Acute hepatopancreatic necrosis disease (AHPND) has caused severe losses in farmed populations of marine shrimp Penaeus vannamei and P. monodon. The causative agents are unique strains of the bacteria Vibrio parahaemolyticus and related Vibrio species. The disease emerged in the People's Republic of China (China) and Vietnam in 2010 and spread throughout South-East Asia; it was later reported in countries in both North and South America. The disease has had significant economic impacts on the shrimp aquaculture industry. From 2010 to 2016, combined losses from China, Malaysia, Mexico, Thailand and Vietnam due primarily to outbreaks of AHPND, including losses at the farm gate and those resulting from a drop in feed sales and exports, were estimated at over US$ 44 billion. Other economic losses include those associated with processing facilities, decreased community revenues resulting from increased unemployment, financial investments, and the costs of implementing diagnostic and control measures. The reduced employment opportunities and increases in debt burden and investment risk have had sociological impacts. The responses to the disease have led to a gradual recovery of the shrimp industry in affected countries. These response efforts have included the implementation of changes in farming systems and management, including, among others, enhanced biosecurity and the use of AHPND-free and AHPND-resistant shrimp. This situation of losses and recovery illustrates the importance of having a multi-level response plan in place to prevent, or to reduce the risk of, outbreaks of disease.
White feces syndrome (WFS) is an emerging problem for penaeid shrimp farming industries in SE Asia countries, Thailand, Malaysia, Vietnam, Indonesia, China, and in India. This occurrence of this syndrome is usually first evidenced by the appearance of white fecal strings floating on surface of the shrimp ponds. The gross signs of affected shrimp include the appearance of a whitish hindgut and loose carapace, and it is associated with reduced feeding and growth retardation. To investigate the nature of the white feces syndrome, samples of white feces and shrimp hepatopancreas tissue were collected from Penaeus vannamei in affected farms in Indonesia, and these were examined histologically. Within the white feces, we found densely packed spores of the microsporidian Enterocytozoon hepatopenaei (abbreviated as EHP) and relatively fewer numbers of rod-shaped bacteria. From WFS ponds, hepatopancreas samples form 30 individual shrimp were analyzed by histology and in situ hybridization. The results showed that all of the shrimp examined were infected with EHP accompanied by septic hepatopancreatic necrosis (SHPN). Midgut epithelial cells were also infected and this increased the number of tissue types being affected by EHP. By PCR, EHP was detected in all the samples analyzed from WFS-affected ponds, but not in those sampled from healthy shrimp ponds. To determine the modes of transmission for this parasite, we performed feeding and cohabitation bioassays, the results showed that EHP can be transmitted through per os feeding of EHP-infected hepatopancreas tissue to healthy shrimp and through cohabitation ofinfected and healthy shrimp. In addition, we found the use of Fumagillin-B, an antimicrobial agent, was ineffective in either reducing or eliminating EHP in infected shrimp.