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Nutritional pathology of fishes
Dr. M. Rosalind George
Assistant Professor (SS)
Department of Aquaculture
Introduction
Nutritional diseases are not common in the wild
fish.
In the case of the farmed fish, complete diets are
provided taking into consideration of the nutrient
requirement for that fish.
In case of pond reared fish, provision of
supplementary diet serves to enhance the growth
rate of fish and they are expected to obtain some
part of nutrition from natural environment.
Nutritional disease has been defined as the
deficiency, excess or improper balance of
components present in a fish diet.
Loss of nutrients happen in artificial diets due to
improper mixing of wet diets /trash fish or during
storage
In case of fish larvae of fast growing fishes when
starved, they reach a stage called point of no
return at which the body damage induced by the
catabolic breakdown cannot be recovered even
when the normal nutrition is resumed
Physiological characterization of nutritional pathology - by
loss of weight and change in body shape. Fish becomes thin
and head becomes relatively larger in proportion.
Skin becomes dark and fish lose appetite. Necropsy shows
anaemia and absence of abdominal lipids.
Liver is shrunken with sharp edges and the intestinal caeca
will be without visceral fat.
Histological- granular degeneration of skeletal muscle
fibres - Digestive tract condensed - Haemopoietic tissue
dark and condensed - increase in melanin content of spleen
and kidney - high level of hemosiderin in
melanomacrophage centres.
Nutritional deficiency and
imbalance diseases
Deficiency diseases are divided into two types
1. deficiency or imbalance of the macronutrients
of the diet – the protein, carbohydrate, lipid and
fibre- and
2. deficiency of the micronutrients – the vitamins
and minerals. Most frequent problems arise in the
lipids and digestible carbohydrate components of
macronutrients.
Protein
All fishes require high levels of high quality protein for
protein synthesis and gluconeogenesis.
Deficiency arises from improper processing or improper
formulation/ or ingredients.
Deviations in the level and availability of essential amino
acids in feeds cause growth impairment.
Lysine deficiency cause dorsal fin erosion
Tryptophan, leucine, lysine, arginine or histidine deficiency
cause spinal abnormalities
Methionine and tryptophan deficiency associated with
cataract
Carbohydrate
Fishes have limited capacity for
carbohydrate metabolism than higher
vertebrates.
Excessive carbohydrate lead to hepatic
degenerative changes and glycogen
deposits. Reports indicate that high level
of carbohydrates in the diet will lead to
excessive glycogen deposits in the liver
and continued intake can result in
extensive lipid deposition in the viscera.
Fats
Dietary lipid disease problems appear to be the most
serious nutritional problems in fish.
Fish tissues contain essential fatty acids (n-3) as well as a
general lipid contribution to calorie requirements.
Deficiency syndrome - fat cells surrounding the lateral
lymphatic sinus are particularly affected with thickening
and deformity of lipid cell walls, increased vascularity and
deposition of a hyaline material between the cells.
Essential fatty acids
Deficiency cause swollen, pale liver with fatty infiltration,
consistent anaemia with lack of secretion of haemopoietin
by compromised liver- mortality
Auto-oxidation lead to reduced availability and the
oxidation of free radicals
peroxides aldehydes and ketones are toxic and react with
other dietary components.
The rancid fat causes lipoid liver degeneration
Essential fatty acids
contd..
Clinical features - extreme anaemia with pale
gills. Liver appears swollen and bronzed with
rounded edges.
Histologically, lipid infiltration
There is inactivity of renal and splenic
haemopoietic tissue and melanomacrophages are
replete with high levels of pale staining pigment.
Fibre
Less ill effects of low levels of fibres.
Catfishes require fibres in the diet to move
nutrients along the absorptive pathways
slowly.
Micronutrients
Fat-soluble vitamins: Due to high levels
of vitamin, liver necrosis and hepatocytes
destruction may occur.
Vitamin A (Retinol):
Hypovitaminosis A - reduced growth,
exophthalmia, keratomalacia, thickening
deformation of the gill arch and operculum.
Hypervitaminosis A – choroidal (vascular tissue of
eyes) inflammation, corneal oedema , nervous
effects. Extensive necrosis of tail, splenomegaly,
hepatomegaly epithelial hyperplasia and osseous
dystrophy. Unless extreme, they are readily
reversible.
Vitamin D (Calciferol):
reduced growth rate and
reduction in body ash, calcium and
potassium levels.
Vitamin E (Tocopherols):
functions as a component of a complex protective system
against the toxic effects of free radicals
metabolism is linked with selenium.
controls architecture of cell membranes.
Clinical conditions - muscular dystrophy (any degenerative
disorder resulting from inadequate or faulty nutrition),
swim-bladder, digestive and cardiac muscle pathology and
anaemia.
Most prominent is polymyopathy syndrome or pancreatitis.
Histologically - myopathy affecting red muscle, cardiac
muscle and oesophagus
Degeneration of pancreatic acini and increased fibrosis of
periacinar fat.
Vitamin K
Involved in blood-clotting mechanism
Has bacteriostatic and coenzyme properties.
Chronic vitamin K deficiency is similar to those of
viral haemorrhagic septicaemia.
Water-soluble vitamins:
In young fish, the general features of poor growth are
anorexia and pigmentation alterations and this rarely
forms clinical features.
Thiamin: Thiamin (Vitamin B1) deficiency caused by
a diet short of thiamine or by presence of thiaminase
enzyme
Thiamin deficiency cause petechial (pin prick type)
haemorrhage, fin necrosis, ataxia (Inability to
coordinate voluntary muscle movements; unsteady
movements and staggering) and nervous signs.
Histology - haemorrhage and degeneration of specific
nuclei of the periventricular areas of the brain
Riboflavin:
This is a coenzyme for oxidase
systems important in respiration of
poorly vascularised tissue like cornea
and lens of the eye.
Lack of riboflavin can cause petechial
haemorrhage in carp and congenital
dwarfism in channel catfish.
Pyridoxine
Deficiency occurs rarely
causes histopathology including renal
ovarian and hepatic degenerative
changes, thyroid colloidal deficiency
and haemopoietic hyperplasia in
farmed Atlantic salmon.
Pantothenic acid:
Deficiency frequently observed.
Causes lamellar epithelial hyperplasia,
progressing proximally from periphery of
the gill as the condition develops.
Erosion of fins and barbels and superficial
skin ulceration
Inositol
Deficiency causes reduced growth
rate and mild ulcerative lesions on
the integument
Responds to the supplementation of
inositol.
Niacin
Deficiency is associated with wide spread
haemorrhages, dermatoses, muscle
spasms and oedema of gastric
submucosa.
It causes erosion of the dorsal epidermis
following exposure to UV light a condition
called as back peel.
A dose of 18 ppm niacinamide is
necessary to avoid skin damage in UV.
Biotin
Biotin is important as coenzyme for many
aspects of lipid and carbohydrate
metabolism.
In experimental biotin deficient diets,
effects such as darkening, anorexia,
reduction in growth, poorer feed
conversion and increased mortality will
occur.
This also causes modifications of epithelial
mucosal cells or mucin production.
Choline:
Lack of choline causes poor growth and
conversion.
Renal haemorrhages
Cyanocobalamin:
Absence result in anaemia and poor
growth accompanied by darkening and
variable erythrocyte depression.
Folic acid:
Is a coenzyme in haemopoiesis.
Lack causes anaemia
Common deficiency of folic acid and
cyanocobalamin causes severe anaemia.
Ascorbic acid: Vitamin C
Deficiency causes reduction in wound healing
capacity and
skeletal malformation syndrome including spiral
lordosis and scoliosis, spinal fracture, opercular
and gill lamellar deformity
A tendency for haemorrhage - may lead to
secondary infection.
Development of deforming diathesis
(Constitutional predisposition to a particular
disease or abnormality) of cartilage and osteoid
replacement of many bony tissues.
Mineral deficiencies and
imbalances
Mineral deficiencies can occur in farmed
fishes – caused by reduced bioavailability
due to dietary imbalance or its interaction
with other dietary ingredients such as
vitamins and fibres.
Within plant proteins the presence of
phytic acid may chelate trace elements
such as iron, copper and zinc.
White fishmeals reduce the bioavailability
of trace elements.
Iodine: Diets with fishmeal, will not have
iodine deficiency.
Deficiency - cause goitre (thyroid
hyperplasia).
Iron: deficiency leads to anaemia
Excess cause Ferric iron toxicity
Copper: absorption from water is easy
and hence deficiency is not reported
High levels shows slight anaemia.
It facilitates pathogenesis of V.
anguillarum in salmonids.
Manganese: def.- Poor growth, dwarfism and
cataract
In Oreochromis mossambicus, Mn def. resulted in
poor growth, reduced food consumption and loss
of equilibrium
Zinc: Def. caused by zinc binding agents such as
phytic acids and calcium.
Causes poor growth and skin and fin lesions,
complemented by bilateral cataract
In salmonids it is associated with riboflavin and
methionine deficiency and physical trauma such
as very low temperature and certain chemical
exposure
Dietary mineral toxicity
General characteristic of mineral toxicity reduced growth and poor food conversion
Cadmium excess - hyperactivity,
hypocalcaemia and osteoporosis.
Lead toxicity - development of black tails
and spinal curvature.
Calcium high levels - reduces toxicity of
lead and zinc in salmonids.
Selenium: Strong relationship exists
between selenium and tocopherol (Vitamin
E)
Selenium supplementation with vitamin E
greatly enhances tocopherol activity in liver
but not in muscle
At higher level selenium is toxic to fish
especially with high level of carbohydrates.
Selenium – copper interaction affects
susceptibility to secondary infections
Calcium
Fish readily absorb calcium ions through gill.
Pathologies are caused by chelating capacity of
calcium leading to metal deficiencies
Two most important problems with calcium is visceral
granuloma and nephrocalcinosis.
Visceral granuloma is a specific condition confined to
the digestive tract of salmonids where local
granulomata develop in the stomach wall and become
mineralised, often resulting in large metastatic
calcified nodules.
Nephrocalcinosis is the precipitation within the renal
tubules of calcium complexes.
Calcium
Excessive levels of dissolved CO2 in water
causes urolithiasis, but it has also been
associated with magnesium deficiency
Selenium toxicity and nephrotoxic heavy
metal complexes in binders used in wet
feeding.
Mycotoxins
natural contaminants of feed components
aflatoxins - produced by Aspergillus flavus
are powerful carcinogens responsible for
wide spread occurrence of hepatocarcinoma
At 80 ppb or more, acute toxic syndrome massive local hepatic necrosis, branchial
oedema and generalised punctate
haemorrhage.
Toxic algae:
Toxic strains of Microcystis aeruginosa and
non-toxic Anabaena cause damage to
fishes.
Toxic marine algae the red tide organisms
are associated generally with acute
necrotizing branchial lesions.
Gyrodinium aureoleum causes severe
enteric and hepatic necrosis when
ingested.
Cottonseeds:
most common substrates for aflatoxicosis
contain 2 toxic components - gossypol, a yellow
pigment causing sudden anorexia and deposition of
large lipid globules within liver and kidney around
which a chronic granuloma is formed. In the kidney, it
also produces glomerular nephritis and tubular
necrosis.
Glandless unpigmented cottonseed kernel derived
from specially selected strains of cotton also carries a
toxic component - cyclopropenoid fatty acids powerful synergists of aflatoxin B1 and its
metabolites.
Ipil-Ipil toxins: The seedpods of
Leucaena or ipil-ipil contain high level of
toxic amino acid mimosine.
Causes poor growth, inappetence and
general cachexic condition.
Anthropogenic chemicals:
pesticides for agricultural crops - lead to
toxicity in fishes
deaths are usually rapid and associated
with massive liver and renal tubular
necrosis often with haemorrhage and
behavioural aberrations
Binders
High level of polycellulose binders in the
diet cause chronic degeneration condition
known as hepatorenal syndrome.
– characterized by vacuolation, necrosis and
ablation of the renal tubules with fibrous of
haemopoietic tissue, cast formation and a
biliary cirrhosis.
– affected fish grow slowly
– become inappetent and darkened
– and die eventually.
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