Aquaculture Disease
Processes
Dr. Craig Kasper
FAS 2253/FAS
2253L
Description of Syllabus
• Course Number and Title: FAS 2253/FAS
2253L, Aquacultural Disease Processes
• Lecture Time/Location: TTH/9:301045am/BSC 212
• Lab Time/Location: TH/11:00a12:40p/BSC 212
• Instructor: Dr. Craig Kasper, BHUM 111,
253-7881, ckasper@hccfl.edu
Description of Syllabus
• Exposure to fundamental and current
disease/health issues pertaining to the
production of aquaculture crops
• Prevention of diseases via practical diagnosis
and real-world decision making!!
• Covers: anatomy and physiology,
immunology, virology, bacterial diseases,
nutritional diseases, parasitology, mycoses,
larval diseases and general health
management
Syllabus
• Text: Fish Disease and Diagnosis (Noga,
Blackwell Publishers).
• Additional readings will be on reserve in the
library.
• Course will consist of weekly two-hour lectures (2)
followed by a two-hour practical lab.
• You will need “grubby” clothes on lab day
• No open-toed shoes in lab!!
• Labs may require observation and checking on
samples outside class period
Syllabus: lecture outline
Date
Topic
8/24
8/29
8/31
9/5
9/7
9/12
9/14
9/19
9/21
9/26
9/28
10/3
10/5
10/10
10/12
10/17
Introduction to Disease
Signs vs. Symptoms? What’s the difference?
Immune Response in Aquaculture Animals, Part 1
Immune Response in Aquaculture Animals, Part 2
Diseases of a Non-infectious Nature (Nutritional)
Exam 1
Common Viral Pathogens of Aquaculture Organisms, Part 1
Common Viral Pathogens of Aquaculture Organisms, Part 2
Common Bacterial Pathogens of Aquaculture Organisms, Part 1
Common Bacterial Pathogens of Aquaculture Organisms, Part 2
Exam 2
Probiotic Bacteria (Part 1)
Probiotic Bacteria (Part 2)
Molds and Fungi (Part 1)
Molds and Fungi (Part 2)
Exam 3
Date
Topic
10/19
10/24
10/26
10/31
11/2
11/7
11/9
11/14
11/16
11/21
11/23
11/28
11/30
12/2
12/7
12/9
Protozoans and Parasites Part 1
Protozoans and Parasites Part 2
Exam 4
Aquaculture Health Programs
Design of High Health Facilities/HACCP/Biosecurity
Practical Considerations
Regulations, Drugs and the FDA
Exam 5
Treatments
Ethics in treating fish.
Case Study (Real World Example)
Case Study (Real World Example)
Thanksgiving Break (No Class)
Presentations
Presentations
Final Exam (non-cumulative)
Lecture 1: Introduction to Disease
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•
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•
•
•
•
•
•
What is disease?
Types of diseases
Dynamics of infectious disease
Epizootiology of infectious diseases
What you have to do to be a disease agent
Disease reservoirs
Transmission
The host
Stages in an epizootic
What is Disease?
• Definition: any alteration of the body
or one of its organs so as to disturb
normal physiological function
• opposite of health = unhealthy or
dysfunctional
Why are diseases of such
concern in aquaculture?
– 1990: WSSV, a virus, devastates shrimp
culture in China, $600 million lost
– 1971: Flexibacter columnaris, a bacterium,
kills 14 million wild fish in Klamath Lake
– the Idaho trout industry loses 10 cents on
every dollar made to disease (death,
weight loss)
– future of finfish and shrimp culture may
hinge on our ability to control vibriosis*
*more on “vibrio” in a later lecture!
Types of Diseases
1) infectious: diseases due to the action of
microorganisms (animal or plant):
–
–
–
–
–
–
viruses: CCV, WSSV, TSV, YHV
bacteria: Vibrio sp.
protozoans
metazoans
fungi: Saprolegnia sp.
crustaceans: O. Isopoda
Types of Diseases
2) non-infectious: diseases due to non-living
causes (environmental, other)
– even a moderately adverse environment can lead
to stress, stress leads to epizootics
– a very adverse environment can cause disease
and mortalities directly (e.g., nitrogen gas bubble
disease, brown blood disease)
– the “other” category refers to nutritional, genetic
and developmental diseases
Types of Diseases
3) treatable vs. non-treatable
– non-treatable diseases are some of the worst
– include pathogens such as viruses, drug-resistant
bacteria, myxozoans
– white spot syndrome virus (shrimp) has no known
treatment
– Vibrio sp.: because of rampant over-use of
antibiotics in Central America, South America,
new, more virulent strains are developing
Dynamics of Infectious
Diseases
• First mode of infection demonstrated by Robert
Koch (1876) and his work with Bacillus anthracis
(anthrax)
• reached epidemic proportions in cattle, sheep
and other domesticated animals
• also can occur in man (as we are well aware!)
• Koch showed that a bacterium caused the
disease by using the following method:
Koch’s Method (Postulates)
• 1) find the organism common to all
infected animals, demonstrate its absence
in healthy ones
• 2) isolate the organism in pure culture
• 3) reproduce the disease in suitable
experimental animals
• 4) reisolate the same organism from
experimentally infected animals
Dynamics of Disease: Germ
Theory
• Koch’s work lead to what is known as the
germ theory: germs cause disease
• if you have germs you are diseased
• Renes Dubos (1955) refined the concept in
the following statement:
“There are many situations in which the microbe is a constant
and ubiquitous component of the environment but causes
disease only when some weakening of the patient by
another factor allows infection to proceed unrestrained, at
least for a while. Theories of disease must account for the
surprising fact that, in any community, a large percentage of
healthy and normal individuals continually harbor potentially
pathogenic microbes without suffering any symptoms or
lesions.”
Dynamics of Disease: stress
• Definition: any stimulus (physical, chemical or
environmental) which tends to disrupt homeostasis in an
animal.
• The animal must then expend more energy to maintain
homeostasis: less energy to combat disease
• Aquatic organisms are fundamentally different from
terrestrials: they are immersed in their environment,
can’t go somewhere else
• some disease agents are almost always present in the
water (ubiquitous)
• examples: Aeromonas sp., Pseudomonas sp., Vibrio
sp.
Dynamics of Infectious
Disease: how it occurs
•
Three-set model:
1. susceptible host
2. pathogenic agent
3. environment unfavorable to host/favorable to
agent
•
•
exceptions??: extremely large numbers
of bacteria, extremely virulent agent
stress throws a wrench into it all
Dynamics of Infectious
Diseases
• infection  parasitism  disease (infection can result
from parasitism, but neither necessarily results in
disease
• symbiosis: any association between 2 species
involving an exchange of matter and energy
• commensalism: symbiosis in which one partner
benefits, the other is neutral
• parasitism: symbiosis in which the parasite
(usually smaller) is metabolically dependent on the
host (larger); some harm intuitive, but not necessary
Epizootiology of Infectious
Diseases: terminology
• epidemiology: branch of medicine describing
occurrence, distribution and types of diseases in
populations of animals at distinct periods of time
and at particular places (usually refers to
humans)
• epizootiology: same as above (non-human)
• epidemiology is the study of the who, what,
when, where, how and why of disease
outbreaks
Epizootiology of Disease:
outbreak terminology
• enzootic vs. epizootic (endemic vs. epidemic)
• incidence: frequency of disease in a population over
time in relation to the population in which it occurs
(cases/yr)
• rate: number of new cases per number of population
(per thousand)
• prevalence: the expression of the frequency of a
disease at a particular point in time in relation to the
population in which it occurs (%)
• proportion: number affected/population
• mortality: the percentage expression of the frequency
of deaths over a period of time in the total population
(not a rate, a proportion)
How to Become a Disease Agent:
6 Commandments of Parasitism
1.
2.
3.
4.
5.
6.
7.
Find a proper host
Somehow get in or access inside
Find a home
Be fruitful and multiply
Get out once done or developed
Be transmitted to a new host
all this obviously involves specificity in the
host:parasite relationship
Host:Parasite Specificity
• Specificity is required for steps 1 and 3, above
(find a proper host, find a home inside)
• host specificity example: Shasta rainbow trout
are highly susceptible to Ceratomyxa shasta
while Crystal Lake individuals are completely
resistant
• reason: physiological specificity (the host must
meet all of the metabolic requirements of the
agent without destroying it immunologically)
Host:Parasite Specificity
• Another example: Why are centrarchids infected
with black spot metacercariae while walleyes
aren’t?
• Answer: ecological specificity -- the host and
agent must overlap in time and space
• Another type of specificity: tissue specificity
For Next Time….
• Will continue with introduction to disease
• Check books on reserve in the library….
• Lab tonight: fish interna/exeternal anatomy,
we provide dissection kits, etc.
Potential for Disease via
Infection: contributors
1.
2.
3.
4.
5.
6.
•
number of organisms (overwhelming)
infectivity (ability to get in)
virulence (ability to produce disease)
susceptibility of the host
agent’s ability to overcome host’s defenses
level of stress (REM!)
probablility of disease (Theobald Smith Model)
= (# agents x virulence of agents)÷(resistance
of host)
Possible Fates of an Agent
within its Host
1. host dies: agent proliferates, overwhelms
host, good parasites don’t do this, $$$$$
2. host lives: largely dependent on stress
–
–
–
host gets sick, but recovers (defense worked)
host doesn’t get sick (agent not virulent, wrong host)
survivors:
•
•
agent either eliminated or
carrier state established (host infected, but no obvious
disease, big problem)
– latent (not easily observed)
– patent (ongoing/observable)
Mortality Curves: bell shaped
25
Mortality Rate (fish/wk)
• Infectious agent or toxic
substance moves into the
population and then, after
time, no longer affects
events in population.
• Transmission is horizontal
with width of curve
proportional to incubation
time and period of
communicability.
20
15
10
5
0
1 2 3 4 5 6 7 8 9
Week
Agent??: typically bacterial
Mortality Curves: sigmoidal
25
Mortality Rate (fish/wk)
• Slight deviation from
bell-shaped curve
due to lag period in
course of disease (lag
phase of growth)
• Also, periods in which
the disease is not
communicable.
20
15
10
5
lag
0
1 2 3 4 5 6 7 8 9
Week
Agent??: typically bacterial
Mortality Curves: point
source
25
Mortality Rate (fish/wk)
• Population at risk was
exposed to agent at a
single point in time.
• All susceptible
members affected.
• Highly virulent
infectious type
disease of toxic agent
• Exposure to toxin.
20
15
10
5
0
1 2 3 4 5 6 7 8 9
Week
Agent??: chemical, viral
• Indicates exposure over
a long period of time
• slow incubation
• slow transmission
Agent??: possibly
nutritional
Mortality Rate (fish/wk)
Mortality Curves: plateaushaped
18
16
14
12
10
8
6
4
2
0
1 2 3 4 5 6 7 8 9
Week
Mortality Curves: multiple
spiked
14
Mortality Rate (fish/wk)
• Due to frequent but
intermittent exposure
to disease agent
• Data usually or
eventually indicate
plateau effect
• Must take care re
frequency of sample
12
10
8
6
4
2
0
1 2 3 4 5 6 7 8 9
Week
Agent??: physical parameter (e.g., low D.O.)
Theoretical Cumulative
Mortality Patterns
Degree of Infection
• Acute: high degree of mortality in short period
of time, external signs might be completely
lacking (e.g., CCV, IHNV, TSV, WSSV)
• Chronic: gradual mortality, difficult to detect a
peak (Aeromonas septicemia, furunculosis)
• Latent: disease agent present, but host shows
no outward sign, little or no mortality, sometimes
associated with secondary pathogen/infection
(CCV and Edwardsiella ictaluri)
The Reservoir Concept
• reservoir: the sum of all sources of the agent, the
natural habitat of the agent, where the agent comes
from
– The size of the reservoir is proportional to the chance of
spread of a pathogen
• transient reservoir: situation in which the epizootic
displays a seasonal pattern of either cases or carriers
• permanent reservoir: usually associated with
disease in which chronic carriers are shown
– good example: water supply, itself
Transmission
•
•
Definition: mode of transfer of disease to
a new host
Method 1) direct transmission: from one
host to another, either a) vertically or b)
horizontally
a) vertical transmission: from parent to offspring
 via male (Girodactylus, trematode in pipefish)
 via female (IHN)
b) horizontal transmission: from one member of a
population to another, one offspring to another
• contact: typically water borne (e.g., fish to fish)
• ingestion of agent or of infected aquatic
Transmission
• Method 2) indirect transmission: infection via
an inanimate vehicle, vector or intermediate
host
– vehicle: an inanimate object such as handling
equipment (nets, waders, etc.) or feed (e.g.,
aflatoxin)
– vector or intermediate host: animate object
• mechanical: vector is not essential to life cycle of
agent
• biological: agent spends some part of life cycle
in vector (e.g., water boatman and WSSV)
Disease Transmission:
getting in the door
Portals of entry, not as easy as they sound:
1. ingestion: e.g., Ceratomyxa shasta, BKD,
Myxobolus cerebralis
2. gill lamellae: e.g., Schizamoeba salmonis,
Ichthyobodo necatur
3. lesions: bacteria (Vibrio sp.), fungi
(Saprolegnia sp.)
4. active penetration: some metazoans,
dinoflagellates
The Host
• The ability of a host to acquire a disease
agent and demonstrate disease symptoms
can be expressed both qualitatively and
quantitatively
• qualitatively: resistance (ability of a host to
withstand the effects of an agent; e.g.,
Litopenaeus stylirostris to TSV)
• quantitatively: susceptibility (a measure of
the host’s ability to tolerate an agent)
Resistance: Primary
Factors
Physical barriers, inflammation, natural immunity,
acquired immunity
1. physical barriers: refers to innate
characteristic of animal body to penetration
(e.g., mucous slime layer, intact skin, mucous
membranes, exoskeleton)
• for fish, the mucous slime layer itself displays
an immune response (phagocytic properties,
antibodies)
Resistance: Primary
Factors
2. inflammation: basic response to any wound,
designed to seal off the area and reduce further
infection/damage
• manifestations (humans) include swelling, reddening,
loss of function, heat, pain
• manifestations (fish) possibly include heat and pain
• histological changes: local edema (swelling);
infiltration of neutrophils (type of white blood cell
produced in bone marrow) , lymphocytes (lymph
proteins), macrophages; fibroplasia (formation of
fibrous tissue in wounds)
Resistance: Primary Factors
3) Immune Response
1. natural immunity: inherited (discussed in detail
later)
2. acquired immunity: either active or passive
a) active: obtains antibody via contact with antigen
b) passive: antibody obtained via donor (vaccination)
–
discussed in following lecture
Resistance: secondary
factors
• Secondary factors associated with disease
resistance are either environmental in nature or
somatic (associated with host, itself)
• environmental factors: mainly stress resulting
from deviation in temperature, dissolved oxygen,
ammonia; inadequate nutrition; mechanical, etc.
• somatic factors: age, sex, species (e.g., IPN
affects only largest fry, potential for exposure,
immune experience via exposure, black
spermataphore, TSV)
Stages in Epizootic
• REM: epizootic is an outbreak of disease
1. incubatory: agent has penetrated host barrier,
found home and multiplying
2. clinical or subclinical: host adversely affected
(manifestations)
– depression (reduced activity)
– color change
– interrupted feeding behavior
– body contortions
– respiratory change
– mortality
Stages in Epizootic
3. terminal: host either dies or recovers
–
•
exception: in some very acute, highly pathogenic
diseases (e.g., MBV) death may occur so fast that
obvious signs don’t develop
NEXT: Immune Response in Aquaculture
Organisms