Fish Diseases and Management

2.2.7 The Respiratory system

Gills are the primary respiratory organs in fishes. Gill being very delicate in structure, its external location and direct contact with the water is liable to damage by any irritant materials, whether dissolved or suspended in the water. The gills are also supplied with a rich source of nutrients and has relative safety of location for the pathogens and so are a favoured site for external protozoan and monogenean trematode parasite. Gill forms a ready route for bacterial and viral infection, both as a site of  primary infections  or as site of invasion leading to vascular or lymphoid dissemination.

Gill primarily consists of a gill arch, gill filaments (primary and secondary gill filaments) and gill rakers.

Secondary gill filaments or gill lamellae act as the primary site of gaseous exchange.

Pillar cells give support to the secondary gill lamellae. Pillar cells contain contractile protein which help the secondary lamellae to withstand the high pressure at which it receives blood supply from ventral aorta. Pillar cells have also been suggested to play a role in controlling lamellar perfusion.

Pathology

Gill arch is a highly calcified or ossified organ, hence does not exhibit much of pathology. The main pathology happens in primary lamellae and secondary lamellae.

Three types of pathological changes are well recognised in fish gill lamellae.

a) Lamellar oedema:

It is the fluid accumulation in the interstitial space of lamella mainly due to alteration in gill membrane permeability. It is reversible and  most frequent following  the exposure to chemical pollutants such as heavy metal, certain pesticide etc. Oedematous separation of primary and secondary gill lamellae with necrosis of lamellar epithelial cells leading to severe respiratory and osmoregulatory distress.

b) Lamellar hyperplasia

Lamellar hyperplasia is generally due to an increase in numbers and migration of the malpighian cells of primary lamella. As the thickness of the lamella increases, the entry of the pathogen into the blood is minimised. In some cases of lamellar hyperplasia caused due to acidification of water it has been found that chloride cells extend on to the surface of the secondary lamellae, and instead of being located in shrunken pits, bulges out on to the surface. This type of hyperplasia may interfere with the ionic flux across the epithelia and normal chloride cell function.

c) Lamellar fusion

Secondary lamellar fusion may take place as an ultimate result of massive lamellar hyperplasia which result in a solid fusion of many or all of the lamellar capillaries within a mass of hyperplastic epithelium. It is irreversible.

Pathology

Lamellar fusion reduces the surface area of lamella exposed to outside and hence lamellar exchange efficiency comes down. In order to fulfill the oxygen demand fish has to increase its water pumping rate, thus diverting more energy towards basic metabolism. Fish with above pathological symptoms may survive well under normal circumstances but as the water temperature increases with consequent increase in metabolic oxygen demand chances of mortality increases.