1. DIFFERENT KINDS OF SWINE
DISEASES

2. ENTERIC PROBLEM
SWINE DYSENTERY:
Caused by Serpulina (Treponema) hyodysenterie which
is sometimes referred to as Vibrionic dysentery, bloody
scours, bloody diarrhea or black scours.

3. CLINICAL SIGNS
 fever (40oC)
 watery feces with blood/mucus in the feces
 loss of appetite
 back is arched and due to the pain in the abdomen the
pig may be seen trying to kick it
 in chronic cases there is dehydration, thirst, weakness,
in coordination and emaciation. Death may result
from dehydration and/or acidosis.

4.  Brownish diarrhea
 Diarrhea progresses to brownish red with a much
more liquid consistency
 Lesions are found in the large intestine.
 Typical shape of Swine
Dysentery-infected pigs

5. PREVENTION
 Prevention is by lessening stress through good housing
and management, maintenance of good hygiene and
cleanliness to limit the multiplication of the bacteria.
Prevent overcrowding.

6. Treatment :
 When treated with antibiotics, may show signs of
improvement (Tylosin, lincomycin, bacitracin, etc.)

7. DYSENTERY

8. SALMONELLOSIS:
 Various strain of Salmonella bacteria can cause
diarrhea. This type of diarrhea is rare in young piglets
and is usually seen from weaning up to 6 months.
Acute deaths can occur.

9. CLINICAL SIGNS
 heavy bacteremia
 high fever
 cyanosis of the skin (bluish skin) specially in the belly
and eartips and skin hemorrhages
 little or no diarrhea before death

10. TREATMENT
 Treatment should start first with isolation of infected
animals to prevent the spread of the disease to the
group or herd. Remove the feed and provide clean
drinking water with electrolytes. Three (3) days
treatment with antibiotics like Ampicillin or
Chloramphenicol (Please note that chloramphenicol is
presently banned for use in food animals in the
Philippines). These should be followed with feed or
water antibiotics for 7 days.

11. PREVENTION
 The disease can be prevented by implementing an all-
in-all-out system in fattening pigs. Maintain good
hygiene and other general preventive measures.
 Also take note that Salmonellosis is a zoonotic disease.

12. Salmonellosis

13. PORCINE PROLIFERATIVE
ENTEROPATHY
 (Ileitis, PIA, Porcine Intestinal Adenomatosis, Red
Gut)
 The causative agent of PPE is Lawsonia intracellularis
an intracellular curved bacteria. The acute form of this
disease occurs in young breeding stock or finishing
pigs while the chronic forms occur in young growing
pigs. Also, the disease, albeit not apparent can affect
from 15 to 50% of the growing herd.

14.  CLINICAL SIGNS
 Acute forms
 death, often the first signs seen
 pale and anemic animals
 depression and reluctance to move
 reduced appetite
 retarded growth
 watery, dark or bright red diarrhea
 abortion may occur in recovering animals often within 6
days of the onset of clinical signs

15. Chronic forms
 very slight with irregular periods of diarrhea and
anorexia
 severe loss of condition and persistent scouring
 terminal peritonitis

16. PREVENTION
 The disease can be prevented by implementing an all-
in-all-out system in fattening pigs. Maintain good
hygiene and other general preventive measures.
 Also take note that Salmonellosis is a zoonotic disease.

17. PORCINE PARVOVIRAL INFECTION
Stillbirth, Mummification, Embryonic Death, Infertility
(SMEDI)
 Both these diseases cause the same disease symptoms,
and they can only be differentiated from each other by
laboratory tests. When these diseases are present in
the herd, they cause no other symptoms except
reproductive failure.

18. Clinical signs:
 too many repeat breeders in the herd
 intervals are often more than 21 days
 early embryonic deaths
 small litter sizes
 mummies, stillbirths, weak piglets

19. Treatment
 There is no treatment for reproductive failure.

20. Prevention
 in a herd free from parvovirus/SMEDI occurrences is very
difficult since these viruses are known to be very stable and
can be infective for long periods. Even with good hygienic
measures and strict quarantine, it can still find its way into
the farm. The most common ways are from new stock,
persons, rodents and other unwanted animals.
 Ensure that gilts and new breeding stock entering the
breeding herd are properly at least one (1) month before
breeding, should be implemented. This establishes a
common micro flora providing a fairly uniform immunity.

21. Still birth, Mummification, Embryonic Death, Infertility (SMEDI)

22. REPRODUCTIVE PROBLEM
BRUCELLOSIS
This disease is caused by a bacterial organism, Brucella suis.

Importance of brucellosis:
 Brucella suis is not a highly infectious organism. It spreads slowly
between and within herds, and you should be able to keep it out of your
herd if you take sensible precautions. But it is a serious disease, and
you must always think of it as such.
 The disease is zoonotic. If brucellosis is suspected in your herd, take
great care that you and the farm caretakers do not get infected. Call in
your veterinarian immediately.
 If it gets into your herd, it is difficult to eliminate. It causes long term
reproductive losses, and some types also cause a very nasty disease
(known as undulant fever) in people.

23. Clinical signs:
 in male breeders
 orchitis (inflammation of the testicles) which may
lead to temporary or permanent sterility
 The organism multiplies in the testicles and/or the
male accessory reproductive glands and is then shed in
the semen for prolonged periods. The infection in the
boar’s reproductive tract is usually permanent. The
damage that it does is irreversible.

24.  in female breeders
 abortion at any time of the gestation period
 high return to service and vaginal discharges
The infection in the sow’s reproductive tract is not
permanent and eventually clears up spontaneously.

25. in newborn piglets
 stillbirths and weak piglets
in adult pigs
 lameness and posterior paralysis
 abscess formation in the extremities or other parts of the
body
A few growing pigs and adults, and a slightly greater
number of suckling piglets and weaners start to develop
partial or total paralysis in their hind quarters. This is the
result of infection and damage to the spine. Some pigs may
become lame with swollen joints.

26. Treatment
 There is no practical treatment for this disease. All
infected animals should be slaughtered and disposed
properly, either by burning or burying.

27. Prevention
 Healthy animals - buy stocks from Brucella-free pigs.
 Proper quarantine procedures - This includes, in
particular, the prevention of exposure of the herd to
infected pigs and the introduction of Brucella-free
replacement pigs.
 Testing animals for brucellosis (blood testing) -
Repeated herd blood tests with removal of positive
reactors is a good preventive measure. However, this
may be effective if only a few pigs are infected but is
likely to be unsuccessful if many pigs are positive.
 Proper disposal of manure and dead animals

28. Brucella - 'orchitis'

29. Mastitis-Metritis-Agalactia (MMA)
Syndrome
Mastitis is the inflammation of the mammary gland
which is responsible for milk production. Mastitis
involving individual udder section is diagnosed by keen,
visual observation and manual examination.
metretis or inflammation and infection of the uterus often
occurs after farrowing, dystocia or abortion. Metritis is part
of the agalactia syndrome so frequently encountered as a
clinical entity in swine practice.
The following organisms are frequently isolated from
animals suffering from metritis: Streptococcus, Escherichia
coli, Enterobacter aerogenes, Klebsiella aerogenes,
Klebsiella pneumoniae.

30. Prevention and Treatment
 There are several factors that can lead to MMA in a
herd, including infection, stress, lack of good nutrition
and toxicity from constipation and uterus infection.
Toxicity can result from constipation brought about by
a lack of exercise and poor diet. Here, we can always
mention the very important contribution of improper
feeding shortly before and after farrowing

31. Retained uterine contents after farrowing may
also result to toxicity. Injections of hormone oxytocin
will help the sow in expelling retained placenta, blood
or any fetal membrane. Moreover, flushing or lavage
using a mild antiseptic (0.1% - 0.2% potassium
permanganate) or herbal decoction (guava leaves) is a
cheaper way of expelling retained uterine contents. A
sow needs plenty of clean, fresh water. Flow rate
should be at least 1.5 liter/minute for proper milk
production.

32. Mastitis

33. Flushing or lavage with the use of a syringe and a catheter facilitates evacuation
of retained uterine contents

34. PORCINE PARVOVIRAL INFECTION
Stillbirth, Mummification, Embryonic Death, Infertility (SMEDI)
Both these diseases cause the same disease
symptoms, and they can only be differentiated from
each other by laboratory tests. When these diseases
are present in the herd, they cause no other symptoms
except reproductive failure.

35. Clinical signs:
 too many repeat breeders in the herd
 intervals are often more than 21 days
 early embryonic deaths
 small litter sizes
 mummies, stillbirths, weak piglets

36. Treatment
 There is no treatment for reproductive failure.

37. Prevention
 Prevention in a herd free from parvovirus/SMEDI occurrences is very difficult
since these viruses are known to be very stable and can be infective for long
periods. Even with good hygienic measures and strict quarantine, it can still
find its way into the farm. The most common ways are from new stock,
persons, rodents and other unwanted animals.
 Ensure that gilts and new breeding stock entering the breeding herd are
properly at least one (1) month before breeding, should be implemented. This
establishes a common micro flora providing a fairly uniform immunity.
 Additionally, prevention in an infected herd is based on immunizing the gilts
providing contact with older sows before they are bred, or even mixing fecal
matter from sows and piglets with their feed. It is also a practice to feed after-
births and fetuses of affected sows (these are either chopped fresh or dried and
mixed with the feed).
 A vaccine is available for parvovirus and is usually given to gilts, boars and sows
(up to second parity only). However, this also depends on the discretion of the
veterinarian whether to continue vaccination until the third or fourth parities.

38. LEPTOSPIROSIS:
 This disease is caused by a bacterial organism,
Leptospira spp. Take note that leptospirosis is
infectious to human beings (zoonotic). The signs are
fever, headache, pain and stiffness of the muscles.

39. Clinical signs:
 animals may show various levels of inappetence, fever
and diarrhea which may last for about 3 days and
which can easily be overlooked
 abortion (more common in the late stage of pregnancy
(D90-D110)
 in cases of abortion, it is common to have piglets dying
at different stages of gestation
 infertility does not occur in leptospirosis cases

40.  . The signs of the disease appear in 1-3 days post-
farrowing. They will be found lying in their beds,
shivering or trembling.
 The temperature ranges from 40oC-41oC.
 The udder is hot and milk flow is inhibited. A thick,
whitish to yellowish discharge from vulva is seen by
the end of the first or second day.

41. Transmission:
 The disease is spread by way of urine. Animals can
remain infectious and continue shedding Leptospira
spp. for years, since the infection persists in the
kidneys where these pathogens cannot be effectively
reached by the immune system.

42. Treatment:
 Treatment is possible using antibiotics. Streptomycin
is most effective in these cases.

43. Prevention:
 isolation of sick animals and new additions to the
herd
 cleaning and disinfection of pens and equipment
 extermination of rats
 administration of leptospirosis vaccines
 keeping different classes of livestock separated
 buying healthy stocks

44. STREPTOCOCCAL ARTHRITIS:
CLINICAL SIGNS
 Mycoplasma hyorhinis is found commonly in the nasal
cavity (nose or snout) of swine and is frequently a
secondary invader following pneumonia. Some of the signs
to look for early in the disease are rough haircoat and
depression. As the disease progresses, the animal suffers
abdominal and chest pains. The pigs show stretching
movements with the front and hind limbs extended
particularly when first aroused. Other signs are labored
breathing, poor appetites and slight temperature
elevations. Pigs may lie on their chest rather than their
sides. Lameness and enlarged joints follow.

45. Prevention
 involves good sanitation in the farrowing house.
 Clipping navel cords and treating them with a
disinfecting solution is helpful.
 A dry, warm, ventilated farrowing house is
recommended for controlling this disease.
 Injections of a combination of penicillin and
streptomycin will work well in the early stages of the
disease. When infection becomes well-established,
complete recovery maybe impossible.

46. Porcine Reproductive and
Respiratory Syndrome (PRRS)
 The porcine reproductive and respiratory syndrome
(PRRS) is a relatively new disease that is caused by an
arterivirus.

47. Clinical Signs:
 When the virus first enters the breeding herd, disease
is seen in dry and lactating sows and suckling piglets.
It has primarily reproductive and respiratory
manifestations. However, one of the early clinical signs
include a blue discoloration of the ears, hence its early
name "blue ear pig disease.“
 ‘red eye symptom’

48. Supportive) Treatment
 vitamins
 high energy diet

49. Weak born piglets, stillbirths
and mummies due to PRRS

50. Diarrhea of Piglets
 While the consistency of manure may vary according
to the diet fed, diarrhea maybe considered to occur
when through small or large intestinal disease there is
a change to a more fluid consistency than normal.
Clinical signs associated with small intestinal disease
may include vomiting, melena, poorly digested feeds
and bulky voluminous feces. Vomiting seldomly occurs
in cases of large intestinal diseases, however, there
maybe bloody stools, gross mucus on the feces, small
and frequent defections and tenesmus.

51. Clinical sign
Diarrhea as the main clinical sign.
Minimal other signs of gastrointestinal
tract disease such as vomiting,
anorexia, or colic.

52. Control and Treatment
 In commercial farms, routine vaccination of sows against E. coli is practiced
coupled with improved husbandry practices. On the other hand, it should be
mentioned that the immunity of piglets due to pre-farrowing vaccination is
also dependent on adequate colostrum and milk production.
 It is therefore very important to ensure adequate colostrum intake. As have
been explained in the preceding discussions, colostrum contains antibodies
which helps protects young piglets during their first few weeks of life. Natural
immunization of gilts during the quarantine period will boost immunity
against common farm pathogens.
 Further, corrections of environmental defects: improve ventilation (to avoid
draughty conditions); daily and routine cleaning; keep bedding dry and clean;
keeping the creep area warm would greatly improve the resistance of young
piglets. Postponement of scheduled piglet activities on weak piglets is also
advisable as these will give additional stress, further reducing their resistance.

53.  The administration of iron is also withheld if diarrhea is due to E. coli.
The explanation is that this bacterium needs iron as a source of
nutrient for multiplication. Iron administered will then serve as an
additional food for them. On the other hand, consult your veterinarian
for proper diagnosis and recommendations.
 Electrolyte solution will help rehydrate the body fluids lost due to
excessive diarrhea. There are many commercially prepared electrolyte
solution available in the market. In some cases, creep feed may cause
diarrhea, withheld creep feed if diarrhea occurs 1-3 days after the
introduction of feed.
 Lastly, evaluate the integrity of the sow. Sometimes the diarrhea of
piglets is due to an infected milk of the sow, or inadequate milk flow
(MMA syndrome, old sow). In such cases, have a closer look at the sow
and check if it causes the problem, and if fostering is possible.

54. E. coli - "yellowish diarrhea"
E.

55. Skin diseases
Greasy Pig Disease (Exudative Epidermitis)
Caused
This is caused by infection of the skin with
Staphylococcus.

56. Clinical sign:
 The disease starts with reddening of the skin then
becomes wet and covered with crusts. It usually starts
around the head then spread over the body. It may
sometimes resemble mange but the crust are easy to
remove and the skin below is wet, rough and reddish.
Pruritus is not common.

57. Prevention:
 Routine disinfection of nursery pens and farrowing crates
is recommended. Provide warm, dry, draft-free
environment. If lice or mange are evident, a control
program should be instituted. Early detection is necessary
for successful eradication of exudative epidermitis.
Therapeutic doses of penicillin or tetracycline injected 3-4
days in the early stages of the disease may help. Once the
lesion becomes extensive, it may help to bathe the animal
with mild soap and water or disinfectant solutions (iodine
or chlorine).

58. Greasy Pig Disease

59. Internal Parasites
 Parasites are very small animals (insects, worms) that live
partly or completely in the bodies of other "host", animals
or plants. Sometimes, they can be seen by the naked eye,
sometimes a microscope is needed, especially for the
younger life stages of the parasites.
 Internal and external parasites are of economic importance
to the swine industry. Actual death losses from parasitism
are extremely low. However, the economic loss is
significant, if proper diagnosis, treatment and prevention
are not carried out. By incorporating standard health
practices for controlling internal and external parasites,
you can help maximize your economic gain with healthy
hogs.

60. Control
Eggs of worms are very resistant. They sometimes remain
infectious for up to five years! Most disinfectants are not effective
against worm eggs. What is important is to keep worm infestation at
the lowest possible level. As such, it is necessary to disrupt the life cycle
of the parasites. This can be achieved in various ways:
 General hygiene, including regular cleaning and disinfection of the
pens will minimize intake of infectious larvae of intestinal and kidney
worms.
 A good deworming program will kill adult intestinal worms.
 A proper disposal of human wastes to prevent infection with bladder
worms.
 Rat and mice eradication programs and cooking of kitchen wastes
prevent swine form infection with muscular worms.
 Confinement of animals prevents infection with lungworm. The
frequency with which you need to deworm will depend upon housing
conditions, types of floor and sanitation.

62. Ascaris suum
Ingested eggs go into the wall of the small intestine,
where they hatch and release larva (immature adults). This larvae
migrate to the liver (where they cause "milk spots"), staying there
for approximately one week before traveling through the blood
stream onto the lungs. In the lungs they will be cough-up and then
swallowed. They go back again to the small intestine where they
finally mature into adults. These adults then produce eggs that are
passed in the feces. Migration predisposes the animal to respiratory
infections and a variety of enteric diseases
Female worms hatched 200,000 eggs/day, which are passed through
the feces. Under warm and moist conditions, these eggs are
infective within eight (8) weeks. Hosts ingest infective eggs and the
cycle continues.

64. Matured ascaris

65. Whipworm

66. Respiratory problem
SWINE INFLUENZA
(Swine flu, flu, influenza)
Swine influenza virus belongs to Influenza virus type A.
The incubation period is from 1-3 days or can be as
short as 4 hours.

67. Clinical Signs
 all ages are susceptible but more common among growers and
fatteners
 rapid onset of disease, 1-3 days after the introduction of the virus
(or infected animal)
 fattening animals develop sneezing, nasal and eye discharge and
coughing often associated with arched back
 animals tend to huddle together and show rapid and labored
breathing especially when they are forced to move
 fever may reach 42oC so there is inactivity, depression and loss of
appetite resulting to weight loss
 recovery is rapid, about 7 days after the onset and mortality is
very low (1%) unless there is another infection

68. Stress factors
 moving pigs
 mixing pigs
 poor isolation facilities
 marked diurnal temperature – p.m.
 overstocking

69. Treatment
 Antibiotics are used to suppress secondary bacterial
complications (e.g. Pasteurella). Antibiotics are
administered either via water or injectable, in-feed
medication is not recommended because affected pigs
are recumbent and have very poor appetite.

70. Swine Influenza

71. MYCOPLASMA HYOPNEUMONIA
(Mycoplasmal Pneumonia of Swine MPS; Enzootic Pneumonia of Swine, EPS)
 Transmission is primarily from pig-to-pig although
long range aerosol transmission is possible. Clinical
signs within the herd are dependent on the degree of
infection, contributing pathogens and environmental
stress. Many producers are utilizing all-in-all-out
system for the farrowing and nursery units.

72. Clinical Signs
 few pigs show specific symptoms, but Mycoplasma
paves the way for other disease condition such as
Actinobacillosis or Pasteurellosis which would make it
more fatal
 typical is a short, dry cough
 low mortality, but effect is more on the growth of the
animal with very high feed conversion ratio

73. Infection in Piglets
 the newborn piglets become infected from their mother
during birth or first days of life, but due to colostral
immunity, signs appear 2-3 weeks after weaning only
 if a newborn does not get enough colostrum (e.g. due to
MMA), or does not get it in time, signs develop at the age of
2-4 weeks
 morbidity reaches highest level (40%-60%) at the age of 4-
6 months, and thereafter the diseased animals decline, if
there are no complications

74. Treatment
 Since Mycoplasma is often complicated by Pasteurella,
Actinobacillus and Bordetella, application of
combined drugs with a wide spectrum is
recommended.
 Use of vaccines reduce lungs lesions with
improvement of weight gain, however no reduction in
the number of Mycoplasma was observed.
 use of drugs or vaccine should always be combined
with an improvement in hygienic conditions.

75. Mycoplasma hyopneumonia

76. ACTINOBACILLUS (HEMOPHILUS)
PLEUROPNEUMONIA
 Subclinical carriers of App are the primary cause of
outbreaks. Serology (30 samples) from pigs at 7-8
weeks of age is important to determine if App carriers
are present. Positive results from these animals
indicate: a recent infection, presence of carriers and in
inactive infection in the herd.

77. Clinical Signs
 low feed intake coupled with high fever
 serious breathing difficulties resulting to sudden
death, or sometimes death within hours
 bloody froth from the mouth/nose immediately
before/after death
 severe damage on growing-finishing farms: market
pigs show inflamed pleura (pleuritis)

78. Predisposing Factors
 draught
 mixing/regrouping of pigs
 origin of fatteners - different farms
 bad micro-climate coupled with high air velocity
 over-stocking

79. Control
 Antibiotics
 Vaccination
 Depopulation/Eradication.

80. Site of lesions (Actinobacillus pleuropneumonia)

81. ATROPHIC RHINITIS
 Caused by toxins produced by Pasteurella multocida,
these bacteria adhere to the cells of the nose causing
degeneration of the turbinate bones resulting to
twisted snouts. Other viruses and bacteria, in
particular Bordetella bronchiseptica. together with
ammonia, dust and cold air all damage the lining of
the nose allowing Pasteurella to colonize the nose. A
scoring system in the slaughterhouse is used in foreign
countries to determine extent of damage.

82. Control strategies
 Antibiotics. First and foremost, proper testing is required
to determine drug sensitivity of the bacteria. Antibiotics
such as oxytetracycline and sulfonamides can be used in
feed medication in the last month of pregnancy to control
the shedding of bacteria from the sow to her subsequent
litter. Injectables are sometimes used on piglet program
consisting of three to four injections in the first 21-28 days
of life.
 Vaccination. The vaccination program is targeted to protect
piglets before infection. Vaccinate sows before farrowing
with a vaccine containing the appropriate toxin. It must be
given 2 weeks prior to natural exposure to bacteria.

83. Note the twisted snout (Atrophic
rhinitis)

84. MISCELLANEOUS CONDITIONS
PARAKERATOSIS.
The major portion of this pig's
skin is wrinkled especially on the abdomen
and legs. It does not appear to be irritating to
the pig, although if there is secondary mange
infection, irritation will occur. Most consider
this as zinc deficiency, but mineral imbalances
involving calcium play an important role.

85. PARAKERATOSIS

86. STAPHYLOCOCCAL INFECTION
ON LACTATING SOWS
Can easily lead to mastitis and irritation
of the sow causing its refusal
to let her piglets suckle.

87. STAPHYLOCOCCAL INFECTION
ON LACTATING SOWS.

88. STAPHYLOCOCCAL INFECTION.
This can easily be mistaken for mange
problem. The characteristic
lesion is one of pus-filled insect bite-like
wounds.

89. STAPHYLOCOCCAL INFECTION.

90. ACUTE PERITONITIS.
On opening the abdominal cavity, a greenish watery
fluid with strands and sheets of fibrin escaped. The
viscera, especially the intestine, has 'bunched up' from
the irritating peritoneal fluid which is usually gastric
fluid and bile. Maybe due to a chronic illness or
ascarid infection which punctured or damaged the
biliary system (gall bladder).

91. ACUTE PERITONITIS

92. FIBRINOUS PERITONITIS
Many strands and clumps of fibrin are scattered in
the abdominal cavity. A castration wound is just
visible between the legs. This might be the source of
infection and the most probable point of entry is the
inguinal canal. Without an accountable wound, one
should suspect Hemophilus spp. (Glasser's disease) in a
poly serositis case.

93. FIBRINOUS PERITONITIS

94. AURAL HEMATOMA.
 Before (left) and after (right) the hematoma
disappears. Such conditions maybe due to fighting
injuries or circulatory failure. The condition
disappears by itself and it would help if the affected
animal will be isolated.

95. AURAL HEMATOMA

96. VULVAR FISTULAE.
Usually caused by injuries. On pregnant animal,
there will be difficulty in farrowing, while on dry sows,
this could lead to an internal infection.

97. VULVAR FISTULAE

98. IMPERFORATE ANUS.
 The piglet has been partially necropsied to explain
the cut tissue in the lower part. The area just above
the tail should be open. In this anomaly, the
proctodeum (anus) did not open. On female animal,
megacolon may develop and may survive. This
condition is to be differentiated from atresia recti in
which the rectal lumen is constricted more cranially in
the GI tract allowing insertion of a finger or blunt
instrument into the anus, at least as far up as the
constriction.

99. IMPERFORATE ANUS

100. LEG WOUNDS/ABRASIONS.
Due to rough floors, weak piglets or perhaps
insufficient milk. Later on, it could lead to arthritis,
pneumonia or meningitis, or simply unthrifty animal.

101. LEG WOUNDS/ABRASIONS

102.  Facial wounds caused by faulty toothclipping
technique. This can lead
to greasy pig disease, if not, death of piglet can happen
due to massive infection.

103. EPISTAXIS (Nosebleed).

104. EPISTAXIS (Nosebleed).
In living or recently dead animals, one should suspect
things such as trauma, foreign bodies, atrophic
rhinitis, pneumonia or even bleeding gastric ulcers
with vomiting when one sees relatively fresh blood or
blood mixed with mucus or froth from the nose or
mouth. It can also be seen with extreme exertion and
dyspnea.

105. EPISTAXIS (Nosebleed).

106. GASTRIC TORSION.
The abdomen was well distended and tense prior to
opening in a recently dead animal. The spleen is seen
here on the right side which is abnormal and the
intestine and stomach are gas-filled. This condition
regularly occurs on pregnant sow.

107. GASTRIC TORSION.

108. RECTAL PROLAPSE.
Rectal prolapse in a farrowing sow. The animal
recovered after replacement of the prolapse.

109. RECTAL PROLAPSE.

110. RECTAL PROLAPSE
Rectal prolapse in a 16-kg. weaner, two days after onset.

111. RECTAL PROLAPSE

112. CLASSICAL SWINE FEVER, HOG CHOLERA
Hog cholera is one of the most commonly
occurring viral disease in South East Asia and the
Pacific Region affecting all ages of pigs. The disease is
caused by a virus under the Family Togaviridae.

113. Importance of Hog Cholera
 Hog cholera is one of the most economically-
damaging pandemic viral diseases of pigs in the world.
 In a susceptible or unvaccinated herd almost all the
pigs are affected. Mortality is high.
 There is only one serotype of the virus, and attenuated
vaccines are highly effective. Also, it does not spread
on the wind or on insects or birds, so standard
precautions of farm biosecurity should keep it out.
However, it persists in uncooked and cured meat.


114. Mode of Infection
 Infection usually occurs via the oro-nasal route and
occasionally through the conjunctiva, genital mucosa
or skin lesions. The infection is classified into three (3)
categories. They are acute, chronic or persistent and
congenital infection. Usually, clinical signs appear
after 2-6 days of incubation. Chronic or persistent
infection is usually caused by low to moderate
virulence viruses. Pigs my survive the infection
showing prolonged and intermittent disease periods.
There can be clinical improvement, relapse or death.

115. Clinical Signs
 Clinical signs and symptoms in suckling piglets and growing pigs will
be discussed in Module 6 (Fattener Operation - Health) of this course.
The chronic and persistent type of infection will be discussed in some
detail in this section since it affects breeder animals.
 The virus can cross the placenta and infect the piglets in the sow’s
uterus. If the virus crosses the placenta before the piglets’ immune
systems have developed, the following may happen:
 They may be born apparently healthy although possibly weak.
 They may grow on to be persistent carriers without at first showing
clinical signs.
 They shed virus, so they are dangerous to other pigs.
 At several weeks or months of age, they may develop typical clinical
signs. These are likely to be milder, last longer and without the
characteristic high temperatures.

116. Prevention and Control
 Importation of breeders, pork or pork products from
countries positive with hog cholera should be
prohibited. Kitchen left-overs from aircrafts and ships
should not be used as pig feeds and has to be
destroyed.
 Vaccination is widely practiced in all countries with
hog cholera using the modified live virus vaccine.
Thorough cleaning and disinfection should be done.
NO PRACTICAL TREATMENT AGAINST HOG
CHOLERA VIRUS.

117. Hog Cholera
Pigs affected with hog cholera appear weak, staggering and tend to sit like a dog.

118. PSEUDORABIES/AUJESKY’S
DISEASE
 Pseudorabies or Aujesky’s Disease is a herpes virus
infection characterized by nervous and respiratory
signs associated with a rise in temperature and often
leading to death in young pigs. Infection in adults
maybe inapparent or associated with stillbirth or
abortion.

119. Clinical signs:
 Piglets - Clinical signs begin 3-7 days after infection. Piglets
may vomit and may show diarrhea and then become
depressed with trembling and nervous symptoms (circling,
dog-sitting position, spasms, opisthotonos, head pressing)
and death within 24 hours.
 Adults - Up to 50% of affected pregnant animals abort or
give birth to mummified or macerated fetuses.
Reproductive failure may follow these abortions or early
weaning consequent upon death of a litter. Boars may be
affected. Semen quality declines from 10-14 days post-
infection for 1-2 weeks. Sperm abnormalities may occur

120. Treatment and Control
 No treatment is possible at present. Antibiotics will prevent secondary
infections particularly of the respiratory system and also reduce
bacterial damage.
 Routine vaccination is recommended in enzootic and high risk areas.
There is only one main serotype of the pseudorabies virus which
produces a strong long-lasting immunity. Vaccinated pigs can become
infected, but multiplication of the virus in the pigs' tissues is limited,
and so less is shed into the environment. Vaccination also prevents the
virus from crossing the placenta of pregnant sows to infect the unborn
piglets.
 Piglets, which are suckling from vaccinated sows, receive colostral
protection which lasts about 6-8 weeks. This is the age when the
virulent pseudorabies virus would do most damage. During this time
the pigs cannot be vaccinated successfully because the maternal
antibodies neutralize the vaccine virus before it has had time to
stimulate an immunity (see p. 43 for vaccination schedule).

121. Measures to aid in disease
eradication
 proper disposal of dead pigs (burning or burying)
 buying of tested breeding stocks and isolation for at least
30 days
 avoid buying feeder pigs if breeder stocks are being raised
 getting of feeder pigs from a farm that did not have the
disease
 keeping visitors away from swine premises
 keeping stray dogs, cats and wildlife off the premises5
 keeping swine and cattle separate
 isolation of show stock for 30 days after the fair is over

122. IMAGES