Abstract

Many fish use a gas-filled swimbladder as a buoyancy organ. The swimbladder originates as an unpaired dorsal outgrowth of the posterior foregut, the pharynx. While in physostomous fish the embryonic connection to the pharynx persists, in physoclistous fish it is lost during early development. In most fish larvae, initial inflation of the swimbladder is achieved by gulping air shortly after hatching, but some species have been reported to inflate the swimbladder without surfacing. Failure to inflate the swimbladder reduces viability. Hydrostatic pressure increases with increasing water depth. Accordingly, the volume of the flexible-walled swimbladder is reduced during descent and increases during ascent. In order to keep the swimbladder volume and thus the buoyancy status constant, fish must secrete gas into the swimbladder during descent and gas must be resorbed from the swimbladder during ascent. Gas secretion into the swimbladder requires the activity of gas gland cells, which acidify the blood and thus induce a decrease in its gas-carrying capacity. As a consequence, gas partial pressures in the blood increase, providing a pressure head for the diffusive transport of gas from the blood into the swimbladder. In a second step, the initial increase in gas partial pressure in the blood is multiplied by back-diffusion and countercurrent concentration of gas molecules in a countercurrent system, the rete mirabile. Thus, very high gas partial pressures can be achieved in swimbladder blood vessels, high enough to explain the presence of gas-filled swimbladders at a water depth of several thousand meters.

Abstract

Histamine (or scombroid) fish poisoning (HFP) is reviewed in a risk-assessment framework in an attempt to arrive at an informed characterisation of risk. Histamine is the main toxin involved in HFP, but the disease is not uncomplicated histamine poisoning. Although it is generally associated with high levels of histamine (≥50 mg/100 g) in bacterially contaminated fish of particular species, the pathogenesis of HFP has not been clearly elucidated. Various hypotheses have been put forward to explain why histamine consumed in spoiled fish is more toxic than pure histamine taken orally, but none has proved totally satisfactory. Urocanic acid, like histamine, an imidazolecompound derived from histidine in spoiling fish, may be the “missing factor” in HFP. cis-Urocanic acid has recently been recognised as a mast cell degranulator, and endogenous histamine from mast cell degranulation may augment the exogenous histamine consumed in spoiled fish. HFP is a mild disease, but is important in relation to food safety and international trade. Consumers are becoming more demanding, and litigation following food poisoning incidents is becoming more common. Producers, distributors and restaurants are increasingly held liable for the quality of the products they handle and sell. Many countries have set guidelines for maximum permitted levels of histamine in fish. However, histamine concentrations within a spoiled fish are extremely variable, as is the threshold toxic dose. Until the identity, levels and potency of possible potentiators and/or mast-cell-degranulating factors are elucidated, it is difficult to establish regulatory limits for histamine in foods on the basis of potential health hazard. Histidine decarboxylating bacteria produce histamine from free histidine in spoiling fish. Although some are present in the normal microbial flora of live fish, most seem to be derived from post-catching contamination on board fishing vessels, at the processing plant or in the distribution system, or in restaurants or homes. The key to keeping bacterial numbers and histamine levels low is the rapid cooling of fish after catching and the maintenance of adequate refrigeration during handling and storage. Despite the huge expansion in trade in recent years, great progress has been made in ensuring the quality and safety of fishproducts. This is largely the result of the introduction of international standards of food hygiene and the application of risk analysis and hazard analysis and critical control point (HACCP) principles.

Abstract

The broad phyletic distribution of air breathing among bony fishes, the diversity of this group’s aerial-respiratory specializations, and the diverse ways that bimodal breathing has permeated the natural history of many species provide an important comparative perspective on the evolution and biological significance of this adaptation. The long-term view of fish air breathing emphasizes its importance in the evolutionary transition to vertebrate terrestriality; a key role in this process was played by the fishes which were the first air-breathing vertebrates. On the other hand, air breathing in most extant fishes has not led to terrestriality. Rather, auxiliary air breathing, which has evolved independently in many groups, enables a species to remain in or to exploit an aquatic habitat from which it would otherwise be excluded.

Abstract

The ears of all fishes function like accelerometers and respond to acoustic particle motion. Some species, in addition, have sensitivity to sound pressure via an otophysic connection between the ears and a bubble of gas in the body. All fishes can hear within a frequency range extending from below 50 Hz to as high as 5000 Hz for some species. Most species have a best sensitivity in the range from 100 to about 1000 Hz. All fishes can discriminate between different frequencies with moderate accuracy, and sound detection in all fishes is subject to masking, or interference by external noise.

The ornamental and food fish aquaculture industries continue to flourish and grow, and they form an important part of the economy of the United States. Concomitant with this growth is the discovery of new diseases as well as a greater understanding of diseases that afflict these animals. This article reviews the fungal diseasses of fish, including the diagnosis, pathology, and prevention and treatment of these diseases.