Novel midgut smooth muscle necrosis (MSMN) in translucent or glass post-larvae of whiteleg shrimp.

Abstract

From the Asia-Pacific region, the suspected TPD/GPD specimens of postlarvae (PL) at 9 days of development (PL9) preserved in Davidson's fixative and 95% ethanol were sent to our laboratory to prepare for PCR and histological analysis. Interestingly, PCR tests with the specimens were negative with the VP_HLVD (vtcc2 and vtcc3 gene) primers, but positive with the VP_TPD (vhvp-2 gene) primers. There were no characteristic lesions of acute hepatopancreatic necrosis disease detected in these specimens. However, in the sections of several specimens from two affected tanks, the midgut was cut tangentially in the abdominal region, revealing a novel histopathology characterized by severe necrosis specifically in the thin, smooth muscle tissues underlying the midgut lumen epithelium. This comprised nuclear pyknosis and karyorrhexis limited to the smooth muscle and occasionally affecting the midgut epithelium but not involving the surrounding skeletal muscles. The pathology is called midgut smooth muscle necrosis (MSMN). Such pathology would undoubtedly lead to loss of midgut peristalsis and cessation of feeding, but it could be easily overlooked without careful histological examination using a high magnification microscope objective. No bacterial cells were evident, suggesting that the lesions arose from a virus or from a specific toxin response. This report is an urgent plea for colleagues studying TPD/GPD to review their samples histologically to help in determining whether MSMN is pathognomonic for TPD/GPD.