Goldfish (Carassius auratus): biology, husbandry, and research applications
Ayelén M. Blanco , Suraj Unniappan , in Laboratory Fish in Biomedical Research, 2022
Swim bladder disorder
Swim float disorder or disease is one of the most common goldfish diseases. It tin can exist caused by several factors, including high nitrate levels in the water, sudden h2o temperature changes, a bacterial infection of the swim float, etc. However, the near mutual causes for this disorder are overfeeding and/or feeding a poor diet lacking in cobweb, which sometimes cause gas in the gastrointestinal tract and can lead to astringent constipation that would cause the abdomen to corking, preventing the swim bladder from functioning properly (Mayer and Donnelly, 2013b).
Symptoms: Swimming problems, including fish pond on one side, head up or head down, floating on the surface (sometimes upside down), or resting on the bottom, or struggling to rise.
Treatment: Stop feeding for 3 days, and then gradually start refeeding fish with a small amount of live food or cooked vegetables, peas, or beans.
Ricardo Yuji Sado , ... Bernardo Baldisserotto , in Biological science and Physiology of Freshwater Neotropical Fish, 2020
Swim (gas) bladder
The swim bladder nowadays in most Teleosts lies right above the digestive tract and beneath the spinal vertebrae (consequently right beneath the kidney) and is beside the pinnacle portion of the pleural ribs. Swim bladders may be filled with either air or oxygen, thus playing a key role in maintaining neutral buoyancy and lowering energy costs for fish to remain at any certain depth (Helfman et al., 2009). In some species, such equally the pirarucu, Arapaima gigas, the swim bladder is highly vascularized and functions equally a respiratory organ (Brauner et al., 2004).
The swim float may be connected to the digestive tract, more than specifically with the esophagus and stomach through a structure chosen the pneumatic duct (Fig. 2.sixteen). According to this construction and the evolutionary pattern of the swim bladder, teleost fish can exist grouped every bit physostomous (e.grand., pacu, goldfish, carp) or physoclistous (due east.g., Siluriformes in general). Physostomous fish maintain the connection of the swim bladder-esophagus all through the adult phase (Fig. ii.xvi), whereas physoclistous fish lose the pneumatic duct in the adult phase (Helfman et al., 2009).
Fig. 2.16. Digestive organisation and swim float of grass bother, Ctenopharyngodon idella, a physostomous fish. Presence of the pneumatic duct connecting the swim bladder to the esophagus. Pneumatic duct (Dp), swim bladder (Bn), esophagus (Es). Scale bar: ii cm.
(Courtesy: Carolina Zabini. Reprinted with permission of the author.)
In Clinical Veterinary Counselor: Birds and Exotic Pets, 2013
Basic Information
Definition
Swim bladder disease is a symptom of various underlying etiologies that results in aberrant buoyancy in the h2o cavalcade. The swim float is a gas-filled organ in the dorsal coelomic cavity of fish. Its principal role is maintaining buoyancy, but it is besides involved in respiration, sound product, and mayhap perception of pressure fluctuations (including audio).
Tin be seen in any species of fish but is especially common in globoid fancy goldfish (Orandas, Ranchus, Lionhead, Moors, Ryukins, fantails, etc.)
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Median age, three.five years in 1 study
Clinical Presentation
History, Primary Complaint
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Two clinical presentations of a buoyancy disorder in fish include positive buoyancy ("floaters") and negative buoyancy ("sinkers").
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"Sinkers" cannot maintain neutral buoyancy and may lay on the bottom of the tank in lateral recumbency.
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"Floaters" (the more common presentation in fancy goldfish) volition bladder at the surface on one side or upside down.
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In either presentation, the clinical signs can be transient or permanent.
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Many of these fish remain agile and alert with a good appetite.
Physical Exam Findings
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Physical examination may reveal intestinal distention.
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Secondary pare changes tin occur in both "floaters" and "sinkers" secondary to prolonged contact and desiccation, respectively. Dermatologic findings include erythema, erosions, and ulcerations.
Etiology and Pathophysiology
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Diseases of the swim bladder can outcome in overinflation or underinflation, causing positive or negative buoyancy, respectively.
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The verbal cause of buoyancy disorder is unknown.
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Possibilities include pneumocystis (infectious, idiopathic), swim bladder torsion, anatomic abnormalities of the swim float, mechanical obstruction of the pneumatic duct, poor water quality, low h2o temperature, and neoplasia.
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The status is especially common in globoid fancy goldfish and may be secondary to conformational changes in the torso brought about by selective breeding and genetics.
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Lite, floating foods such as flakes and pellets have been incriminated because they are theorized to expand with water in the digestive tract and occlude the pneumatic duct.
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A large number (up to 85%) of fish with buoyancy disorder may have underlying disease.
Leiomyosarcoma of the swim float in Atlantic salmon (Salmo salar) was outset recognized in pen-reared salmon at a commercial fish subcontract in Scotland in 1976 (Duncan, 1978; McKnight, 1978). The illness was noted in 4.vi% of the fish that were put in a sea muzzle the prior year. These fish were in poor physical condition and had multiple nodular masses on the surface of the swim float (McKnight, 1978). A second outbreak of disease occurred in 1996 in Atlantic salmon nerveless from the Pleasant River in Maine that were housed at a fish hatchery in Massachusetts and used as brood stock for the Atlantic salmon recovery program (Bowser et al., 2012; Paul et al., 2006). Mortality among the afflicted salmon from the Pleasant River peaked at 35% in the leap of 1998. Affected fish exhibited signs of sluggishness, hemorrhages on the fins and body and bloated abdomens that comprise firm nodular masses on the external and internal surfaces of the swim float. The swim bladder of affected salmon was expanded past the presence of these masses.
Histologically, the tumors are comprised of spindle cells organized into interlacing bundles divided by bands of collagen (Fig. 13.4) (Java et al., 2013; Duncan, 1978; McKnight, 1978). Neoplastic cells exhibit moderate anisocytosis, variable nuclear pleomorphism, frequent pyknotic nuclei and abundant mitotic figures. Tumor cells stain positive for desmin and weakly positive for smooth muscle actin, consistent with the diagnosis of leiomyosarcoma.
Figure xiii.4. Photomicrograph of Atlantic salmon swim bladder leiomyosarcoma.
Electron microscopy was used to examine neoplastic tissue collected from Atlantic salmon during the first outbreak of disease in 1976, which revealed the presence of budding retroviruslike particles (Duncan, 1978). These observations led investigators to pursue a molecular approach to place possible retrovirus sequences in swim float leiomyosarcomas collected from the second outbreak. Degenerate PCR primers that target conserved sequences in the RT genes of retroviruses were used to amplify a tumor-associated retroviral sequence (Fig. 13.2) (Bowser et al., 2012; Paul et al., 2006). The consummate sequence of Atlantic salmon swim bladder sarcoma virus (SSSV) was obtained and plant to be x.9 kb in length. SSSV contains gag, pro, pol and env genes and utilizes a methionine-tRNA as a primer for replication. Total-length viral transcripts and singly spliced env transcripts are detected in tumors (Paul et al., 2006). The virus has not been propagated in cell culture.
SSSV is an exogenous retrovirus that does not contain viral accessory genes, which distinguishes information technology from the complex fish retroviruses WDSV and WEHV. Phylogenetic analysis places SSSV between the Gammaretrovirus and Epsilonretrovirus genera. Unlike mammalian and avian simple retroviruses, related endogenous copies of SSSV are not present in the Atlantic salmon genome (Paul et al., 2006). SSSV-associated tumors contain high proviral re-create numbers (≥xxx copies per jail cell) and a polyclonal integration pattern (Paul et al., 2006). The mechanisms that lead to the accumulation of proviruses in tumors are not known.
Gross and microscopic features are used to confirm the presence of swim float leiomyosarcoma. The presence of SSSV can exist detected in blood of salmon by PCR (Bowser et al., 2002a,b). Salmon tin be screened for infection with SSSV using viral-specific PCR primers. At that place are no vaccines available.
In Fenner's Veterinary Virology (Fifth Edition), 2017
ATLANTIC SALMON SWIM Float LEIOMYOSARCOMA VIRUS
Sarcomas of the swim bladder in captively-reared Atlantic salmon (Salmo salar) have been described in both Scotland and Maine. These tumors appear equally smooth, firm, pale-tan masses that can constrict the swim bladder and cause languor, inappetance, and a significant level of mortality. The tumors, which are associated with an exogenous retrovirus, are composed of spindle-shaped cells that are variably immunopositive for α-smooth musculus actin and strongly immunopositive for desmin, characteristics consistent with their existence of shine muscle origin (ie, leiomyoscarcoma). The genome of Atlantic salmon swim bladder sarcoma virus differs from that of the epsilonretroviruses of walleye in being a uncomplicated retrovirus with, at well-nigh, 1 potential coding region in improver the gag, political leader, and env genes. Nevertheless, unlike nearly elementary exogenous retroviruses, no endogenous homologue was found in the Atlantic salmon genome, perhaps indicating the species is a contempo host and that the oncogenic potential of the virus is due to a viral gene production such as Env equally shown for Jaagsiekte sheep retrovirus. The Atlantic salmon swim bladder sarcoma virus is most closely related to an endogenous retrovirus of zebrafish (Danio rerio).
Bernd Pelster , David Randall , in Fish Physiology, 1998
B. Generation of High Oxygen Partial Pressures
In the swim bladder, high partial pressures of gas are generated in ii steps: an initial increase in partial pressure and a subsequent countercurrent multiplication (Kuhn et al., 1963). The initial increase in partial pressure level is achieved by a decrease in concrete gas solubility and/or a release of gas molecules from a chemical binding site; for oxygen, this is accomplished by liberation from the hemoglobin via the Root effect.
To initiate the Root effect, blood must be acidified during passage through the swim bladder, and this is accomplished by the metabolic and secretory activity of gas gland cells in the swim bladder epithelium. Gas gland cells are cuboidal or cylindrical with a size ranging from 10–25 μm to giant cells of 50–100 μm. Gas gland cells may be lumped together, forming a compact gas gland as in cod, or spread over the whole swim float epithelium every bit in the eel. They are polar with extensive basal membrane foldings, typical for secretory cells. In contrast to other secretory cells, however, these infoldings are not associated with large numbers of mitochondria. But a few microvilli are observed on the luminal surface of gas gland cells (cf. Pelster, 1997).
The metabolism of gas gland cells is highly specialized for the production of acidic metabolites. It is fueled by blood glucose, which, even under hyperoxic conditions, is largely converted into lactic acrid (D'Aoust, 1970; Boström et al., 1972; Ewart and Driedzic, 1990; Pelster and Scheid, 1993; Pelster, 1995a). Although aerobic metabolism appears to be almost negligible in gas gland cells, some of the glucose is decarboxylated by the enzyme 6-phosphogluconate dehydrogenase in the pentose phosphate shunt, forming CO2 without concomitant consumption of oxygen (Walsh and Milligan, 1993; Pelster et al., 1994).
Lactic acrid every bit well equally CO2 are released into the bloodstream (Steen, 1963; Pelster and Scheid, 1993) and acidify the blood. Though CO2 easily diffuses into the blood and into the red cells, the situation is more than circuitous for lactic acid. Experiments on gas gland cells in principal culture advise that the acid secretion from these cells may involve sodium-dependent pathways and in function be due to the activity of a V-ATPase (Pelster, 1995b). This acid release results in a remarkable acidification of the claret (Fig. iv). In the European eel, pH values as low as half-dozen.half dozen–six.viii accept been measured in blood afterwards passage of the gas gland cells (Steen, 1963; Kobayashi et al., 1990).
Fig. 4. Metabolic end products of glucose in gas gland cells are lactate (lactic acrid) and CO2, formed in the glycolytic pathway and in the pentose phosphate shunt (PPS) and tricarboxylic acrid cycle (TCA), respectively. Both metabolites are released into the bloodstream, causing an acidification. This acidification induces the Root shift and thus the release of oxygen from the hemoglobin, resulting in an increase in claret PO2.
In vitro measurements characterizing the oxygen-binding backdrop of Root event hemoglobins have shown that blood pH values below 7.0 usually are sufficient to provoke a maximal Root upshot. In the European eel, for instance, anodic components, which exhibit a Root effect, brand up well-nigh 60% of total hemoglobin and can be deoxygenated at pH values below seven.0 (Pelster and Weber, 1990). Titration of blood with CO2 indeed revealed that about 40–50% of eel blood is deoxygenated at an extracellular pH of seven.1 or beneath (Pelster et al., 1990). Given a hematocrit of about twenty–30%, typically observed in fish, deoxygenation of 40% of the respiratory pigment results in a remarkable increase in oxygen fractional pressure (Pelster and Weber, 1991).
The time courses of the initiation of the Root issue acquired by the release of COtwo and of lactic acrid should be different. Improvidence of CO2 and the presence of carbonic anhydrase activeness in the extracellular infinite (Pelster, 1995b), besides every bit in the erythrocyte, will allow for a rapid increase in reddish cell proton concentration, and thus for a rapid activation of the Root effect. On the other manus, membranes are not easily penetrated past protons so that ion transfer is required to bring the protons out of the gas gland cells and into the ruby cell. In consequence, proton transfer into the scarlet prison cell is much slower than improvidence of COtwo, peradventure resulting in a transient disequilibrium in extracellular pH. In this example, liberation of oxygen from the hemoglobin would occur just after leaving the capillary system of the secretory bladder, when the blood is already on its fashion to the venous rete mirabile. Gas deposition into the swim bladder initially would exist diminished, but oxygen dorsum-diffusion in the rete mirabile would exist enhanced so that the oxygen is non lost for gas deposition.
Acid production and release from the gas gland cells cause a significant acidification of the blood, but conscientious analysis of the acid–base of operations status of the blood during passage of the swim bladder revealed that, in the European eel, blood pH decrased from 7.82 ± 0.06 to seven.33 ± 0.04 during arterial passage of the rete mirabile (Kobayashi et al., 1990); i.e., the blood was acidified fifty-fifty before reaching the gas gland cells. This acidification is caused by dorsum-diffusion of acid—mainly CO2—in the rete mirabile (Pelster et al., 1990; Kobayashi et al., 1990). The high rate of CO2 production and release from gas gland cells assures that the PCO2 in blood returning to the venous rete mirabile exceeds arterial PCOii and establishes partial pressure gradient for CO2 from the venous to the arterial rete capillaries. The formation of COii in the pentose phosphate shunt of the gas gland cells not only contributes to the acidification of blood during passage of the gas gland cells, but also sets the phase for dorsum-diffusion of COtwo and acidification of the blood in the countercurrent system.
In analyzing the Root effect, both steps have to be taken into account, every bit shown in Fig. five. At pH 7.8, observed in the arterial blood supplying the swim float, about consummate saturation of the hemoglobin can be expected. Acidification of the blood downwards to pH vii.3, induced past back-improvidence of acid during passage of the rete, is sufficient to reduce the oxygen-carrying capacity of the hemoglobin by nigh 20%. The release of acrid from gas gland cells into the blood causes a farther decrease in pH to seven.1 and adds another fifteen–20% reduction (Fig. five). Thus, the acidification of blood in two steps during passage of the swim bladder ensures an nigh maximal reduction in the hemoglobin oxygen-carrying capacity.
Fig. 5. The subtract in the ratio O2 cap/(O2 cap)max with decreasing pH in whole blood of the European eel (Auguilla anguilla) in vitro, and pH and PO2 values in blood samples taken from swim bladder vessels of an in situ training of the eel. Co-ordinate to the pH values actually measured in swim float claret and the in vitro oxygen-binding characteristics of the blood, a severe subtract in the oxygen-carrying capacity tin be predicted to occur in the blood during passage of the swim bladder.
The importance of acid dorsum-improvidence in the rete mirabile for the generation of high POtwo values was demonstrated by experiments of Kobayashi et al. (1990), in which, due to a high charge per unit of oxygen degradation into the swim bladder, only a very small POii gradient was measured between the venous blood returning to the rete mirabile and arterial blood leaving information technology. Nevertheless, POtwo increased remarkably during arterial passage of the rete and dropped in the venous capillaries. These POii changes, however, were not accompanied by changes in oxygen content, precluding oxygen back-improvidence equally the underlying mechanism. Thus, the observed sevenfold increase in PO2 during arterial passage of the rete was induced solely by acrid back-diffusion in the rete, switching on the Root effect and partially deoxygenating the hemoglobin (Kobayashi et al., 1990). According to the bones concept of countercurrent concentration, the acidification of blood achieved by acid release from gas gland cells represents the single concentrating effect (Kuhn et al., 1963), the initial increase in gas partial pressure induced by a decrease in the effective gas transport capacity of hemoglobin (without change in the whole blood gas content). In a second step, this initial increment in gas partial pressure is then multiplied by back-diffusion in the countercurrent system, which results in increasing gas fractional pressures and gas concentrations on the arterial side of the countercurrent organization (Kuhn et al., 1963; Pelster and Scheid, 1992). The magnitude of the final gas fractional pressure that can be achieved largely depends on the magnitude of the single concentrating upshot (Kobayashi et al., 1989). Due to the action of the Root result, the single concentrating effect for oxygen by far exceeds that of inert gases and CO2 (Pelster et al., 1990). As model calculations take shown, extremely high PO2 values can be achieved by such a big single concentrating issue and subsequent countercurrent multiplication, certainly sufficient to explicate the presence of fishes with a gas-filled swim bladder at a water depth of several thousand meters (Kuhn et al., 1963; Kobayashi et al., 1989, 1990).
P.W. Hochachka , G.Northward. Somero , in Fish Physiology, 1971
B. High O2 Tensions
A master function of the swim bladder in those fishes which use this organ in hydrostatic function appears to be the secretion of O2 from the blood into the swim bladder, at times confronting exceedingly loftier concentration gradients. During gas degradation, lactic acid enters the blood circulating through the bladder epithelium. The pH of this blood drops to values approaching 1 pH unit lower than the pH of the blood entering the rete organization. This pH modify is brought nigh largely, if not solely, by lactic acid which is presumably produced as an end product of glycolysis in the swim bladder epithelium (Steen, 1963). These conditions raise two important bug: (1) high glycolytic rates are not normally expected in the presence of high concentrations of Otwo because of the Pasteur upshot (inhibition of glycolysis by loftier O2); and (2) the variability in intracellular pH may be expected to be high, being a function of the charge per unit of O2 secretion.
The Pasteur outcome is brought near by the development of a high energy accuse in the prison cell and the subsequent inhibition of the PFK reaction by high ATP concentrations. In swim bladder, the Pasteur event is absent (Brawl et al., 1955), probably because mitochondrial metabolism is reduced (Steen, 1963). Also, it is possible that swim bladder epithelium possesses forms of PFK which are not sensitive to inhibition past loftier ATP.
We accept little information on the pH responses of enzymes of the bladder epithelium. Swim float LDH, particularly at loftier substrate values, appears to exist less sensitive to pH change than do other LDHs examined (Hochachka, 1968b); in this way, this item enzyme appears to exist well adjusted for function in the microenvironment of the swim bladder epithelium. We do not know if the same is true for other enzymes.
The initial gaseous inflation of the swim bladder of larval fishes is accomplished past gulping air at the water surface, followed by transfer of air to the swim bladder via the pneumatic duct (Woolley and Qin, 2010). Although this is considered the mechanism for swim bladder filling in all species, Elsadin et al. (2018) suggested that initial filling of the swim bladder in white grouper (Epinephelsu aeneus) is achieved, at least in part, by means of oxygen unloading from hemoglobin to the swim bladder via the rete mirabile, and that dissolved CO2 may impair this crucial step in development. A limited amount of research has been conducted on the effects of dissolved COii on larval fishes in civilisation. Arguably, this is because biomass loads are much lower than in abound out production systems, and it is assumed that good water quality, including dissolved gases, are easier to maintain. However, aquaculture facilities for larval rearing are still based on recirculation technology with limited water exchange, and while biomass may exist low, feeding rates are high, and the possibility of CO2 accumulation cannot be ignored. Elsadin et al. (2018) investigated the furnishings of three levels of dissolved CO2; 0.8, 5.six, and 28.six mg Fifty− 1, on swim bladder inflation rate and volume in white grouper. In the normocapnic treatment, 79% of all fish had normal swimbladder inflation at 105 days mail hatch, only 57% of fish in the moderate hypercapnic successfully inflated their swim bladder, and only 42% were capable in the high CO2 group. How CO2 interferes with swim bladder filling if the procedure is physostomous, (i.e. by filling the swimbladder with engulfed atmospheric air via a pneumatic duct in the alimentary canal) is unknown, merely improper swim bladder inflation is a common problem in larval culture, and the potential role of dissolved CO2 warrants farther attention. Following swim bladder filling, gas regulation is achieved by unloading oxygen to the swim float via the rete mirabile, and in this process, dissolved CO2 appears to have an result, for reasons equally yet unknown. White grouper that had been exposed to medium and loftier concentrations of COii, but had successfully inflated swim bladders, showed over a 50% reduction in swim bladder volume (Elsadin et al., 2018). In the absenteeism of successful swim bladder inflation, fish are unable to properly orient themselves in the water column, tend to display erratic swimming and elevated metabolic rates, and have much higher bloodshed rates (Lund et al., 2014). It is generally causeless that larval fishes are more than sensitive to dissolved COtwo, therefore future work on hypercapnia in aquaculture should as well include aspects of larval husbandry, particularly at more moderate levels relevant for such rearing systems.
Q. Bone , in Encyclopedia of Ocean Sciences (Second Edition), 2009
Buoyancy
Well-nigh teleosts possess a gas-filled swim bladder of sufficient book to counterbalance the dumbo components of their bodies and render them neutrally buoyant. For most fish this requires a swim bladder around 5% of body volume in seawater, and 7% in fresh water, just there are fish with dumbo scales and heavier than normal bones that exceed these values: for instance, gurnards need a swim bladder around 9% of torso volume for neutral buoyancy, while in the gar Lepisosteus with its dense scales, the swim float occupies 12% of body volume. Neutral buoyancy is advantageous for several reasons, and is found in fish from the surface to the depths of the sea, but the use of swim bladder gas to achieve information technology demands remarkable physiological adaptations, including special backdrop of the blood, ingenious counter-current flow rete mirabilia serving the swim bladder gas gland, and a simple method of preventing gas diffusing out of the bladder. Since swim bladders obey Boyle's law most perfectly, depth changes can pose difficult bug. Ambient force per unit area changes by 1 atm (101.iii Pa) for every x-chiliad depth change, then it is small wonder that many fish like mackerel (Scomber) or tunas, which hunt up and down from the surface, either reduce or lose their swim bladders. Midwater and deep-sea fish suffer little from small depth changes, since a 10-m depth change at say 400 m volition inappreciably impact swim bladder volume. Nevertheless, numbers of fish similar myctophids undergo a daily vertical migration of hundreds of meters, following their vertically migrating copepod casualty, and information technology remains unclear whether they can retain neutral buoyancy over this broad depth range. That this is a real problem is suggested by the way that many adult myctophids replace the gas in their swim bladders with lipids like wax esters where the static lift provided alters little with depth.
Elasmobranchs lack swim bladders, and avert the complexities of gas regulation within them. Instead, sharks like basking sharks or the deep-sea squaloids gain static lift instead from depression-density oils like squalene stored in their livers, which offers lift that changes little as the fish changes depth. Even so, oil storage has its problems too, for there take to be complex biochemical controls to maintain buoyancy lipid split from that used for other purposes, including fuel for locomotion.
By-catch, underutilized species and underutilized fish parts as food ingredients
I. Batista , in Maximising the Value of Marine By-Products, 2007
8.iv.five Fish maws
Dried fish maws ways the stale swim bladder from different fish species. The swim bladder is a part ordinarily discarded in European fisheries, although dried cod maw is available in some niche markets where it is considered a delicacy. All the same, every bit reported by Clarke (2004) the foreign trade in fish maws to or through Hong Kong has been very of import for many decades. In the Far East dried fish maws are consumed equally a nutrient, simply information technology is also believed that they take medicinal properties. Fish maws are produced from a variety of species (Nile perch, Lates niloticus; croaker such every bit Bahaba taipingensis and Otolithoid.es brunneus; jew fish, Pseudosciacna sp.; eel, Muraemesox talaboieds, amongst others). The main characteristics looked for in the fish maws are shape, size, colour (transparency), species and gender. The processing involves splitting open the maw, washing and drying it in the sun. Fish maw is simply boiled with other ingredients to prepare a soup or broth or is cooked with beans. In Hong Kong the smaller fish maws are fried (dim sum) and consumed as a snack food, especially for breakfast. Swim float is also a potential source of gelatin (Regenstein, 2004).
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