrimp was decreased to 46 to 59% of the initial body weight in the AFB1-treated groups but not in the control group. Histopathological findings indicated hepatopancreatic damage by AFB1 with biochemical changes of the hemolymph. These results show that aflatoxin contamination in shrimp feed may cause economic losses by lowering the production of shrimp. Feed contaminated at the level of 20 ppb or lower (i.e., at the observed natural contamination level) may pose a very low risk, if any, to human health.

SUMMARY: Experimental infection of Tetrahymena pyriformis was conducted on ornamental fishes with skin wounded by acetic acid treatment. Among fishes used in this experimental infection, guppy Poecilia reticulata, pristella Pristella maxillaris, neontetra Paracheirodon innesi and cherry barbs Puntius titteya proved to be sensitive to challenge, while medaka Oryzias latipes, dwarf gourami Colisa lalia, goldfish Carassius auratus, platy Xiphophorus maculatus and angelfish Pterophyllum scalare were resistant. In catfish Corydoras aeneus infection was unsuccessful. Exposure to Tetrahymena at ≥100 cells/mL at 25 to 30°C and at pH of 6.0 to 8.0 resulted in the successful infection of some sensitive fish species. Histological and bacteriological observations suggest that deeply destroyed skin tissues from the acid‐treated method are the primary factors in successful infection.

Betanodavirus infection was diagnosed in larvae of farm-raised tilapia Oreochromis niloticus (L.), in central Thailand. Extensive vacuolar degeneration and neuronal necrosis were observed in histological sections with positive immunohistochemical staining for betanodavirus. Molecular phylogenetic analysis was performed based on the nucleotide sequences (1333 bases) of the capsid protein gene. The virus strain was highly homologous (93.07-93.88%) and closely related to red-spotted grouper nervous necrosis virus (RGNNV).

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