– Faeces become pale white, float on water surface
– Hepatopancreas becomes whitish and soft, shrunken.
– Transformation, sloughing and aggregation of hepatopancreatic
microvilli into vermiform bodies resembling gregarines
– Associated loose exoskeleton and epibiotic protozoa leading to
dark discolouration of the gills.
– Reduced feed intake (increased FCR)
– Weak animals, and mortality
– Worst after 50-90 DOC


– 1996. Malaysia, “Soft body-white faeces syndrome” (Yang et al.,1999)
– 2009. Thailand (Tourtip et al , 2009; Limsuwan, 2010)
– 2010. China (Huang, Jie and So (2010, 2011)
– 2010. Vietnam (Ha et al, 2010)
– 2010. Malaysia (Thong, 2016)
– 2014. Indonesia (Thong, 2016)
– 2015. India (Durai et al , 2015; Mastam, 2015)

Info from Indonesia:

– Outbreak in all areas of Indonesia.
– Prevalence in 2017 from 3% to 15% according to areas
– Outbreak mostly in high density farming (>150 PLs/m2)
– Doubts on causes but hepatopancreas damage clear
– All shrimp size affected, with outbreak also seen early in the crop
– No effect of salinity
– No effect of season


– Poor feed quality (mycotoxins, etc)
– Gregarines
– Cyanobacteria (toxins or low digestibility)
– Vibrio
– Enterocytozoon hepatopenaei (EHP)


Impact of mycotoxins (ex: aflatoxin B1)
– Hepatopancreatic damage/changes (Bautista et al., 1994)
– Severe degeneration of hepatopancreatic tubules (Boonyaratpalin et al., 2001)
– Modification of digestive processes and abnormal development of the hepatopancreas (Burgos-Hernadez et al. 2005)
– Histological changes in the hepatopancreas, eg loss of structure of the cells and tubules, desquamation, necrosi (Gopinath & Raj, 2009)
– Alterations of hepatopancreas tissue, eg irregular tubular structure, separation between myoepithelial layer and epithelium (Zeng et al., 2015)

Use and properly store quality feed from trusted supplier

– Impact of anti-nutritional factors
– Present in soybean and other plant based- protein sources
– Reported effects: protein utilization and digestion (e.g. protease inhibitors, tannins,
lectins), mineral utilization (e.g. phytate, gossypol pigments, glucosinolates), etc
(Francis, Makkar & Klaus 2001).
– Anti-oxidative ability and immune response damaged after fish-meal decreased from
25% to 15% (Xie et al., 2016)
– Adaptation mechanisms of shrimp
– Homeostasis of the digestive system when fed anti-nutritional soybean trypsin
inhibitor (Maytorena-Verdugo et al., 2017)
– Benefit of Bacillus probiotics in 100% fish meal replacement by soybean meal
(Olmos et al., 2011)

Use and properly store quality feed from trusted supplier
Consider the benefit of microbial additive


– Common parasites (protozoa) of the digestive tract of shrimp, affecting food intake, but also facilitating bacterial infection. Typically utilize a mollusc as intermediate host.
– Gregarine parasites found in only 2% of all sampled shrimp, diseased and healthy, collected form farms on Chantaburi affected by white faeces (Somboon et al., 2012)
– White faeces syndrome from transformation, sloughing and aggregation of hepatopancreatic microvilli into vermiform bodies superficially resembling gregarines (Sriurairatana et al., 2014)

No evidence of link between gregarines and white faeces


– Necrosis observed, with lumina of the hepatopancreatic tubules in filled with sloughed epithelial cells (Morales-Covarrubias etal., 2016)
– Severe damage to the gastrointestinal linen (e.g. cell desquamation, loss of integrity), thought to interfere with food absorption (Pérez-Linares et al., 2003)


– Indonesia (Supitoi et al, 2016) V. alginolyticus, V. parahaemolyticus, V. vulnificus
– Indonesia (Jayadiet et al, 2016) V. parahaemolyticus, V. vulnificus, V.cholerae and V. anguillarum
– India (Mastan, 2015) V. parahaemolyticus, V. fluvialis, V. mimicus, V. alginolyticus, Vibrio sp.
– Thailand (Limsuwan, 2010; Somboon et al, 2012) V. vulnificus, V. fluvialis, V. parahaemolyticus, V. alginolyticus, V. mimicus, V. cholerae and Photobacterium damselae.
– China (Cao et al.,2015) V. cholerae


– India (Rajendran et al., 2016)
Higher prevalence of E. hepatopenaei in shrimp from ponds affected with White Feces. But no conclusive association!

– Vietnam (Sriurairatan et al., 2014).
The cause of White Feces WFS in Vietnam was attributed to E.hepatopenaei (Ha et al, 2012), but this was later shown to be very unlikely based on closer study of natural and laboratory infections of E. hepatopenaei in Thailand.

– Thailand (Thitamadee et al., 2015).
laboratory tests on transmission by cannibalism did reveal that transmission was not accompanied by white feces even though EHP is often found in shrimp exhibiting White Feces. There is some possibility that EHP may be a component cause or predisposing agent for White Feces.


Hepatopancreas samples collected from P. vannamei exhibiting white feces syndrome (Tang et al. 2016)
(E) Hematoxylin and Eosin staining of midgut epithelial cells showing EHP inclusions
(F) in situ hybridization with EHP probe Scale bars = 25 μm.

Comparative prevalence of EHP in P. vannamei collected from ponds with and without white faeces syndrome (Rajendran et al., 2016)

Link with AHPND (Aranguren et al., 2017)

Link with other Vibrio infection, such as Septic Hepatopancreatic Necrosis. Histology of 100 shrimp collected from 19 grow-out pond in 2015-2016.
SHPN = generalized atrophy of the hepatopancreas tubules with multifocal necrosis and hemocytic nodules, some melanized (Aranguren et al., 2017)

– E. hepatopenaei associated with white feces
– E. hepatopenaei alone does not cause white feces
– E. hepatopenaei, by affecting the growth rate of shrimp, may increase the risk of overfeeding, and resulting poor rearing conditions.
– E. hepatopenaei, by affecting the shrimp metabolism, may affect the ability of shrimp to fight other pathogens WFS


Poor water quality

– Poor preparation of pond
– Incorrect biosecurity measures prior stocking, aiming at both viruses and bacteria
– Unstable phytoplankton
– Algal bloom and crash, stressing shrimp
– Incorrect N:P balance supporting the growth of cyanobacteria
– Poor management
– Insufficient aeration to maintan DO > 4 or 5mg/L (1HP for 300-400Kg)
– No control of ammonia and nitrite
– No control of sulphide WFS

Poor bottom quality

– Overfeeding
– Higher water temperature  Increased appetite, leading to risk of overfeeding
– Lower shrimp growth rate than expected  feeding not adapted
– Too high application of molasses, etc
– Unstable phytoplankton
– Algal bloom and crash, creating anaerobic sediment
– Poor management
– Accumulation of waste in pond bottom
– Insufficient aeration to support degradation of waste


Start with clean and healthy animals (broodstock, larvae, PLs)

Work with clean environment

Control EHP in previously affected pond

Pond sediment treatment:
– Apply CaO (quick lime,burnt lime, unslaked lime or hot lime) at 6 MT/ha
– Plough the CaO into the dry pond sediment (10-12 cm) and then moisten the sediment to activate the lime
– Leave for one week before drying or filling
– After application of CaO, the soil pH should rise to 12 or more for a couple of days and then to the normal range as it absorbs carbon dioxide and forms CaCO3


Control of vibrio during culture, using probiotic treatment

Control of vibrio during culture, using probiotic treatment


– Removal of white faeces, moults
– Control organic waste, using microbial products alone or in combination with oxidizing agents

– Control Vibrio load in the sediment/water, using probiotics that are and remain active in the farm conditions

– Control Vibrio load in the sediment/water, using probiotics that are and remain active in the farm conditions

Less Vibrio in the sediment

– Control Vibrio load in the shrimp gut

– Reduced Vibrio and improved utilization of nutrients

Better growth and FCR


– Prevent pathogen(s) transfer from one phase to the other
– Focus on EHP and Vibrio
– Prevent pathogens from (re)colonizing shrimp through waste removal/control
– Consider nutrition, health and environment


Source: Society of Aquaculture Professionals(SAP)


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