Taura at last

[Sean Stevens]

Dear Folks-

A while ago I posted requests for info regarding a vrus referred to in a 
NY Times article as 'Taura virus' which was the equivalent of shrimp 
Ebola (even the times gets into the hype). The article appeared June 14 
and was on page A16. Several of you asked if I had the name incorrect or 
if I found anything out to post here. I am happy to say that I didn't 
screw the name up, and through the help of several people much more 
knowledgeable than myself one article was found and faxed to me by Dr. 
Paul Frelier (thanks Paul!) I summarize it here:

D. V. Lightner, R. M. Redman, K. W. Hasson, and C. R. Pantoja

³Taura syndrome in Penaeus vannamei (Crustacea: Decapoda): gross signs, 
histopathology and ultrastructure² 

Diseases of Aquatic Organisms  Vol. 21 pp. 53-59 (1995)

Abstract:

	Taura syndrome (TS) is an economically important disease of Penaeus 
vannamei (Crustacea: Decapoda) that was first recognized in commercial 
penaeid shrimp farms located near the mouth of the Taura river in the 
Gulf of Guayaquil, Ecuador, in June 1992. The syndrome is now known from 
shrimp farms throughout the Gulf of Guayaquil, as well as from single or 
multiple farm sites in Peru, Colombia, Honduras, and Oahu, Hawaii, USA. 
Both toxic and infectious etiologies for TS have been proposed, but TS 
appears to have a viral etiology due to a previously unrecognized agent 
now called Taura syndrome virus or TSV. The disease has peracute and 
recovery (or chronic) phases, which are grossly distinguishable. 
Peracute episodes of TS are the most common manifestation of TS and 
occur in juvenile shrimp (of 0.1 to 5.0 g) within 14 to 40 d(ays) of 
stocking into grow-out ponds or tanks. Gross signs displayed by moribund 
shrimp with peracute TS includeexpansion of the red chromatophores 
giving the affected shrimp a pale reddish coloration and making the tail 
fan and pleopods distinctly red. Peracutely affected animals usually die 
during the process of molting. Those with peracute or acute TS that 
survive molting either recover or are chronically affected by TS and 
typically display multiple melanized cuticular lesions suggestive of 
Œshell disease¹. Shrimp acutely affected with TS display a distinctive 
histopathology that consists of multifocal areas of necrosis of the 
cuticular epithelium and subcutis (of the general cuticle, gills, 
appendages, foregut and hindgut), which are characterized by the 
presence of several to extremely numerous, variably sized eosinophilic 
to basophilic cytoplasmic inclusion bodies that give TS lesions a 
characteristic Œpeppered¹ or Œbuckshot¹ appearance, which is considered 
to be composed of an amorphous, granular, electron-dense matrix in which 
are often embedded numerous needle-like crystals of presumed calcium 
phosphate. The purpose of the present paper is to provide a definition 
of TS (based primarily on gross signs and histopathology supported by 
electron microscopy) as a basis for future studies on the disease.


	Apparently, this paper, and many of the ones referenced within it, are 
not found within medline, hence my difficulties in researching it. The 
discussion includes some interesting points. The initially recognized 
outbreak in Ecuador coincided with the first aerial spraying of 
agricultural fungicides in lands that drained directly into the Taura 
basin, and included several sterols. This prompted the theory that one 
of the sterols in question, ergesterol, which structurally resembles the 
crustacean molting hormone ecdysone, could be responsible for the TS 
etiology. This theaory was especially compelling in light of the 
peracute deaths at the molting stage. However, a number of industrial 
and academic studies have not supported this theory.

	The histopathology, the authors conclude, is consistent with a severe 
disruption of calcium metabolism, resutilng in calcium phosphate 
accumulation in the affected tissues. Although this may support a toxic 
basis for the disease, they state that researchers in Hawaii and Arizona 
(in press) have isolated a small (30 nm), icosahedral, cytoplasmic virus 
which induces TS when injected into healthy shrimp via cell-free 
homogenates. (Brock, J. A., Gose, R., Lightner, D. V., and Hasson, K. W. 
(in press) An overview on Taura syndrome, an important disease of farmed 
P. vannamei. Proceedings of the special session ŒSwimming Through 
Troubled Water¹. J. World Aquacult. Soc.)

	The authors note that although infectious and noninfectious disease of 
penaeid shrimp affect the same target tissues, none are sufficiently 
similar to be confused with TS. They specifically mention that 
infectious hypodermal and hematopoietic necrosis virus (IHHNV) has been 
ruled out based upon etiology, histopathology and in situ hybridzation 
with IHHNV-specific probes. In addition, yellowhead virus (YHV) can be 
distinguished by its predilection for the lymphoid organ, whereas TS 
creates no observable effects upon this organ.

	If anyone can get a hold of the article in press, I would appreciate a 
copy-there does not seem to be many resources for marine research here 
in midtown Manhattan! I would like to thank those of you who expressed 
an interest in this and cited this article. In particular I would like 
to thank Dr. Paul Frelier at Texas A+M who faxed me a copy of this 
article and was such a good sport about my pestering.
 
	Several people have mentioned to me over e-mail that this smells like a 
baculo-related virus. Do these symptoms support this notion or is the 
jury still out? I am still intrigued by the timing of the Ecuadorian 
outbreak and the fungicidal spraying. Could spraying cause a heightened 
mutation rate, creating a more virulent form of a previously weaker 
virus? In the NY Times article it is noted that many of the outbreaks 
seem to Œjump¹ from place to place (ie Oahu, Hawaii) with no apparent 
carrier. Is it possible that there is a quiescent or hidden phase to the 
infection, perhaps an integration event that after stress will erupt 
into an infectious phase? Also interesting is the fears expressed in the 
Times article that the spread of the disease is deliberate-a form of 
industrial sabotage. I am curious about the fact that wild shrimp appear 
unaffected-although they do not exhibit the disease, has anyone looked 
at whether they are carriers?

	Okay, that is more than enough out of me. I am curious how the rest of 
you think about this. E-mail me or post here if you would like to talk 
some more!

Sean Stevens  The Rockefeller University
stevens at rockvax.rockefeller.edu

P.S.-Can anyone tell me why the line count on all my postings (in 
parenthesis after my name) is always (0)?