AQUACULTURE EXTENSION MANUAL NO.

16 JULY 2000
SECOND EDITION

Diseases of Penaeid Shrimps

in the Philippines
C.R. L A V I L L A - P I T O G O , G . D . L I O - P O , E.R. C R U Z - L A C I E R D A ,
E.V. A L A P I D E - T E N D E N C I A and L . D . D E L A P E Ñ A

A Q U A C U L T U R E DEPARTMENT
S O U T H E A S T ASIAN FISHERIES D E V E L O P M E N T C E N T E R
Tigbauan, Iloilo. Philippines
 Aquaculture Extension Manual No. 16
Second Edition
July 2000

Diseases of Penaeid Shrimps in

the Philippines

Celia R. Lavilla-Pitogo
Gilda D. Lio-Po
Erlinda R. Cruz-Lacierda
Eleonor V. Alapide-Tendencia
Leobert D. de la Peña

Aquaculture Department
Southeast Asian Fisheries Development Center
Tigbauan, Iloilo, Philippines
AQUACULTURE EXTENSION MANUAL NO. 16
Second Edition
JULY 2000

ISBN 971-8511-43-1

Published and printed by:

Aquaculture Department
Southeast Asian Fisheries
Development Center
Tigbauan, Iloilo, Philippines

©Copyright 2000
Aquaculture Department
Southeast Asian Fisheries
Development Center
Tigbauan, Iloilo, Philippines

ALL RIGHTS RESERVED

No part of this publication may be

reproduced or transmitted in any form or
by any means, electronic or mechanical,
including photocopy, recording, or any
information storage and retrieval system,
without the permission in writing from
the publisher.

For comments
and inquiries Fish Health Section
SEAFDEC Aquaculture Department
Tigbauan, Iloilo 5021, Philippines
Fax (63-33) 335 1008
E-mail [email protected]
[email protected]
AQD website http://www.seafdec.org.ph/
 Foreword
Aquaculture is one of the fastest growing food producing sectors of the
world. However, disease outbreaks are increasingly recognized as significant
constraints to aquaculture production and trade affecting both economic
and social development in many countries.

Within the shrimp culture sector, the number of diseases has expanded
steadily with expansion and intensification of large-scale commercial
cultivation. Shrimp disease is considered as the single most limiting factor
to successful commercial production. There is therefore a pressing need to
develop and implement practical solutions to this problem.

Several countries in the Southeast Asian region have already begun to

take real and meaningful strides towards this end. The Southeast Asian
Fisheries Development Center, Aquaculture Department (SEAFDEC/AQD)
in its pursuit for responsible aquaculture has come up with a revision of
the manual Diseases of Penaeid Shrimps in the Philippines, to include
newly discovered diseases. We hope that this manual will be of considerable
help to shrimp farmers in identifying the disease and lead to prevention or
early disease diagnosis and control.

ROLANDO R. PLATON, Ph.D.

Chief SEAFDEC Aquaculture Department
 Table of Contents
Foreword
Introduction

Viral Diseases
Monodon Baculovirus (MBV) Disease 2
Infectious Hypodermal and Hematopoietic Necrosis Virus
(IHHNV) Disease 5
Hepatopancreatic Parvo-like Virus (HPV) Disease 8
White Spot Syndrome Virus (WSSV) Disease 10
Yellow Head Virus (YHV) Disease 12

Bacterial Diseases
Luminous Bacterial Disease (Hatchery) 14
Luminous Bacterial Disease (Grow-out) 17
Shell Disease, Brown/Black Spot, Black Rot/Erosion, Blisters,
Necrosis of Appendages 19
Filamentous Bacterial Disease 22

Fungal Disease
Larval Mycosis 26

Protozoan Diseases
Ciliate Infestation 30
Microsporidiosis, White Ovaries, Microsporidian Infection 33
Gregarine Infestation 35

Nutritional, Toxic and Environmental Diseases

Incomplete Molting 38
Swollen Hindgut Syndrome 40
Chronic Soft-shell Syndrome, Soft-shelling 43
Black Gill Disease 45
Blue Disease, Sky Blue Shrimp Disease, Blue Shell Syndrome 47
Red Disease, Red Discoloration 49
Underfeeding 52
Muscle Necrosis 54
Cramped Tails, Bent Tails, Body Cramp 56
Acid Sulfate Soil Syndrome 57
Asphyxiation, Hypoxia 58
Bamboo Back Syndrome 59

Appendices 62
Glossary 72
References 77
Acknowledgement 83
 Introduction
Cultured shrimp is a major export commodity of the Philippines. Because of
its high yield, monoculture of shrimps in semi-intensive and intensive
systems has been the preferred production method. However, this approach
led to the proliferation of diseases resulting in growth retardation, physical
deformity, reduced fecundity, physiological malfunction, and mortality.
Even if they are outrightly rejected, diseased shrimps command a lower
price in the market.

Diseases of penaeid shrimps may be caused by living agents like viruses,

bacteria, fungi, and epicommensals and parasites. Moreover, stress from
nutritional deficiency in the shrimp, exposure to toxic substances, and
advance rearing water parameters may also lead to disease. To sustain the
production of good quality shrimps, there is a need to understand disease
and the factors that contribute to its development and outbreak. Although
many solutions to disease problems need long-term study and research,
early detection and diagnosis are crucial factors to well-timed and prompt
control. Therefore, the shrimp farmer must be familiar with potential shrimp
disease problems that may occur.

It has been ten years since the first edition of this manual. Most of the
disease that were originally presented are included because of their
continued adverse consequence on shrimp culture systems. In addition
two viral diseases: white spot virus disease and yellow-head virus disease
are included. Both viruses have negative impacts on shrimp survival and,
therefore, of economic significance to the farmer. The devastating luminous
bacterial disease, which was the scourge of the shrimp hatchery industry
in the 1980s, found its way into pond culture systems causing massive
losses of stocks and disruption of a majority of pond operations in key
shrimp growing areas in the country. The continued appearance of new
shrimp diseases locally and globally has increased awareness in the
aquaculture community of the importance of diseases. Major efforts at
disease surveillance, containment and eradication are primary factors to
prevent its spread.

This manual aims to provide information on diseases observed among the

three major species of shrimps cultured in the country: Penaeus monodon,
P. merguiensis, and P. indicus. It includes the common name of the disease,
causative agent, species affected, stages affected, gross signs, effects on
the host, and methods of prevention and treatment. Although not all
diseases included have been photographed to show gross signs for
effective pond-side diagnosis, simple diagnosis using a microscope, can
be performed on site. Also included are diagrams to help readers recognize
the specific organs where histological sections in the figures are located.
Appendices, a Glossary and a Reference List are included for detailed
information about the diseases.

In cases where diagnosis has been established and chemical treatment is

indicated, it is necessary to test the tolerance of a small number of shrimps
to the chemical. Water parameters vary from place to place and what may
be effective and tolerated in one place may not be true for another. Moreover,
the indiscriminate use of drugs must be avoided because of the danger of
developing drug-resistant strains of the pathogen. Since, many of the drugs
available in the market are used for treatment of human diseases and thus
would consequently lead to public health problems.

The threat of viral and bacterial diseases as well as the deterioration of

culture environments and water source continue to make shrimp culture
challenging. The emergence of new shrimp diseases will continue with
intensification in shrimp culture. Fortunately, much of the historical data is
there for us to learn from.
 Viral Diseases

Monodon Baculovirus
(MBV) Disease
Infectious Hypodermal and
Hematopoietic Necrosis
Virus (IHHNV) Disease
Hepatopancreatic Parvo-
like Virus (HPV) Disease

White Spot Syndrome

Virus (WSSV) Disease
Yellow Head Virus (YHV)
Disease
Common name: MONODON BACULOVIRUS (MBV) DISEASE

Causative agent: Penaeus monodon-type baculovirus (75 - 300 nanomicrons)

Species affected: Penaeus monodon, P. merguiensis

Stages affected: Mysis, postlarvae, juveniles, adults

Gross signs:
• Affected shrimps exhibit pale-bluish gray to dark blue-black coloration
• Sluggish and inactive swimming movements
• Loss of appetite
• Retarded growth
• Increased growth of benthic diatoms andfilamentousbacteria may cause fouling
on the exoskeleton/gills
Infected pond-reared shrimps at 45 days of culture (DOC) stocked at 4 to 100
2
per m manifested slow growth rates and pale yellow to reddish brown
hepatopancreas
• High incidence of bacterial infections expressed as localized "shell disease"
• Significant mortalities can occur during stress and crowding

Effects on host:
• Causes destruction of the hepatopancreas and lining of the digestive tract
• Spherical, occlusion bodies fill up enlarged nuclei of hepatopancreatic cells
(Figure la and b) and discharged into the lumen (Figure 1c) after cells have
been destroyed. This maybe followed by necrosis with secondary bacterial
infection.
PL 3 is the earliest stage found infected with MBV. However, experimental
waterborne inoculation of MB V to mysis 2 (M 2), postlarvae 3 (PL 3), PL 6, PL 9
and PL 11 resulted in MBV infections within 12 days post-inoculation.
• Incidence rate of MB V reported was 20-100%
• Accumulated mortality of 70% was observed among P. monodon juveniles
cultured in raceways and tanks
Preventive methods:
• Use MBV-free postlarvae
• Eggs washed with ozone-disinfected seawater yielded 68% survival of PL 7
compared with untreated ones yielding 31% survival
• Reduce stress by good husbandry practices and good nutrition
• Experimental feeding of shrimp juveniles (0.2 - 0.3 g) using feeds with 100 ppm
phosphated ascorbic acid (MAP) for 92 days showed that shrimps with initially
moderate to severe infection of MBV displayed improvement in the histological
profile of the hepatopancreas and the absence of MBV occlusion bodies in the
cells
• Destroy infected shrimp juveniles by burning or burying in pits lined with lime
• Disinfect rearing facilities (Appendix I)
Treatment: None reported
Figure 1a. A squash preparation of the hepatopancreas of postlarval shrimp
infected with monodon baculovirus (MBV). The multiple intranuclear
occlusion bodies (arrows) are diagnostic for MBV. (Malachite green,
400X).

Figure 1b. High magnification of the distal region of the hepatopancreas of a

shrimp juvenile heavily infected with monodon baculovirus (MBV)
showing numerous multiple occlusion bodies within infected cells
(arrows). (Hematoxylin and Eosin (H&E) stain, 200X).
Figure 1c. Low magnification of the sagittal section of the hepatopancreas of
a shrimp juvenile heavily infected with monodon baculovirus
(MBV). Note the numerous multiple occlusion bodies within
infected cells and the lumen (arrowheads). (H & E,100X).
Common name: INFECTIOUS HYPODERMAL AND HEMATOPOIETIC
NECROSIS VIRUS (IHHNV) DISEASE

Causative agent: Parvovirus (20 ~ 22 nanomicrons)

Species affected: Penaeus monodon

Stages affected: Postlarvae, juveniles, adults

Gross signs:
• Shrimps show erratic swimming behavior, rising slowly to the water surface,
hanging and rolling over until the ventral side is up
• Shrimps become weak and lose their appetite for food. They repeat the process
of rising to the surface and sinking until they die usually within 4-12 hours.
• Decreased preening and delayed molting
• Acutely affected shrimps develop white opaque abdominal muscles, bluish to
distinctly blue cuticular color often with mottled buff to tan pigment patches in
the hypodermis and very soft cuticles

Effects on host:
• Affects the epidermis, lining of foregut and hindgut, nerve cord and nerve
ganglia, hematopoietic organ, antennal gland, connective tissues, muscles,
heart, gonad, mandibular organ, and hemocytes of shrimp
• Induces the development of eosinophilic inclusion bodies (Figure 2a) in the
affected cells in the early acute stage of the disease, followed by necrosis and
inflammation of target tissues
• Presence of the virus can cause death of the cells of the cuticle, blood-forming
tissues and connective tissues of the shrimp which leads to abnormal metabolism
and, eventually, mortality
• Inclusion bodies are common early in acute infections, later decreasing in
number followed by necrosis and inflammation of target tissues
• Poor resistance to stress; susceptibility to secondary infection
• Mortality rates of above 90% were observed among penaeid juveniles in
intensive culture systems
• Has been linked to the runt deformity syndrome (RDS)
• Some survivors of epizootic may carry the virus for life

Preventive methods:
• Use IHHNV-free stocks
• If the disease agent is suspected among cultured shrimp stocks, destroy exposed
shrimps and disinfect contaminated premises
• Strict hygiene
• Disinfection of ponds and inlet canals
• Use of only dry commercial feeds
• Pasteurize fresh feed at 60°C for 15 min
 • Fine screening of inlet water
• Refrain from exchanging water for at least three days after infected ponds have
been discharged
• Ban importation of non-indigenous shrimps
• Compliance with the Hazard Analysis and Critical Control Point (HACCP)
programs for product safety

Treatment: None reported

Figure 2a. Histological section of the antennal gland of juvenile shrimp infected
with infectious hypodermal and hematopoietic necrosis virus
(IHHNV) showing eosinophilic intranuclear inclusion bodies
(arrows). (H & E, 400X).

Figure 2b. Sagittal section of the heart of Penaeus monodon juvenile stained
with ShrimProbe (Diagxotics, Inc.). Note abundant probe-positive
cells (blue color). (100X).
Common name: HEPATOPANCREATIC PARVO-LIKE VIRUS (HPV) DISEASE

Causative agent: Parvovirus (22 ~ 24 nanomicrons)

Species affected: Penaeus monodon, P. merguiensis, P. indicus

Stages affected: Postlarvae, juveniles, adults

Gross signs:
• Retarded growth
• Loss of appetite
Benthic diatoms, protozoans such as Zoothamnium sp., and filamentous bacteria
may cause fouling on the exoskeleton
Occasional white opaque areas on the tail/abdominal muscles

Effects on host:
• Enlargement of the hepatopancreatic nuclei with development of a prominent
occlusion body (Figure 3)
• Affects the distal tubules of the hepatopancreas causing death of cells and
shrinkage of the organ
• Damage in this organ can cause abnormal metabolism and, eventually, death
• Postlarvae (PL 1 - PL 19) from three hatcheries in Iloilo showed prevalence rates
of 7.8 to 26.4%
Mortalities among P. merguiensis may reach as high as 50% within 4-8 weeks of
disease onset

Preventive methods:
• Use HPV-free stocks
• Destroy infected stocks

Treatment: None reported

Figure 3. Histological section of the hepatopancreas of juvenile shrimp with
heavy hepatopancreatic parvo-like virus (HPV) infection showing
single inclusion bodies (arrowheads) within infected nuclei. (H & E,
200X).
Common name: WHITE SPOT SYNDROME VIRUS (WSSV) DISEASE, WHITE SPOT
VIRUS (WSV) DISEASE, WHITE SPOT BACULOVIRUS (WSBV),
SYSTEMIC ECTODERMAL AND MESODERMAL BACULO-LIKE VI-
RUS (SEMBV)

Causative agent: Baculovirus (100-140 X 270-420 nanomicrons)

Species affected: Penaeus monodon, P. indicus, P. merguiensis

Other species affected: P. semisulcatus, P. setiferus, P. chinensis, Litopenaeus stylirostris,

L. vannamei, Scylla serrata, Charybdis feriatus, Portunus pelagicus, Ascetes
sp., P. sanguinolentus

Stages affected: Mysis, postlarvae, juveniles, broodstock

Gross signs:
• Presence of distinct white cuticular spots (0.5 - 3mm in diameter) most apparent
at the exoskeleton and epidermis of diseased shrimp about 2 days after onset
• The white spots start at the carapace and 5th and 6th abdominal segments
which later affect the entire body shell
• Moribund shrimp display red discoloration and have loose cuticle
• Surface swimming and gathering at pond dikes with broken antennae
• Reduction in food consumption and empty gut
• Rapid onset and high mortalities in 3 to 10 days of up to 100% with dead
shrimps at the pond dikes/pond bottom

Effects on host:
• Affects a wide host range and targets various tissues (pleopods, gills,
hemolymph, stomach, abdominal muscle, gonads, midgut, heart, periopods,
lymphoid organ, integument, nervous tissue and the hepatopancreas) resulting
in massive systemic infection
• Presence of inclusions within the nuclei of affected cells (Figure 4a)
• Shrimps 4-15g are particularly susceptible but the disease may occur from mysis
to broodstock
• Pre-moulting shrimps are usually affected
• Penaeus indicus suffers earlier and greater losses compared to P. monodon.
Crabs, krill and other shrimps are viral reservoirs
• Pandemic epizootic occur in extensive, semi-intensive and intensive culture
systems regardless of water quality and salinities

Preventive methods:
• Use WSV-free stocks
• Feeding with peptidoglycan (PG) at 0.2 mg/kg body weight/day for 2-3 months
• Stress test PL with 100 ppm formalin for 30 min with aeration
• Destroy infected stocks
• Strict hygiene
• Disinfection of ponds and inlet canals
Use of only dry commercial feeds
• Pasteurize fresh feed at 60°C for 15 min
Fine screening of inlet water
Refrain from exchanging water for at least three days after infected ponds have
been discharged
Ban importation of non-indigenous shrimps
• Compliance with the Hazard Analysis and Critical Control Point (HACCP)
programs for product safety
Fucoidan (an extract from the seaweed Cladosiphon okamuranus) application
at 60-100 mg/kg shrimp/day for 15 days

Figure 4a. Histological section of the stomach of shrimp with white spot
infection showing intranuclear inclusions in hypertrophied nuclei.
(H & E, 200X).
Common name: YELLOW HEAD VIRUS (YHV) DISEASE

Causative agent: Rhabdovirus (40-50 X 150-170 nanomicrons)

Species affected: Penaeus monodon, P. merguiensis, P. setiferus, Acetes spp.

Stages affected: Juveniles, sub-adults, broodstock

Gross signs:
• Light yellowish, swollen cephalothorax
Whitish, yellowish or brown gills
• Abnormally high feed intake and rapid growth prior to cessation of feeding and
the onset of rapidly accelerating mortality
Marked reduction in feed consumption
• Moribund shrimp swim slowly near the surface at the edge of the pond
• Acute epizootic in juvenile to sub-adult shrimps about 20 days post-stocking
especially during the 50-70 days grow-out culture period
• May be associated with unstable phytoplankton bloom, bad pond bottom,
high stocking density or exposure to pesticides

Effects on host:
• Systemic infection associated with virus assembled in the cells of the gills,
lymphoid organ, connective tissues, and hemocytes
• Massive necrosis due to the replication of the virus in these cells
• Can cause a total crop loss within 3 to 5 days of onset of clinical signs
• Incubation time is 7-10 days
• Viral extracts in water remain infective up to 72 h
• Reservoirs of infection include Palaemon styliferus
• In the Philippines, a recent sampling of 250 shrimps reported positive YHV in
16% of specimens

Preventive methods
Use YHV-free stocks
• Destroy infected stocks
• Strict hygiene
• Disinfection of ponds and inlet canals
• Use of only dry commercial feeds
• Pasteurize fresh feed at 60C for 15 min
• Fine screening of inlet water
• Refrain from exchanging water for at least three days after infected ponds have
been discharged
• Ban importation of non-indigenous shrimps
• Compliance with the Hazard Analysis and Critical Control Point (HACCP)
programs for product safety

Treatment: None reported

 Bacterial Diseases

Luminous Bacterial Disease

(Hatchery)
Luminous Bacterial Disease
(Grow-out)

Shell Disease, Brown/Black

Spot, Black Rot/Erosion,
Blisters, Necrosis of
Appendages

Filamentous Bacterial
Disease
Common name: LUMINOUS BACTERIAL DISEASE (HATCHERY)

Causative agent: Vibrio harveyi, V. splendidus

Species affected: Penaeus monodon, P. merguiensis, P. indicus

Stages affected: Eggs, larvae, postlarvae

Gross signs:
• Larvae become weak and opaque-white
• Heavily infected larvae exhibit a continuous greenish luminescence when
observed in total darkness. When viewed under the microscope, the internal
tissues of these larvae are densely packed with highly motile bacteria
• Infected larval tissues streaked on nutrient agar medium show luminescent
colonies after 18-24 hours incubation (Figure 5a)

Effects on host:
• Systemic infections result in mortalities in larvae and postlarvae, reaching up to
nearly 100% of affected population
• Route of infection is oral
• Bacteria form plaques on the mouth apparatus of infected larvae (Figure 5b)
• Bacteria colonize the eggs (Figure 5c) which may then serve as sources of
infection upon stocking in the rearing tanks

Preventive methods:
• Prevent the entry of luminous bacteria into the hatchery system by using
chlorinated water (Appendix II), or ultraviolet-irradiated water, or by employing
a series of filtration equipment (sandfilters, filter bags, cartridge filters, 0.45
micron pore-sized microfilter, etc.). Higher levels of chlorine may be used if
necessary, but care must be taken to ensure complete dechlorination prior to
use
• Use only previously chlorinated water during spawning and rearing to ensure
a clean environment for newly hatched and developing larvae
• Remove the mothers from the tanks immediately after spawning and rinse the
eggs with chlorinated water to prevent its colonization with luminous bacteria
prior to hatching
• Rinse Artemia nauplii and other zooplankton before introducing them as food
into larval rearing tanks
• Siphon out sediments and debris from the tank bottom since these could serve
as substrates for bacterial growth
Disinfect infected stock before finally discarding them followed by a complete
clean-up and disinfection of hatchery paraphernalia after every larval rearing
period (Appendix III)

Treatment:
• At the height of infection, water change must be 80-90% replacement daily
Note: The application of chemotherapeutics can been done with limited results as
most luminous bacteria have acquired resistance to many chemotherapeutants
(please refer to Baticados et al. 1990b).

Figure 5a. Nutrient agar culture of the luminous bacterium, Vibrio harveyi.
Photo taken in total darkness.

Figure 5b. Scanning electron micrograph (SEM) showing bacterial plaques on

the mouth of moribund Penaeus monodon (mysis 1 stage) after
challenge with Vibrio harveyi for 48 h (SEM, 4000X).
Figure 5c. Scanning electron micrograph of Penaeus monodon egg colonized
by actively dividing cells (inset) of Vibrio harveyi.
Common name: LUMINOUS BACTERIAL DISEASE (GROW-OUT)

Causative agent: Vibrio harveyi and other luminescent vibrios

Species affected: Penaeus monodon

Stage affected: Juveniles

Gross signs:
• Heavily infected and moribund juveniles are luminescent when observed in the
dark
• Infected shrimp swim near the edge of ponds with their heads poised near the
water surface
• Occasionally, the region near the hepatopancreas appears dark. These clumps
of brownish tissues are melanized tubules of the hepatopancreas (Figure 6)
• Green colonies predominate on thiosulfate citrate bile sucrose (TCBS) agar, a
selective culture medium for vibrios

Effects on host:
• Infection results in mass mortality of juveniles especially in the first 45 days of
culture
• The hepatopancreas shows atrophy and massive inflammatory response in
and around the tubules
• Damaged tubules in the digestive organ become non-functional. This could
lead to slow growth among survivors if a significant portion of the organ is
affected

Preventive methods:
• Since the onset of mortality is preceded by the dominance of luminous bacteria
in the rearing water, monitoring of the bacterial profile using microbial culture
media should be done regularly especially in the first 45 days of culture
• Rearing water that is known to harbor a bacterial profile dominated by luminous
vibrios should not be used for culture. Avoid prolonged exposure of postlarvae
and juveniles to luminous bacterial counts of more than 102 colony-forming-
units (cfu) per ml.
• Use reservoirs where settling of sediments, disinfection, conditioning and
effective monitoring of bacterial load of the rearing water can be done
• Monitor the bacterial load of postlarvae for stocking. The associated flora
should not be dominated by luminous vibrios
• Establish and maintain microbial diversity in the rearing environment through
the green water culture system or the application of microbial bioaugmentation
agents (commonly called probiotics)

Note: Administration of various antimicrobials had been tried with variable results.
Figure 6. Histological section of a pond-reared Penaeus monodon juvenile
with luminous bacterial infection. The central region of the
hepatopancreas is atrophied with fibrosis and hemocyte infiltration
in the intertubular spaces. Most of the tubules are melanized. (H &
E, 40X).
 Common name: SHELL DISEASE, BROWN/BLACK SPOT, BLACK ROT/EROSION,
BLISTERS, NECROSIS OF APPENDAGES

Causative agent: Shell-degrading bacteria belonging to Vibrio, Aeromonas and

Pseudomonas groups

Species affected: Penaeus monodon, P. merguiensis, P. indicus

Stages affected: Larvae, postlarvae, juveniles, adults

Gross signs:
• Appearance of brownish to black erosion on the carapace, abdominal segments,
rostrum, tail, gills, and appendages (Figures 7 a - c)
• Blister containing gelatinous fluid may develop on the carapace and abdominal
segment (Figure 7d). The blister may extend to the underside of the lower
section of the carapace creating a bulge.
• In larval and post-larval stages, the affected appendage shows a cigarette butt-
like appearance (Figure 7a)

Effects on host:
• In larval or postlarval stages, shell disease occurs when there is a build-up of
chitinoclastic bacteria on the shell following molting failure or organic fouling
of the rearing water. Progressive erosion of these exoskeletal lesions follows
upon multiplication of bacterial pathogens in the affected area. The infection
may lead to loss of the affected appendage(s), or to the perforation of
exoskeleton where localized infection in the underlying musculature may also
follow. When these occur, normal locomotion or molting is hampered and may
result in shrimp mortality
• The affected shrimp becomes susceptible to cannibalism or dies from stress or
energy exhaustion
• In juvenile shrimps, infection may be initiated at sites of punctures or injuries
made by either the telson or rostrum, cracks on the abdominal segment from
sudden flexure of the shrimp body, or from other damage caused by cannibalism

Preventive methods:
• Maintain good water quality
• Keep organic load of the water at low levels by removing sediments, especially
dead shrimps and molted exoskeletons which harbor high numbers of bacteria
on the lesions
• Provide adequate diet
• Minimize handling and avoid overcrowding
• Avoid injuries to the exoskeleton of the shrimps to prevent the development of
primary portals of entry

Treatment:
• Induce molting as the condition is eliminated upon molting except when
underlying tissues are damaged
Figure 7a. Wet mount of postlarval Penaeus monodon with necrotic appendages
and melanized blister on the carapace. (arrows).

Figure 7b. Scanning electron micrograph showing necrosis of appendages of

postlarval Penaeus monodon (arrows). (SEM, 94X)
Figure 7c. High magnification view of a necrotic appendage showing a colony
of bacteria gradually 'eating away' the affected appendage of a
Penaeus monodon postlarva. (SEM, 3000X).

Figure 7d. Shell erosion and black spot on the carapace of adult Penaeus
monodon.
Common name: FILAMENTOUS BACTERIAL DISEASE

Causative agent: Leucothrix sp.

Species affected: Penaeus monodon, P. merguiensis, P. indicus

Stages affected: Larvae, postlarvae, juveniles, adults

Gross signs:
• Presence of fine, colorless, thread-like growth on the body surface and gills as
seen under a microscope (Figures 8 a - b)

Effects on host:
• Infected eggs show a thick mat of filaments on the surface which may interfere
with respiration or hatching
• If found on the gill surface, filamentous bacteria block respiratory surfaces and
cause respiratory problems (Figures 8 c - d)
• In larvae and postlarvae, filamentous growth on appendages and body surface
may interfere with normal movement and with molting, and may entrap other
microorganisms (like fungal spores), which may initiate a new infection
• Larval shrimps are less prone to infestations by filamentous bacteria than post-
larval, juvenile, and adult stages due to the rapid succession of molts throughout
the different larval stages. Frequent molting does not allow adequate time for
the bacteria to accumulate on the exoskeleton
• In larger shrimps, filamentous bacteria on the gills and other body surfaces may
result in respiratory distress at the point of attachment. An indirect effect of
such filamentous growth on the host is entrapment of algae and debris which
interfere with respiration and promote further fouling
• Mortalities due to direct and indirect effects of filamentous bacteria have been
reported

Preventive methods:
• Maintain good water quality with optimum dissolved oxygen (>5 ppm) and low
organic matter levels

Treatment:
• 0.15 ppm copper (Cutrine-Plus) in 24-h flow through treatments or 0.5 ppm
copper in 4 to 6 h static treatments for postlarva 2 or older. For treatment
guidelines, see Appendix IV.
Figure 8a. Strands of filamentous bacterium Leucothrix sp. on heavily infested
gills of juvenile Penaeus monodon. At upper left is the protozoan
Zoothamnium. (Wet mount, 200X).

Figure 8b. Wet mount of Penaeus monodon postlarva with filamentous bacteria
(arrowheads) on the appendages.
Figure 8c. Scanning electron micrograph of the gills of Penaeus monodon
postlarva showing strands of filamentous bacteria attached to the
lamellae. (SEM, 540X).

Figure 8d. 'Rosettes' of bacterial filaments (arrowheads) colonize the lamella

and block respiratory surfaces (SEM, 1100X).
Fungal Disease

Larval Mycosis
Common name: LARVAL MYCOSIS

Causative agents: Lagenidium callinectes, Lagenidium sp., Haliphthoros

philippinensis, and Sirolpidium sp. In Lagenidium, zoospores are developed
in a vesicle which is formed at the end of discharge tube. Haliphthoros does
not form vesicles but has long discharge tubes, whereas Sirolpidium has short
discharge tubes and forms no vesicle. These aquatic fungi produce highly
motile zoospores that can easily invade other hosts.

Species affected: Penaeus monodon

Stages affected: Eggs, larvae, early postlarvae

Gross signs:
• Infected eggs, larvae, and postlarvae appear whitish, become weak, and may
eventually die
• Signs, such as presence of fungal filaments and their reproductive structures
within infected tissues (Figure 9), are readily apparent when disease is already
widespread

Effects on host:
• Heavy mortalities up to 100% within 2 days may occur. The fungal hyphae
replace the internal tissues of the shrimp and extend outside the shrimp body to
form discharge tubes. Infected eggs do not hatch and larvae lose equilibrium
and exhibit respiratory difficulties.

Preventive methods:
• Siphon sediments and dead shrimps
• Reduce stocking density
• Increase water circulation
• Disinfect materials and tank with 100 ppm detergent (Tide*) for 24 h
• Observe rigid water management and sanitation
• Disinfect eggs with 20 ppm detergent for 2 h at least 6 h before hatching; for
spawners, use 5 ppm Treflan* for 1 h. (Appendix V)
• In areas where larval mycosis is known to occur, Treflan* or trifluralin may be
used at prophylactic levels of 0.1 ppm every 2-3 days
• Dispose infected stocks only after disinfection with 100 ppm detergent
• Regular monitoring of the stock species through microscopic examination is
important

Treatment:
• 0.2 ppm Treflan* or trifluralin for 24 h (Appendix VI)

* Mention of brand name does not mean endorsement of the product.

Figure 9. Filaments of Lagenidium in the tail of Penaeus monodon larva
(arrows). Zoospores in a vesicle (arrowhead) are about to be
released by the fungus. (Wet mount, 100X).
Protozoan Diseases

Ciliate Infestation
Microsporidiosis, White
Ovaries, Microsporidian
Infection
Gregarine Infestation
Common name: CILIATE INFESTATION

Causative agents: Vorticella, Epistylis, Zoothamnium, Acineta, and Ephelota. Vorticella

is solitary and has a contractile stalk. Zoothamnium and Epistylis are both
colonial, but only the former has a contractile stalk. Acineta and Ephelota are
suctoreans equipped with feeding tubules (Figure 10a)

Species affected: Penaeus monodon, P. merguiensis, P. indicus

Stages affected: Eggs, larvae, postlarvae, juveniles, adults

Gross signs:
• Fuzzy mat on shell and gills of heavily infected juveniles and adults
• Reddish to brownish gills
• Loss of appetite

Effects on host:
• Microscopically, protozoans may be observed attached to any external part of
the shrimp
• The protozoans may cause locomotory difficulties when present in large numbers
Respiratory problems occur when they are present in large numbers on the gills
(Figure 10b), particularly at low dissolved oxygen levels

Preventive methods:
• Maintain good water quality
• Avoid high organic load, heavy siltation, turbidity, and low oxygen levels

Treatment:
• Among juveniles in nursery tanks, application of 1.1 ppm chloroquin
diphosphate for 2 days was reported to be effective against the ciliates after
three treatments
• Zoothamnium infestation in adults was reported to be effectively treated with
50-100 ppm formalin for 30 min
• Epistylis infestation in juveniles was observed to be eliminated by 30 ppm
formalin
• Change water by draining from the pond or tank bottom daily to remove excess
feeds, fecal matter, and other organic wastes
Figure 10a. The protozoans a. Vorticella, b. Epistylis, c. Zoothamnium
d. Aniceta and e. Ephelota.
Figure 10b. The ciliate Zoothamnium on gills of Penaeus monodon adult. (Wet
mount, 200X).
Common name: MICROSPORIDIOSIS, WHITE OVARIES, MICROSPORIDIAN
INFECTION

Causative agent: Microsporidia. These are endoparasitic protozoans that may be

diagnosed only through microscopic examination of the infected
tissues.

Species affected: Penaeus monodon, P. merguiensis, P. indicus

Stages affected: Juveniles, adults

Gross signs:

• Affected tissues/organs turn opaque white (Figure 11)

Effects on host:
• Spores and other stages of the parasite replace the affected tissues
• Infection may result in sterility of spawners with white ovaries
• Infection rate is relatively low (usually<10%) but the parasite is highly pathogenic
Preventive methods:
• Disinfect culture facilities with chlorine or iodine-containing compounds
• Isolate and destroy infected shrimps by burning or boiling

Treatment:
• None reported
Figure 11. Microsporidian infection of the abdominal muscles of Penaeus indicus
(top) and ovary of P. monodon (bottom).
Common name: GREGARINE INFESTATION

Causative agent: Gregarines. These are protozoan parasites commonly found in the
digestive tract of penaeid shrimps. They utilize a mollusc species
as intermediate host.

Species affected: Penaeus monodon, other penaeids may also be affected

Stages affected: Larvae, postlarvae, juveniles, adults

Gross sign:

• Gregarines may be detected in the digestive tract microscopically (Figures 12 a - c)

Effects on host:
• Large numbers of this protozoans could interfere with particle filtration through
the gut or the hepatopancreatic duct
• Infection rate in pond-grown prawns was reported to reach 94%
Preventive method:
• In the hatchery, filter or chlorinate seawater used for rearing
• In grow-out ponds, eliminate the molluscan intermediate host

Treatment:
• None reported

Figure 12a. Gregarines (arrows) in the gut of Penaeus monodon postlarva. (Wet
mount, 200X).
Figure 12b. Histological section showing gregarines in the anterior midgut cecum
of pond-reared shrimp juvenile. (H & E, 200X).

Figure 12c. Histological section showing gregarines in the stomach of pond-

reared shrimp juvenile. (H & E,100X).
Nutritional, Toxic and
Environmental
Diseases

Incomplete Molting
Swollen Hindgut
Syndrome
Chronic Soft-shell
Syndrome, Soft-
shelling
Black Gill Disease
Blue Disease, Sky
Blue Shrimp
Disease, Blue
Shell Syndrome
Red Disease, Red
Discoloration
Underfeeding
Muscle Necrosis
Cramped Tails, Bent
Tails, Body Cramp
Acid Sulfate Disease
Syndrome
Asphyxiation, Hypoxia
Bamboo Back
Syndrome
Common name: INCOMPLETE MOLTING

Causative agent: Unknown, although this occurrence is closely associated with low
rearing water temperature

Species affected: Hatchery-reared Penaeus monodon; may also affect other species of
penaeids

Stages affected: Zoea and mysis stages, occasionally in postlarvae

Gross signs:
• Presence of old skeleton attached to newly molted larvae, especially in the area
of the appendages (Figures 13 a - b)

Effects on host:
• Abnormal swimming movement which could lead to easy predation
• Mortality

Preventive methods:
• Maintain optimum temperature in the rearing water

Treatment:
• Use of heaters to raise and maintain temperature at optimum levels
a.

b.

Figure 13. Incomplete molting in mysis stage larva. The old exoskeleton remains
adhered to the abdominal segments (a), and the anterior appendages
and carapace of the larvae (b). Photo in Figure 13a is a wet mount
while Figure 13b is a scanning electron microphotograph.
Common name: SWOLLEN HINDGUT (SHG) SYNDROME

Causative agent: Unknown, but condition may be triggered by poor feed quality such
as senescent and contaminated phytoplankton

Species affected: Hatchery-reared Penaeus monodon

Stages affected: Postlarvae

Gross signs:
• The normally triangular hindgut (Figure 14a) becomes swollen and bulbous
(Figure 14b)
• In some cases, swelling occurs in the midgut-hindgut junction (Figure 14c)
• Melanization may sometimes appear giving the hindgut a brown color (Figure
14d)

Effects on host:
• Affected postlarvae fail to expel their fecal pellets due to the cessation of
rhythmic movements of the rectal pads
• Delayed development due to molting failure
• Cumulative mortality of up to 65% in postlarvae exhibiting severely swollen
hindgut

Preventive methods:
• Rigid sanitary procedures in water management and handling of natural food
• Proper storage of artificial feeds

Treatment:
• Complete reversal of swollen hindgut syndrome has been observed under
experimental conditions after 10 days of rearing affected postlarvae in UV-
sterilized seawater with rinsed Artemia nauplii as its sole food source
Figure 14a. The sixth abdominal segment of a Penaeus monodon postlarva
showing normal hindgut (arrow). (Wet mount, 200X).

Figure 14b. Penaeus monodon postlarva with severe swollen hindgut syndrome
showing necrotic and distended hindgut pad tissues (arrow). (Wet
mount, 200X).
Figure 14c. Penaeus monodon postlarva with severe swollen hindgut syndrome
affecting the midgut-hindgut junction. The hindgut pads appear
slightly affected, but there is a dense accumulation of fecal material
(arrow) resulting from the cessation of rhythmic movements to expel
them. (Wet mount, 200X).

Figure 14d. Penaeus monodon postlarva with slightly swollen hindgut with
melanization (arrow) in the anterior portion of the hindgut pads.
(Wet mount, 200X).
Common name: CHRONIC SOFT-SHELL SYNDROME, SOFT-SHELLING

Causative agents:
• Nutritional deficiency; pesticide contamination; and poor pond water and soil
conditions
• Exposure of normal hard-shelled shrimps to pesticides and piscicides. Aquatin
or Gusathion A at 75-150 ppb, rotenone at 10 - 50 ppm, and saponin at 100 ppm
for 4 days induced soft-shelling in initially hard-shelled stocks.
• Pond surveys also indicated that the occurrence of soft-shelling could be
predicted with 98% accuracy under conditions of high soil pH, low water
phosphate, and low organic matter content in the soil. Of the ponds that were
surveyed and had soft-shelling of shrimps, 70% had high soil pH (>6), low
water phosphate (<l ppm), and low organic matter content (<7%).
• Inadequate feeding practices like improper storage of feeds, use of rancid or
low-quality feeds, and lack of supplementary feeding in ponds with relatively
higher stocking densities were also highly correlated with significantly high
incidence of soft-shelling
• Insufficient or infrequent water exchange was highly correlated with soft-shelling

Species affected: Penaeus monodon

Stages affected: Juveniles, adults

Gross signs:
• Shell is thin and persistently soft for several weeks, shell surface is often dark,
rough and wrinkled, and affected shrimps are weak (Figure 15)
• The disease must not be confused with the condition of newly molted shrimps,
which have clean, smooth, and soft shells that harden within 1-2 days

Effects on host:
• Affected shrimps are soft-shelled, grow slowly, and eventually die
• Shrimps become more susceptible to wounding, cannibalism, and surface fouling
by Zoothamnium and other epicommensals
• Histopathology of shrimps exposed to Gusathion A shows slight hyperplasia
of the gill epithelium, delamination of the cells lining the tubules of the
hepatopancreas, and general necrosis and degeneration of these tissues

Preventive methods:
• During pond preparation, flush ponds thoroughly particularly when pesticide
contamination is suspected
• Maintain pond water and soil of good quality
• Feed shrimps adequately and use only good-quality feeds
Treatment:
• Provide rigid water management, e.g., water change of 20-50% daily in ponds
• Provide supplementary feed, e.g., mussel meat at 8-14% of the body weight
daily for 2-4 weeks, or a diet containing 1:1 ratio of calcium-to-phosphorus
• Water must be changed immediately, particularly when pesticide contamination
is suspected

Figure 15. Penaeus monodon with soft shell syndrome showing dark, rough
and soft shell.
Common name: BLACK GILL DISEASE

Causative agents:
• Chemical contaminants like cadmium, copper, oil, zinc, potassium permanganate,
ozone, ammonia, and nitrate in rearing water
• Ascorbic acid deficiency
• Heavy siltation
• High organic load due to residual feed, debris, and fecal matter on pond bottom
(i.e., the black soil)

Species affected: Penaeus monodon

Stages affected: Larvae, postlarvae, juveniles, adults

Gross signs:
• The gills show reddish or brownish to black discoloration, and atrophy at the
tip of the filaments (Figure 16)
• In advanced cases, most of the filaments are affected and the gills become
totally black
Dorsal side of the body may be covered with fog-like substance
• Loss of appetite
• Mortalities

Effects on host:
• Histological observation shows that the blackening of the gills may be due to
the heavy deposition of black pigment at sites of heavy hemocyte activity
(inflammation)
• Extensive accumulation of blood cells in the gill filaments may result in respiratory
disturbances
• Absorption of silt on the gills may also result in respiratory difficulties
• Secondary infections by bacteria, fungi, and protozoans via the dying cells of
the gills

Preventive methods:
• Avoid overfeeding
• Change water frequently
• Remove black soil by scraping after harvest and draining from the bottom or
"vacuuming" during culture period
• Flush out ponds several times during pond preparation
• Avoid heavy metal discharge of nearby factories from getting into the rearing
facilities

Treatment:
• If the disease is due to heavy siltation or chemical contamination, change water
immediately and daily by draining from the bottom
• If the disease is due to ascorbic acid deficiency, supplement diet with adequate
amounts of ascorbic acid (>2000 mg/kg of feed) or fresh algae
Figure 16. Penaeus monodon juveniles showing severely discolored and blackish
gills.
Common name: BLUE DISEASE, SKY BLUE SHRIMP DISEASE, BLUE
SHELL SYNDROME

Causative agents:
• Soil-water quality problems, e.g. acid-sulfate soil, high organic wastes, and low
dissolved oxygen levels. The disease is commonly observed in intensive culture
systems toward the end of the grow-out culture period.
• Low levels of carotenoid astaxanthin in the diet

Species affected: Penaeus monodon

Stages affected: Juveniles, adults

Gross signs:
• Sky-blue color instead of the normal brown-black (Figure 17)
• Lethargic shrimps show shells that are soft and thin with rough surface
• The shell becomes prone to shell disease
• Absence of intense red color after cooking

Effects on host:
• Hispatological changes in the hepatopancreas, e.g., disruption of the tubules

Preventive methods:
• Incorporate Vitamin A or carotenoid sources, like yellow corn, in the diet 45
days after stocking
• Change 10 to 15% of the water volume daily to diminish the hydrogen sulfide-
rich bottom layers of water
• Reduce stocking density
• Provide high quality food

Treatment:
• Supplement diet with carotenoid sources
Figure 17. Penaeus monodon adults with blue shell syndrome (2nd and 4th
from left).
Common name: RED DISEASE, RED DISCOLORATION

Causative agents:
• Rancid feeds due to prolonged storage at high temperatures
• Presence of aflatoxin B (produced by the fungi Aspergilus spp.) in feeds or
1

feed ingredients
• High water pH due to large inputs of lime (2-6 tons/ha)
Prolonged exposure to low salinity (6-15 ppt)

• Secondary infection with Vibrio parahaemolyticus and V. harveyi

Species affected: Penaeus monodon, may also affect other cultured penaeids

Stages affected: Late postlarvae, juveniles, adult

Gross signs:
• The first sign of the disease is a sudden drop in feed consumption
• The animals then become lethargic and show general body weakness; death
ensues within minutes after being lifted out of the water
• Many of the affected animals are confined to shallow waters at the pond periphery
• Body and appendages of affected shrimp become yellowish, then yellowish
pink, then pink and eventually red (Figure 18a)
• Red, short streaks on gills
• Brown to brownish red fecal matter
• Increased fluid in the cephalothorax emitting foul odor
Effects on host:
• Yellow to red discoloration in affected shrimps
• Slow growth and reduced resistance to stress
• Increased susceptibility to systemic bacterial infection and shell disease
• Aflatoxin B levels of 75 parts per billion (ppb) or more in feed causes atrophy
1

and necrosis of the hepatopancreas after 60 days of continuous feeding

• Histopathology of the hepatopancreas shows hemocytic infiltration in the
spaces in between the tubules; more advance lesions are in the form of fibrotic
and melanized encapsulation of necrotic tissues, either in the tubule itself or the
sinuses around it (Figures 18 b - c)
• Experimental infection through injection of healthy shrimp with V.
7 6 5
parahaemolyticus (10 , 10 , 10 colony-forming-units (cfu) per shrimp) and V.
7
harveyi (10 cfu per shrimp) reproduced the characteristic red discoloration in
juvenile shrimp suggesting bacterial involvement in some cases

Preventive methods:
• Use only recently manufactured feeds
• Store feeds properly in well-ventilated and cool rooms for not more than 2
months
• Submit suspected batches of feeds for aflatoxin B and rancidity analysis
1
 • Withdraw and stop giving contaminated feeds as rations
• Prepare pond bottom properly
• Reduce lime input during pond preparation
• Maintain a low organic load in the environment to prevent the proliferation of
potentially pathogenic bacteria

Treatment: None reported

Figure 18a. Penaeus monodon adults with red disease. Left: early signs, natural incidence; right:
red discoloration after 3 weeks of exposure to aflatoxin B 1
Figure 18b. Histological section of the hepatopancreas of a pond-reared juvenile
with advanced red disease. Note the melanized tubules, and fibrosis
and hemocyte infiltration in the intertubular spaces. Affected tubules
are non-functional at this state. (H & E. 40X).

Figure 18c. Hepatopancreas of shrimp experimentally exposed to 200 ppb

aflatoxin B for 60 days via feed. Note the presence of melanized and
1

necrotic tubules similar to red disease in the proximal tubules of the

hepatopancreas (arrows). (H & E. 40X).
 Common name: UNDERFEEDING

Causative agent: Lack of food

Species affected: Penaeus monodon, may also affect other species of

crustaceans

Stages affected: Juveniles to adults

Gross signs:
• Loose shells, reduced muscular mass in the abdominal segments
• Histological sections show the marked absence of storage vacuoles, which are
abundant in the hepatopancreas of normal shrimp (Figure 19a), in the
hepatopancreas of affected shrimp resulting in atrophy of cells (Figure 19b)

Effects on host: Slow growth or weight loss in severely starved shrimps

Preventive methods:
• Provide supplemental feeds
• Exclude or eliminate competitors from the ponds
• For extensive ponds, apply fertilizer to induce a healthy bloom of algae and
trigger a good growth of zooplankton and natural food

Treatment: Same as above

Figure 19a. Normal structure of the hepatopancreas of juvenile shrimp showing
well vacuolated cells lining the tubules. (H & E, 100X).

Figure 19b. Hepatopancreas of underfed shrimp juvenile showing severely

atrophied tubular cells due to the absence of storage vacuoles. (H &
E, 40X).
Common name: MUSCLE NECROSIS

Causative agent: Stressful environment conditions like low oxygen levels, temperature
or salinity shock, overcrowding, and severe gill fouling

Species affected: Penaeus monodon

Stages affected: Postlarvae, juveniles, adults

Gross signs:
• Opaque white areas on the abdomen (Figure 20a)
Blackening on edges of the uropod followed by erosion
• Liquid-filled boils at the tip of uropods in advanced stages
• Weakness and, eventually, death
• In postlarvae appearance in distinct lines in the abdominal muscles giving it a
"wood grain" appearance (Figure 20b)

Effects on host:
• The disease causes gradual death of cells of affected parts such as uropods
and musculature leading to erosion especially in the tail portion
• Affected areas may serve as portals of entry for a secondary systematic infection
by bacteria

Preventive methods:
• Reduce stocking density in ponds
• Give adequate feed but do not overfeed
• Maintain good water quality avoiding extreme fluctuations in salinity, temperature
and dissolved oxygen

Treatment: None reported

 Figure 20a. Penaeus monodon juveniles with necrosis in the abdominal muscles.

Figure 20b. Penaeus monodon postlarva with "grainy" abdominal muscles.

Common name: CRAMPED TAILS, BENT TAILS, BODY CRAMP

Causative agents: Unknown, but the disease had been associated with mineral imbalance,
and to abrupt change in water and air temperatures, e.g., during handling
of shrimps in air warmer than the culture water

Species affected: Penaeus monodon

Stages affected: Juveniles, adults

Gross signs: Partial or complete rigid flexure of the tail in live shrimps (Figure 21)

Effects on host:
• Partially cramped shrimps swim with a humped abdomen whereas fully cramped
individuals lie on their sides at the pond/tank bottom
• The condition may result in cannibalism of cramped shrimps by unaffected
ones, and death

• Injured muscle fibers may turn brown as an outcome of the wound repair process

Preventive methods: Avoid possible causes

Treatment: None reported

Figure 21. Penaeus monodon juvenile with body cramp.

Common name: ACID SULFATE SOIL SYNDROME

Causative agent: Low water and soil pH

Species affected: Penaeus monodon, P. merguiensis, P. indicus

Stage affected: Juveniles

Gross signs:
• Poor growth
• Decreased molting frequency
• Yellow to orange to brown discoloration of the gill and appendage surfaces
• Reddish to orange color of the pond soil (Figure 22)

Effects on host:
• Normal metabolism of the shrimp is hindered resulting in retarded growth and
eventual death

Preventive methods:
• Correct low pH soil condition by liming and flushing of pond bottom before
stocking.
• Regularly monitor water pH

• Broadcast lime on pond dike surfaces or hang lime bag as the need arises

Treatment: Correct low pH conditions as above

Figure 22. Pond with acidic soil (left).

Common name: ASPHYXIATION, HYPOXIA

Causative agent: Very low levels of dissolved oxygen (DO)

Species affected: Penaeus monodon, P. merguiensis, P. indicus

Stages affected: Larvae, postlarvae, juveniles, adults

Gross signs:
Surface swimming
Sudden mass mortalities

Effects on host:
Prolonged respiratory distress leads to death
Below optimum oxygen levels may cause impairment of metabolism resulting in
growth retardation

Preventive methods:
Monitor DO levels late in the afternoon and early in the morning
Provide aeration facilities and water pump for ready water change
Decrease stocking density if aeration and water-change facilities are not available
Control feeding of artificial diets according to consumption rates to prevent
accumulation of high organic matter
Common name: BAMBOO BACK SYNDROME

Causative agents: Unknown, but may be to be due to nutritional deficiency

Species affected: Penaeus monodon

Stages affected: Juveniles, adults

Gross sign:
• Succeeding exoskeletal plates of the abdominal segments do not overlap properly
allowing the muscles to protrude giving the shrimp a bamboo-like appearance
• Shorter rostrum and tail region

Effect on host:

• Protruding muscles become prone to injury and secondary infection

Preventive methods: None reported

Treatment: None reported

 Appendices
Glossary
References

Acknowledgement
 Appendices
Appendix I. Procedure for disinfection of rearing facilities.

Hatchery
1. Disinfect used and infected rearing water with 220 ppm available chlorine. Soak
all used hatchery paraphernalia overnight in this tank.
2. Drain disinfectant. Scrub tank bottom and sidewalls with freshly prepared
disinfectant of the same concentration.
3. Rinse thoroughly with clean freshwater several times.
4. Allow to dry under the sun and let stand for several days.
5. Wooden materials used when infection occurred should be burned and replaced
for the next operation.
Ponds
1. Used pails and other pond paraphernalia should be soaked overnight in 220
ppm available chlorine. Wash thoroughly with clean water before using. Dry
under the sun.
2. Infected ponds may be disinfected immediately after harvest by applying lime
while the soil is still wet. The soil pH should rise to 9.
3. Infected ponds should be dried thoroughly (until the soil cracks) before using
these for the next operation.
4. Tilling should be done to expose the sub-surface layer.
Appendix II. Procedure for disinfecting rearing water using calcium hypochlorite (70%
chlorine activity).

1. Using Table I, dissolve the required amount of powder for a desired volume of
water in a small volume of water (500 ml). For example, if the water volume is 0.5
ton or 500 liters and the desired concentration is 15 ppm, the amount of calcium
hypochlorite needed is 10.7 g.

Table 1. Guide for determining the amount of calcium hypochlorite (g) to be used for
water disinfection.

Volume of water Chlorine concentration

5 ppm 10 ppm 15 ppm 20 ppm

0.25 ton (250 liters) 1.8 3.6 5.4 7.2

0.50 ton (500 liters) 3.6 7.1 10.7 14.3
1.0 ton (1,000 liters) 7.1 14.3 21.4 28.6
2.0 tons (2,000 liters) 14.3 28.6 42.9 57.1
3.0 tons (3,000 liters) 21.4 42.9 64.3 85.7
5.0 tons (5,000 liters) 35.7 71.4 107.1 142.9
10.0 tons (10,000 liters) 71.4 142.9 214.3 285.7

The amount of calcium hypochlorite may be multiplied by different factors to obtain

other chlorine concentrations. Ex.: To obtain 400 ppm chlorine solution in 1 ton water,
multiply 28.6 g by 20 or 14. 3 by 40.

2. Fill the tank with the desired volume of water, then add the dissolved calcium
hypochlorite solution.
3. Keep chlorinated water for at least 12 hours, up to 24 hours, then check the
residual chlorine level using portable kits available in the market. Neutralize
remaining chlorine with equal amount for sodium thiosulfate (Na S O ) before
2 2 2

using the water.

Table 2. Guide for determining the amount of bleach (ml) for water disinfection.
Volume of water Chlorine concentration
5 ppm 10 ppm 15 ppm 20ppm
0.25 ton 25 50 75 100
0.50 ton 50 100 150 200
1.0 ton 100 200 300 400
2.0 tons 200 400 600 8,000
3.0 tons 300 600 900 1,200
5.0 tons 500 1,000 1,500 2,000
10.0 tons 1,000 2,000 3,000 4,000
Appendix III. Guidelines for discarding infected larval stocks.

Disease-infected larval stock should not be drained back into the sea without prior
disinfection. Failure to disinfect would introduce large numbers of disease-causing
organisms in the nearshore environment. The following steps are recommended:

1. Calculate the total volume of the contaminated rearing water.

2. Weigh the amount of calcium hypochlorite needed to disinfect the contaminated

water volume so that the resulting active chlorine concentration would be
equivalent to 200 ppm.

3. Allow the disinfectant to act for at least 1 hour.

4. Drain. Discarded water/dirt/larvae from the hatchery should not be thrown

directly into the sea. The dumping area should be located in the sandy portion
several meters above the high-tide waterline.
Appendix IV. Guidelines for treatment of shrimp diseases.

1. Clean rearing facilities before treatment. This may be accomplished by siphoning

out sediments from the tank bottom and by water change. Organic matter present
in dirty tanks could absorb part of the drug being used thus reducing its
effectiveness.

2. Apply treatment only during the coolest part of the day (i.e., nighttime). The
drug used should provide the least environmental hazard or stress.

3. Monitor dissolved oxygen levels before and during treatment since stressed
shrimps need more oxygen. Provide additional aeration if necessary.

4. Always make sure that your computations are correct by having someone else
check figures if possible. Unexpected mortalities due to drug overdose may
happen.

5. Follow recommended protocol strictly. Regular use of drugs at levels lower

than recommended could result in the development of resistant strains of
bacteria. Continued use of the drug at the recommended levels but beyond the
prescribed period of exposure could result in physical deformities among treated
shrimps.

6. Keep records of all treatments, their purpose, and results for future reference.
Appendix V. Chemical prophylaxis against larval mycosis.

Eggs

1. Prepare 20 ppm laundry detergent.

Total volume of water Weight of detergent

(liters) (gram)

1 0.02
5 0.01
10 0.2
100 2.0
500 10.0
1000 20.0

2. Dissolved the detergent in a small amount of freshwater, add to the egg culture
tank, and mix gently.
3. Let stand and aerate for 2 hours.
4. Transfer eggs to an egg washer and rinse eggs thoroughly using flow-through
seawater to remove detergent.
5. Chemical prophylaxis should be done long before hatching. Do not let eggs
hatch in detergent solution.

Spawners

1. Prepare 5 ppm Treflan.

Total volume of water Volume of Treflan

(liters) (milliliters)

100 0.5
250 1.25
500 2.1
1000 5.0

2. Mix the chemical in a small amount of freshwater, add to the spawning tank, and
aerate for 1 h.
3. Cover tank with a black cloth to prevent photodegradation of Treflan.
4. Transfer spawner to another tank with fresh seawater and rinse thoroughly
with flow-through seawater to remove the chemical.
Appendix VI. Treatment of larval mycosis with Treflan using drip method.

1. Prepare 0.2 ppm Treflan. Mix the chemical in a small amount of freshwater (for 1
ton culture water, use 1 liter freshwater) and add to the culture water tank. Mix
thoroughly.

Total volume of water Volume of Treflan

(ton) (ml)

0.5 0.1
1.0 0.2
2.0 0.4
3.0 0.6
4.0 0.8
5.0 1.0

2. After 1 h, prepare a second set of Treflan solution of equal concentration as in

#1 and place in dextrose bottles. Hang the bottles inverted so that the solution
would drip into the culture water through the plastic hose.

3. Adjust the drip regulator to release 1/4 to 1/3 of the amount of the solution into
the water per hour. Administer contents of the bottle within 3-4 h. One ml is
equivalent to 15-20 drops, so the flow rate from the bottle would be approximately
60-100 drops per minute.

4. Cover tanks with a black cloth during treatment especially at daytime to prevent
photodegradation of Treflan. Treat only during cool times of the day.
Appendix VII. External and internal anatomy of penaeid shrimps, (after Motoh, 1981)

External

Internal
Appendix VIII. Guidelines for sending specimens for disease diagnosis

1. In the absence of facilities or personnel capable of diagnosing shrimp diseases,

samples for diagnosis may be sent to a disease diagnostic laboratory (Fish
Health Section of the Southeast Asian Fisheries Development Center,
Aquaculture Department, Tigbauan, Iloilo). If the laboratory is located nearby,
live samples may be sent by packing these in clean, aerated culture water in
plastic bags. Diseased shrimps must always be separated from normal ones and
stocking density during transport must be reduced by at least 25%. For larval
and post-larval stages, at least 20 diseased individuals and an equivalent number
of normal shrimps are needed to make a diagnosis. All types of examination and
diagnostic procedures may be done on live samples.

2 If the diagnostic laboratory is quite far from the hatchery/farm and there are no
facilities for immediate and fast transport, fixed or iced samples may be sent.
Specimens are fixed by injecting Davidson's* fixative directly into the tissues
of LIVE specimens. Inject an equivalent of 5-10% of the shrimps's body weight
until all signs of life should cease and the shrimps appear cooked (orange
color). Fixed specimens should be immersed in fixative at a ratio of 1 part shrimp
tissue to 9 parts fixative. If Davidson's fixative is not available, 10% formalin
with 1.0% salt may be used.

3. The same number of specimens are sent as for live samples. Diseased animals
must be separated from normal ones. Only direct microscopic examination (for
parasites and fungi) and hispathological examination may be done on fixed
samples.

4. Iced samples are sent by packing adult/juvenile shrimp in plastic bags (separate
diseases from normal) and placing these in between layers of ice in a styrofoam
box. Like fixed samples, very limited diagnostic procedures may be done on
iced samples.

5. All pertinent data/information must be sent with the samples.

6. Notify the laboratory of the delivery and arrival of samples

* Davidson's Fixative (1 liter)

95% Ethyl alcohol 330ml

Formalin (saturated formaldehyde solution) 220 ml
Glacial acetic acid 115 ml
Distilled water 335 ml
7. Aside from the Fish Health Section at SEAFDEC, samples may also be
sent to:

(a) Fish Health Section

Bureau of Fisheries and Aquatic Resources (BFAR)
Arcadia Bldg., Quezon Ave
Quezon City

(b) Regional Offices of BFAR throughout the Philippines

(c) Negros Prawn Producers Marketing Cooperative, Inc.

JTL Bldg., B.S. Aquino Drive
Bacolod City
Appendix IX. Water quality suitable for rearing penaeid shrimp (Chen, 1985 in Licop,
1988)

Hatchery

Parameter Range

Temperature 24°-31°C
pH 7.5-8.5
Dissolved oxygen (D.O.) >5 ppm
Salinity 28-33 ppt
Turbidity <50FTU
Hg <0.01 ppb
Heavy metals <0.01 ppm
Biological oxygen demand (B.O.D.) <1.0 ppm (5 days)
Unionized ammonia (NH ) 3 <0.1 ppm
Nitrate (NO -N)
2 <0.02 ppm

Grow-out ponds

Parameters Range

Temperature 28°-33°C
pH 8.0-8.5
D.O. (critical) 3.7 ppm
Salinity 15-25 ppt
Heavy metals
Hg 0.0025 ppm
Cu 0.1 ppm
Cd 0.15 ppm
Zn 0.25 ppm
Hydrogen sulphide (H S)
2 0.33 ppm
NH 3 0.1 ppm
 Glossary
Acute a condition or disease process with a rapid trend

Aflatoxin B1 a highly toxic substance produced by the fungus Aspergillus

flavus which induces tumors in some animals

Antennal gland the organ found in the base of the antennae of shrimps which has
an excretory function

Astaxanthin a violet crystalline carotenoid pigment found in the shell of

crustaceans

Atrophy reduction in the size of tissue or organ

Bacteria one-celled microorganisms which lack well-defined nucleus. There

are three shapes of bacteria: rods, round, and spiral

Basophilic cell structures that are easily stained with basic stains like
hematoxylin

Benthic related to the bottom of the pond or other aquatic environment

Bioaugmentation the addition of benign bacteria into the rearing water to promote
ecological balance within the system and to digest accumulated
organic waste materials

Broodstock adult animals maintained as a source of eggs and sperms to

establish a new population

Chemotherapeutant a drug or chemical used in the treatment of disease

Chitin the complex carbohydrate that makes up the exoskeleton of

shrimps

Chitinoclastic that which is capable of digesting chitin

Ciliate protozoan possessing hair-like structures for movement known

as cilia

Clinical signs signs based on direct observation

Cuticle the non-living outer layer of skin

Cyanotic possessing bluish skin due to presence of large quantities of
deoxygenated blood in the minute vessel

Diatoms any of the one-celled or colonial algae having a cell wall with
silicon components

Discharge tube an exit tube formed in the asexual reproductive body of a fungus
that penetrates through the host cell wall to the outside; zoospores
may be directly released through this tube or maybe formed in a
vesicle at the tip of this tube

Distal anatomically located far from the point of reference

Ectoderm the outermost layer of the three primary germ layers of the embryo

Endoparasitic parasites living inside the body of the host

Eosinophilic cell structures that are readily stained by eosin

Epicommensal a microorganism that lives on the external surfaces of another

organism and derives benefits from it without causing any harm

Epizootic a disease affecting many animals of one kind at the same time

Fibrosis excessive proliferation of fiber cells

Fouling the presence of organisms or organic material on the surface of

an animal

Fungus a general term for a group eukaryotic protists (e.g., mushrooms,

yeasts, molds, etc.) characterized by the absence of chlorophyll
and the presence of a rigid cell wall

Green water an innovative system by which shrimp is cultured with water

culture system where algae grow abundantly. This green water comes from a
pond where Tilapia is grown.

Hematopoietic organ the blood-forming structure in crustaceans

Hemocyte a blood cell of shrimp and other arthropods

Hemolymph the equivalent of blood in crustaceans

Hepatopancreas the digestive organ of shrimp which also functions in absorption
and storage of food

Histology the study of tissue structure at a microscopic level

Hypha a tubular filament which is the unit structure of fungi

Hypertrophied overly developed cell structure or tissue

Inclusion body any body of material within a cell

Incubation time elapsed time between exposure to infection and the appearance
of disease symptoms

Inflammation/ is a non-specific response to injury which involves the

inflammatory accumulation of blood cells and the deposition of the pigment
response melanin

Intermediate host host in which the larval stages of the parasite develop

Latently infected infected animal that does not manifest the disease signs but has
the potential of transferring the disease agent to other stages of
the same or another species

Lethargy weakness or sluggishness

Luminous/ living organisms which give off cold light

luminescent

Melanin a dark brown or black pigment produced in response to injury or

infection

Mesoderm the middle layer of the three primary germ layers of an embryo

Microsporidia a type of protozoa capable of producing resistant spores

Mollusc an invertebrate animal with a soft body usually covered with a

hard shell

Molting the process of shedding the exoskeleton or skin

Mycosis any disease caused by fungi

Mysis a larval stage of higher crustaceans having all the thoracic

appendages developed
Nanomicron one billionth of a micron
Necrosis the state wherein the cells and the tissues lower their activity and
eventually die

Occlusion body a specialized form of inclusion which contains virus particles

Pasteurize partially sterilize by heating below the boiling point

Pathogenic disease-causing

Peptidoglycan a substance composed of two sugar derivatives found in the

rigid layer of the cell wall of both Gram-negative and Gram-positive
bacteria

Phytoplankton minute free-floating aquatic plants

Piscicide substance that selectively kill fish

Postlarva the molt stage after mysis where the immature shrimp begins to
assume the appearance of a miniature adult

Prevalence the proportion of diseased animals in population at a specified

point in time

Probiotics benign bacteria which are added into feeds or encapsulated into
natural food to stimulate the population of 'friendly bacteria' and
prevent the colonization of pathogenic microorganisms in the gut

Protozoa a single-celled organism with a nucleus

Quarantine restrictions placed on animals entering or leaving premises;

detention on account of suspected disease agents

Secondary pathogen a disease-causing organism which causes infection only after

host has been weakened by other causes such as entry of another
pathogens

Spawner a mature female shrimp that produces eggs in large numbers

Stress the sum of the biological reactions to any adverse stimulus that
tends to disturb an organism's physiological stability

Suctoria a class of protozoa having cilia only early in development and in

which the mature form is fixed to the substrate
Syndrome a pattern or group of signs which may be associated with more
than one disease organism or process

Systemic affecting the whole animal

Toxin a poison

Vacuole a tiny cavity in the cell of animals

Vesicle a thin, bubble-like structure in which zoospores are formed

Virus a minute infectious agent which can only be resolved in high-

powered microscopes. It lacks independent metabolism and is
able to replicate only within a living cell

Zoea an early larval form of shrimps

Zooplankton microscopic animals that freely drift in natural bodies of water

Zoospore motile spores produced by means of asexual reproduction

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 Acknowledgment
We thank M.C.L. Baticados, M.C. dela Cruz, R.C. Duremdez-Fernandez, and R.Q. Gacutan,
co-authors of the first edition and former colleagues at SEAFDEC, whose efforts helped
lay down the foundation of this Second Edition. We also thank Dr. J.H. Primavera and
Mr. P.F. Cruz for providing some photos.
About SEAFDEC
The Southeast Asian Fisheries Development Center
(SEAFDEC) is a regional treaty organization estab-
lished in December 1967 to promote fisheries devel-
opment in the region. Its Member Countries are Japan,
Malaysia, the Philippines, Singapore, Thailand,
Brunei Darussalam, the Socialist Republic of Viet
Nam, and Myanmar.
Representing the Member Countries is the Council of
Directors, the policy-making body of SEAFDEC. The
chief administrator of SEAFDEC is the Secretary-
General whose office the Secretariat, is based in
Bangkok, Thailand.
Created to develop fishery potentials in the region in
response to the global food crises, SEAFDEC under-
takes research on appropriate fishery technologies,
trains fisheries and aquaculture technicians, and dis-
seminates fisheries and aquaculture information. Four
departments were established to pursue the objectives
of SEAFDEC.
• The Training Department (TD) in Samut Prakan,
Thailand, established in 1967 for marine capture
fisheries training
• The Marine Fisheries Research Department
(MFRD) in Singapore, established in 1967 for fish-
ery post-harvest technology
• The Aquaculture Department (AQD) in Tigbauan,
Iloilo, Philippines, established in July 1973 for
aquaculture research and development
• The Marine Fishery Resources Development and
Management Department (MFRDMD) in Kuala
Terengganu, Malaysia, established in 1992 for the
development and management of the marine fishery
resources in the exclusive economic zones (EEZs)
of SEAFDEC Member-Countries.