Photo: Graeme Finsen

Deformities

Deformities in rainbowfishes are occasionally found in wild population. However, such abnormalities are quite common among rainbowfishes kept in captivity. The cause of the deformities is often unknown, but often results from a wide range of causes, including genetic variance (hereditary factors), significant environmental changes, namely temperature, pH, disease, nutritional deficiencies, injury and environmental contamination. Intense inbreeding can also elicit such abnormalities in fish species but in the absence of sound evidence no single specific reason for deformities can be established. However, I believe that most deformities in rainbowfishes we see today in captivity are the results of inbreeding.

Available evidence suggests that deformities in aquarium bred rainbowfishes usually develop very early during the larval/juvenile stages. The most common deformities observed in rainbowfishes include spinal malformations (lordosis, scoliosis, coiled vertebral column), deformed operculum and fin malformations. Spinal malformations increased steadily with growth. Deformities become more common with inbreeding within a small gene pool over a span of several generations.

Deformities as a result of inbreeding have been observed in many hatchery reared fishes in aquaculture (Tave, 1986). The same trend has been observed in limited studies of aquarium fishes. There are cases of reproductive failure, growth reduction, bodily deformities, and behavioural changes in Amatitlania nigrofasciata, Brachydanio rerio, Poecilia reticulata, Carassius auratus and a number of other species due to inbreeding depression. In some species such as Poecilia reticulata, which have been exposed to sustained selective breeding for more than fifty years, a great many deleterious alleles have been eliminated. The rainbowfish breeder may like to establish 'pure lines' also, but in practice this is much more difficult to achieve.

The inbreeding depression observed in the convict cichlid (Amatitlania nigrofasciata) is comparable to the results seen from inbreeding rainbowfishes. Amatitlania nigrofasciata appears to be unable to survive extensive laboratory inbreeding without deleterious genetic effects (Winemiller & Taylor, 1982). No major deleterious inbreeding effects were noted until the F4 and F5 generations. Of the surviving (5 months) fry from nine F4 broods, 26.4% were moderately deformed and 58.1 % were severely deformed. Moderately deformed fish exhibited abnormal fins (often shortened with an absence of dorsal spines), a pronounced vertical slope of the forehead, shortened, flared opercula (exposing the gills at all times) and a permanently depressed hyoid apparatus. The position of the spinous dorsal fin frequently deviated laterally from the dorsal midline of deformed fish. Severely deformed fish were characterised by the same abnormalities, but in a more pronounced form. Severely deformed fish frequently exhibited moderate lordosis and abnormal swimming behaviour, wherein the head remained lowered and the lateral undulations of the body appeared grossly exaggerated. Of the surviving F5 fry (five broods), 17.6% were moderately deformed and 65.9% showed severe deformities. All deformed fish appeared to develop normally until the end of their most rapid growth phase (2-3 months). The variety of morphological and behavioural abnormalities observed in F4 and F5 inbred generations indicate that a number of genetic factors may act singularly or together.

The Zebra Danio, Brachydanio rerio inbred for four generations, exhibited vertebral abnormalities, a lack of swim bladders, protrudent jaws, opercular deformities, oedema and behavioural irregularities (Piron, 1978). Larval deformity occurred in a study (Badger, 2004) of Melanotaenia splendida as well i.e., in the larvae hatched from eggs obtained from fish fed a 20% lipid content diet. It is surmised that the high lipid content in the diet was the likely cause of larval deformity as it was not seen in the larvae from the 12% or 9% lipid diet trials.

In one study, deformed operculum was the most common deformity (37.6%) observed in Cyprinus carpio. The deformities were first observed at two months of age and the degree of deformity was variable but in most cases operculum was usually shortened with involuted edges. In some fish it was minimally shortened, while others had an operculum that was so malformed that the posterior gill lamellae were exposed. The deformity usually occurred only on one side; however, some of the fish had a bilateral deformed operculum. Fish with this kind of deformity swam normally, but growth was very slow. In some studies it was reported that operculum deformity was found to be non-inheritable and was associated with ascorbic acid (Vitamin C) deficiency in the diet.

It is also reported that some deformities in rainbowfish larvae, particularly spinal deformities, are greatly affected by dietary ascorbic acid levels during early rearing. Feeding trials (Ako et. al., 1999) using Pseudomugil furcatus found an unusual number of the fish had crooked spines at the end of the grow-out trials. The next batch of fry was fed brine shrimp enriched with a product containing ascorbic acid and the crooked spines largely disappeared. This points out the importance of early nutrition in fish rearing. Low doses (25-50 ppm) of ascorbic acid are reported to have a positive effect on growth and to reduce skeletal deformities. Duckweed can provide vital bio-pigments that are required for the development of improved colouration for captive bred rainbowfishes, and can also be a rich source of ascorbic acid (2.78 - 4.90 mg/100 grams dry weight).

Non-inflation of the swim bladder (belly-sliders) is another common problem often encounter in larval/juvenile stages of rainbowfishes. Swim bladder inflation is a fundamental developmental step during the early larval stage of most fish larvae. Initial inflation occurs when air, gulped by larvae from the surface, passes through the gut and is transferred via a pneumatic duct to the swim bladder lumen. Because the pneumatic duct exists for only a brief period of time in larval development before it regresses, inflation must occur during this narrow window of opportunity. Once the physical connection between the gut and swim bladder lumen has degenerated, swim bladder inflation cannot occur. This is one of several critical stages of larval development that may cause high mortality or swim bladder problems. Swim bladder inflation failure is common in intensively reared fish species. Non-inflation of the swim bladder commonly appears to affect about 5% of rainbowfish larvae. The swim bladder of rainbowfishes usually inflates within the first 12 hours of hatching.

Although the exact causes of swim bladder non-inflation remain uncertain, factors such as genetics, nutritional status or water conditions, probably play an important role. The use of surface skimmers to prevent build-up of surface oils on the water has been found significant to optimise swim bladder inflation. In several fish species spinal malformation was found to be associated with the absence of a functional swim-bladder. Swim bladder problems can also be caused by bacterial infection.

Predisposing factors that can cause deformities:

• Disturbance of fertilised eggs during the first 12 hours of embryonic development.
• Elevated levels of dissolved gases (CO2 etc.) during embryonic, larval and juvenile development.
• Accelerated water flows in the larval/juvenile tanks.
• Alterations in water quality.
• Fluctuations in water pH.
• Elevated levels of light intensity during larval development.
• Vitamin deficiency: There are numerous reports of deformities in aquarium fishes due to ascorbic acid and calcium deficiency. High levels of vitamin A have been observed to cause spinal effects in some species.
• Amino acid deficiency: Amino acids may be absent in foods due to improper formulation, extended storage or excess heat in processing.
• Hereditary: Mostly as a result of inbreeding - most prominent in aquarium fish.
• Heavy metals (arsenic, copper, lead, mercury), have been recorded as causes of vertebral defects.
• Spinal deformities associated with organophosphate, organochlorine and carbamate pesticides.
• Antibiotic therapy: Spinal deformities and decreased growth rates have been frequently observed in fish fed with therapeutic doses of Oxytetracycline.
• Infectious disease (particularly of bacterial origin).

Management and Prevention

• If the proportion of deformed larvae exceeds 25~30%, reject the whole batch.
• Careful selection, nutrition and conditioning of brood-stock.
• Proper collection and incubation of fertilised eggs.
• Meticulous control and recording of water parameters and larval management.
• Avoid inbreeding by using two independent lines from the same fish species.

Literature
Ako, H., L. Asano, M. Fukada and C.S. Tamaru (1999). Culture of the rainbowfish Pseudomugil furcatus and the use of a Hawaii-specific feed, Tropical Gold. I'a O Hawai'i. 2: 1-9.

Al-Harbi, A.H. (2001) Skeletal Deformities in Cultured Common Carp Cyprinus carpio L. Asian Fisheries Science 14: 247-254.

Badger, A. C. (2004) The effects of nutrition on reproduction in the Eastern Rainbowfish, Melanotaenia splendida splendida. Masters (Research) thesis, James Cook University.

Fracalossi, D., M. E. Allen, D. K. Nichols and O. T. Oftedal (1998) Oscars, Astronotus ocellatus, have a Dietary Requirement for Vitamin C. Journal of Nutrition 128: 1745-1751.

Heupal, M.R., Simpfendorfer, C.A. and Bennett, M.B. (1999) Skeletal deformities in elasmobranchs from Australian waters. Journal of Fish Biology 54: 1111-1115.

Piron, R.D., 1978. Spontaneous skeletal deformities in Zebra Danio (Brachydanio rerio) bred for fish toxicity tests. Journal of Fish Biology 13: 79-83.

Tave, D. (1986) Genetics for Fish Hatchery Managers. AVI Publishing, Westport, Connecticut, 299 pp.

Tave, D. (1999). Inbreeding and brood stock management. Fisheries Technical Paper No. 392. Rome, FAO. 122 pp.

Winemiller, K.O. and Taylor, D.H. (1982) Inbreeding depression in the convict cichlid, Cichlasoma nigrofasciatum (Baird and Girard). Journal of Fish Biology 21: 399-402.

Yousefian, M. and Nejati, A. (2008) Inbreeding Depression by Family Matching in Rainbow Trout (Oncorhynchus mykiss). Journal of Fisheries and Aquatic Science 3 (6): 384-391.

© Copyright Adrian R. Tappin
Created January, 2009