Here is an article for you to read as some parasites can cause fish tb.Not the author of this information.
Microsporidiosis
Neural microsporidiosis in zebrafish was first reported in 1980 in France (de Kinkelin 1980). The parasite has now been identified in zebrafish at many research and commercial facilities, and was recently assigned to a new genus and species, Pseudoloma neurophilia by Matthews et al. (2001). The infection appears to be linked to severe emaciation (often referred to as ‘skinny disease’), but its precise role (primary cause or secondary opportunist) has yet to be resolved. The infection is also found routinely in normal, healthy appearing fish. In a preliminary prevalence study at the University of Oregon Huestis Hall facility, 97% (29/30) of "skinny" fish and 30% (10/30) of normal, healthy appearing adult fish have microsporidial spores detectable by wet mounts of dissected spinal cords, and the former had heavier infections.
Microsporidia are obligate intracellular parasites with a complicated life cycle. The life cycle concludes with the production of an infectious and resistant spore, which is the only stage of the parasite that can live outside of the host cell. With most microsporidia, transmission occurs via the ingestion of the infective spore stage, and we have found the infection in exposed fish as soon as 8 wk after feeding infected tissues. There have also been reports of vertical transmission in other microsporidia of both vertebrates and invertebrates (Bandi et al. 2001; Dunn et al. 2001). We detect the spores of Pseudoloma in the ovaries and within eggs of zebrafish, and the role of vertical transmission of Pseudoloma in the spread of the infection is currently under investigation in our laboratory. Enhanced methods for diagnosis and treatment of the infection, and the link between the microsporidian and skinny disease are also topics that we are studying.
Clinical Disease and Gross Pathology. Emaciation and spinal curvature, such as scoliosis, are common in infected fish.
Microscopy. The primary site of infection is the central nervous system (spinal cord and hindbrain). Spores and associated inflammation are also noted occasionally in the skeletal muscle surrounding vertebrae and ventral nerve roots.
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Clinical signs of microsporidosis.
A. emaciation ("skinny disease")
and
B. scoliosis.
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Pseudoloma from brain. Giemsa stain
A. and wet mount with Nomarski’s optics
B. Bar = 10 ìm.
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Pseudoloma in histological sections.
A. Sagittal section showing spinal cord. X = xenomas in spinal cord. Xenomas also occur in ventral nerve roots (arrows) with associated inflammation (In).
B. High magnification of xenomas in spinal cord.
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Pseudoloma in histological sections – other sites of infection.
A. Low magnification showing inflammation in skeletal muscle. Bar = 100 ìm.
B. High magnification of muscle showing spores (arrows) in phagocyte.
C. Egg filled with Pseudoloma spores (X).
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Fungi-Fluor stained histological sections.
A. Low magnification showing numerous spores (stained blue with DAPI filter) in spinal cord xenomas (arrow).
B. High magnification of spores (S) in ovaries.
Diagnosis. The infection can be detected in wet mounts of the central nervous system that have been carefully dissected from infected fish. Because this is tedious and laborious, histology is the routine method by which the infection is observed. Spores are ovoid to pyriform, with a prominent posterior vacuole, and average 5.4 x 2.7 Fm. The microsporidium produces xenomas within the spinal cord and hindbrain of fish, and xenomas contain sporophorous vesicles with up to 16 spores. Sporoblasts and presporoblast stages (probably sporonts) are found rarely in small aggregates dispersed randomly throughout xenomas. Fungi-Fluor (Polysciences, Warrington, PA fluorescent stain binds nonspecifically to beta-linked polysaccharides found in cells containing chitin. As chitin occurs in spore walls of microsporidia, this stain is excellent for demonstrating spores in either tissue smears or histological sections. Weber et al. (1999) describes a related stain (Calcofluor) and other staining techniques for the identification of microsporidia.
Control and Treatment. Fumagillin has been widely used as an oral treatment for fish microsporidosis, usually with good success (see review by Shaw and Kent 1999). Fumagillin was first developed for treating Nosema apis infections in honey bees. Kano et al. (1982) reported that fumagillin was effective against the microsporidium H. anguillarum in eels (Anguilla japonica). Since this first report on treating microsporidiosis in fish with fumagillin, the drug has been used to treat N. salmonis infections in chinook salmon (Hedrick et al. 1991) and Loma salmonae infections in chinook salmon (Kent and Dawe 1994). However, this has not been tested with zebrafish microsporidiosis. The best method for control as this time is to remove and euthanize all emaciated and moribund fish as soon as possible to prevent cannibalism and further transmission.
Microsporidian spores may be resistant to disinfectants (Shaw et al. 1999), and at present it is not known if the levels of chlorine routinely used to surface disinfect eggs (chlorine 25 ppm for 5 min) will kill the spores. Moreover, we have observed eggs filled spores of Pseudoloma. The spores within intact eggs could be protected from chlorine, even if this concentration is effective for killing spores. It is recommended that all nonviable, unfertilized eggs be removed prior to the bleaching procedure.
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