- Pathophysiology of fish diseases
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2.1.1. Introduction |
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Pathology:
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Pathology is defined as study of disease and their causative
agents.
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2.1.2 Disease |
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Disease
is due to the change in condition i.e. some change from the normal metabolism
or activity of the animal.
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Disease
is the combination of three factors namely (i) Animal (ii) Environment
(iii) Pathogen / causative agent; which are present in culture system
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2.1.3 Pathogens |
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Pathogens
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Pathogens
are the causative agent. Pathogens are of two types namely
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i)
Obligate pathogen
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ii)
Opportunistic pathogen
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i)
Obligate pathogen
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Organism
which will cause disease because of the mere presence in the culture system is
said to be obligate pathogen. This is mainly due to the interaction between
animal and environment. eg. Aeromonas salmoniclda
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ii)
Opportunistic pathogen
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Organism
which will not cause disease even if it is present in the culture
system. organism that is normally a commensal or does not harm its host
but can cause disease when the host's resistance in low.
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Eg.
Vibrio sp in shrimps,
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Aeromonas
hydrophila (It is a
fresh water species universally present which cause disease when the condition
is favourable).
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2.1.4 Stress |
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Selye
(1950) defined stress as the sum of all the physiological responses by which an
animal tries to maintain or re-establish a normal metabolism in the face of a
physical or chemical force.
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In
general change in normal condition i.e. change in chemical, physical, biological, physiological factors or parameters that cause stress.
When the stress increases in a moment it can cause disease.
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The
changes which occur in response to environmental stress are termed as General
Adaptation Syndrome, by which animal tries to adopt to
its original condition.
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These
adaptations normally occur in three phases.
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i)
Alarm reaction
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ii)
Stage of resistance
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iii) Stage
of exhaustion
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i)
Alarm reaction
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This
is due to physical response of the animal to stressor i.e animal
escape due to the external stimuli eg:handling nething change in physiology
if D.O reduces significantly and the animal comes to the
surface, chemical change i.e. change in pH or dissolved oxygen or range amount
of ammonia.
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ii)
Stage of resistance
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During
this period, adaptation to achieve homeosatasis under the changed circumstances
takes place.
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iii)
Stage of exhaustion
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When
the animal is unable to achieve homeostasis i.e. resistance / change.
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the
animal gets exhausted. If it reaches this stage, it may lead to disease.
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When
an animal course these three stages and comes back to the normal condition, the
animal does not have disease.
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2.1.5.1 Production of GAS |
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The
changes occurring during the GAS are non specific ie, neither species
specific nor stressor specific eg. anoxia, infection, fright, forced exercise,
anaesthesia and many other stressors provoke similar responses in higher and
lower vertebrates.
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.1.5.2 Adaptation of animals in GAS |
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The
events comprising GAS are mediated by a hormonal and nervous
reaction. Hypothalamic Pituitary Interrenal(HPI) axis plays a central role
in regulating the response of animals in presence of a stressor. The
hypothalamus senses the stress by environmental stimuli received through
sensory neurons. Hypothlamus responds to these signals by activating the
pituitary. The pituitary which is the master gland controls the endocrine
system.Pituitary responds to the activation by secreting proper tropic factors
which in turn activate the respective glands to secrete their hormones.
Interrenal axis picks up the signals from the pituitary gland and gives stress
hormone namely
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a)
Cortisol (involved with glucose metabolism)
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b)
ACTH (Adrenocorticotropic hormone is involved with retention of Na+ and
Cl- and excretion of k+)
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The
response generated by the secretion of one endocrine hormone will result in activation
of other downstream components of endocrine system resulting in a consequent
change in the physiology, biochemistry and metabolism of the animal.
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Temperature
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It
is the most important stressor affecting the balance between the fish host and
the environment. As the temperature approaches the maximum and minimum range
for the animal the chances for pathogenic invasion increases. Alteration in
temperature may affect the rate of multiplication of micro-organisms, the
amount of dissolved oxygen in the water, the rate of excretion of metabolites
or, most importantly, the host immune response.
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Other
stressors include accumulation of waste, very high stocking density, presence
of predators, life stage of the animal etc.
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Inflammatory
response
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Inflammatory
response may be defined as the series of changes that take place following
injury, however caused, provided that the injury is not severe as to completely
destroy the affected tissue. Since fishes bare poikilotherms,
change in temperature has a great influence on its inflammatory response.
Principally protective in nature but at times may initiate severe disease in
certain sites.
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2.1.7 Inflammation in higher vertebrates |
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Inflammation – It is a change happening in the animal due to a
stressor. The cardinal signs of inflammation in the higher vertebrates are
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a)
Rubor (Redness). This is due to the dilation of capillaries mainly due to
increase in the blood flow in blood vessels.
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b)
Tumor (swelling). When the capillaries are dilated the fenestrae (pore in the
capillaries) size grows up allowing the largest serum protein molecules such as
fibrinogen and immunoglobulin to exude into the tissues .
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c)
Calor (heat). This is due to increased physical activity
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d)
Dolore (pain). The nerve endings will be stretched which carry message and
cause pain.
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e)
Et functio laesa (Loss of function). It happens when the integrity of
the system is damaged or broken. This is due to a combination of pawi,
swelling and destruction of tissues.
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2.1.8 Inflammation in vertebrates |
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Inflamatory
response occur following the release of pharmacodynamic amines (especially
those found in mast cells histamine and 5-hydroxy tryptamine). They may be
released by an agent capable of causing tissue damage, as almost all tissues
have some component of mast cells. The most common causes of such are
microbes and their excretory products (toxins), physical and chemical trauma,
death of cells from circulatory insufficiency and the immune reactions. White
blood cells migrate through the fenestrae to the affected tissue. The degree of
cellular migration depends to a considerable extent on the stimulus.
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The
cells which leave the blood include
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1)
Neutrophils (Polymorphonuclear leucocytes)
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2)
Monocytes or Mononuclear macrophages
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3)
Lymphocytes
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4)
Thrombocytes
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2.1.9 Types of Inflammation |
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Basically
all the inflammatory responses can be categorised into two forms.
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They
are:
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1)
Acute Inflammation
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2)
Chronic Inflammation
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2.1.9 Types of Inflammation |
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Basically
all the inflammatory responses can be categorised into two forms.
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They
are:
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1)
Acute Inflammation
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2)
Chronic Inflammation
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2.1.9.1.1 Resolution |
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The
cause of inflammation is countered rapidly and tissue returns to normal by means
of repairing of damaged tissue through local proliferation
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2.1.9.1.2 Exudates |
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Exudates
are the result of the continued production of the products of the inflammatory
response and depending on the site and stimulus may rarly be suppurative,
catarrhal, fibrinous, serous or diptheritic.
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2.1.9.1.3 Necrosis |
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Necrosis
is the death of the cell. Resolution and exudation is reversible. But necrosis
is nonreversible. This is caused due to prolonged inflammation and at this stage the inflammatory response ends.
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Types
of necrosis
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i)
Liquefactive necrosis
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It
results from the enzymatic digestion of cells.
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Enzyme
can be produced either by host cell (such as neutrophils) itself or
by lytic toxins released by infecting bacteria
.e.g:- acute furunculosis and vibriosis of teleost fish.
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ii)
Coagulative necrosis
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It
results due to the loss of blood supply to an area (ischaemia). When the
coagulative necrosed area is invaded by the saphrophytic pathogens which
digest the dead tissue the necrosis
is gangrenous .
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In
section coagulative necrosis
is recognized as an acidophilic area where the cell nuclei is destroyed but
outline of cells are still visible .
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iii)
Fat necrosis
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It
is a rare form of necrosis
where necrotised area is found to be associated with soapy fat consistency and
is usually whitish in colour. It is mainly due to the lipase enzyme released by
the damaged pancreatic tissue.
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Stages
of necrosis
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Stages
of necrosis
nuclear changes observed in recrosed cell and not stages can be recognized
best by observing the nucleus. There are three stages :
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i)
Pyknosis
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ii)
Karyorhexis
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iii)
Karyolysis
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i)
Pyknosis
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Characterised
by the presence of shrunken and very dark nucleus.
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ii)
Karyorhexis
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Refers
to rupture of the nuclear membrane and fragmentation of the nuclear
chromatin.
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iii)
Karyolysis -dissolution of nucleus
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As
the nucleic acid are hydrolyzed, they lose their basophil and the whole tissue
assumed a shiny pink colour. They appear as very dark,haematoxylinophilic,
irregular tadpole or trypanosome – shaped structure usually against a pale
shiny structure less back-ground.
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Chromato
lysis- disappearance of nucleolus
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2.1.9.2 Chronic inflammation |
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Chronic
inflammation
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ailure
of the acute inflammation lesions to resolve leads to chronic inflammation, which in contrast to acute inflammation does not resolve quickly. it is characterized
by simultaneous inflammation and proliferation of neighbouring support tissue.
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Granulomata
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Chronic
inflammation some times lead to a progressive lesion
progressing to fibrosis
and lesion is known as granuloma. Granuloma is defined as a mass of inflamed granulation tissue,
usually associated with ulcerated infections. It is a white to
yellow in colour which may have a cheesy or hard consistency or
even be calcified. It may be caused by foreign bodies such as silicaceous
diatoms, bacteria
such as Myxobacterium tuberculosis and Reninbacterium salmoninarum
or fungi
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