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mucus. Levy et al. (2007) observed that, infected fish sometimes develop a white or brown coloration (“velvet”)
or cloudy appearance, If the primary site of infection is skin, which is most visible when viewed with indirect
lighting such as a flashlight. Such fish may display signs of “flashing” or rubbing on tank walls, the substrate, or
other structures in their environment. Again, feeding behavior likely will be poor and some fish may appear
emaciated. Fish with
Amyloodinium
infection alone do not typically have ulcers, white spots, or fuzzy lesions, but
the skin can seem “hazy” in appearance. If the infection is confined to the gill, the “velvet” appearance will not be
present.
The present study showed that infested European seabass
Dicentrarchuslabrax
with
Amyloodinium ocellatum
appeared distressed, emaciated, and anorexic and showed flashing behavior. Also, there were gasping of air rapid
gill movement and lying on the bottom. There was rapid and mass death of fish. The affected skin showed friable
skin (velvet like appearance), darkened, excessive mucous secretions forming cloudy film of slime. Also, grossly
focal erosion areas were seen on the operculum and caudal tail. Schwarz and Smith (2009) observed by Light
microscopy of moribund and dead fry showed brownish or yellowish, round to oval-shaped trophonts attached to
the body of the fish. The infestation on July resulted to a sudden mass mortality. Some trophonts might have
completed its feeding stage and detached to become a tomont. Lom and Dikov (1992) mentioned that the method
of diagnostic is the identification of the trophont in the skin and gills of infected fish, which can be done through
microscope observation of these tissues. Trophonts are ovoid with 150-350 microns. Gills are first to be infected.
In this study it was concluded that intensity of infection in gill tissues was higher than in skin tissues respectively.
That indicates that primary site of infection and the main target organ of is gill tissues. Also that be confirmed
from the histopathologcal diagnosis that revealed mild hyprer plasia in skin tissue while in gill tissue was sever. In
this study Microscopic examination of skin and gills scrapings of examined D. labrax showed, round to oval small
dark brown mucoid
Amyloodinium ocellatum
stage. Different developmental life stages of
Amyloodinium
ocellatum
were seen in the gill and skin tissues as the two main inhabitant organs. The first stage was trophonts
with its root - like structure (Rhizoids). They showed distended appearance with the presence of feeding stage
trophonts dark brown color lodged between the gill filaments. Also, dislodged trophonts were also observed
between the skin and fin surface. In detached trophonts (feeding stage) the rhizoids root-like structure (that
penetrates deep in to epithelium causing substantial damage to tissue at the attachment site)of the attached
organelle was sometimes visible. The second was tomont stage; trophont stage feeds for several days, detaches,
retracts its rhizoids and becomes tomont. Tomonts (reproductive stage) in division were occasionally observed.
The third was Dinospores, the tomont divides, producing Dinospores, were not observed as it is a free swimming
stage in water. Paperna (1980) and Johnson (1990) mentioned that histologically, affected gills may appear
hyperplastic (a proliferation of cells) and lamellar fusion may be evident. Paperna (1980) suggested that
A.
ocellatum
is attached to and feeds from the host epithelial cell by means of rhizoids, which penetrate the host cell.
The consumed cell gradually degenerates and collapses.
Damage to infected cells leads to focal erosion of the epithelium. Prolonged infection exhausts a generation of
mucus cells and leads to accelerated desquamation. Proliferation of the epithelium causes obliteration of the gill
lamellae, while the inner strata of the epithelium become spongious and in some cases undergo complete lysis.
The histopathological diagnosis in present study revealed mild to severe histopathological changes. Severe
hyperplasia was shown in the gill epithelia and fusion of the secondary gill lamella which was caused by
Amyloodinium ocellatum
trophonts. Also Destructed secondary gill lamellawhich was caused by
Amyloodinium
ocellatum
trophont attachment to gill tissue was observed.
Amyloodinium ocellatum
trophont was surrounded with
tissue debri underneath a scale. Mild Hyperplasia and desquamation of the covering epithelium which was caused
byattachment of
Amyloodinium ocellatum
trophont to the skin tissue. Environmental and seasonal dynamics of
A.ocellatum
infestation is documented by Kuperman and Matey (1999) and Pereira et al. (2010). Noga and Levy
(1995) reported that Infestations of the gilthead seabream by the gill parasite
A. ocellatum
may occur, particularly
during summer. At the end of the growing season, when the water temperature increases within production ponds,
the proliferation of the ectoparasite and the damage done to the developing fish can rapidly reach devastating
proportions in terms of fish production. In Portugal, Menezes (1994) reported several outbreaks of
A. ocellatum
in
