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Swine medicine module 2 and 3
67問 • 1年前
  • Rein
    • 通報

    問題一覧

  • 1

    * Mainly in growing pigs * common in many areas of the world

    Erysipelas

  • 2

    ETIOLOGY * Erysipelothrix rhusiopathiae * remain in carcass even after processing * carrier in pigs can cause re-infection

    Erysipelas

  • 3

    CLINICAL SIGNS * acute septicemia * fever (40 - 42°C) * walk stiffly

    Erysipelas

  • 4

    CLINICAL SIGNS * lie on sternum * erythema of ears, snout, and abdomen * diamond shaped skin lesion all over the body (lateral and dorsal part)

    Erysipelas

  • 5

    LESIONS * swollen spleen * congested lungs * arthritis

    Erysipelas

  • 6

    DIAGNOSIS * penicillin treatment within 24 hours * diamond shape lesion * staining (spleen/ kidney)

    Erysipelas

  • 7

    DIAGNOSIS * culture (blood agar) (tonsil/lymph nodes) * gram staining * bacterial isolation

    Erysipelas

  • 8

    TREATMENT * simple-acting penicillin

    Erysipelas

  • 9

    CONTROL * vaccination (4 - 6 months) * elimination of carrier * sanitation

    Erysipelas

  • 10

    * highly contagious viral disease of pigs * affects pigs of all ages * high morbidity and mortality

    Hog cholera/ classical swine fever

  • 11

    ETIOLOGY * pestivirus from togaviridae family * host specific * virus replicate in cell culture of pig origin * virus survive in bedding for days to weeks, depending on temp

    Hog cholera/ classical swine fever

  • 12

    ETIOLOGY * temperature remain in frozen pork (<4 yrs), chilled and preserve carcass (3 -6months ) * most common route infection is ingestion and replication occur in tonsil * viremia occurs within 24 hrs

    Hog cholera/ classical swine fever

  • 13

    ETIOLOGY * direct contact (most common mode of transmission) * infected pigs shed virus in body excretion/ secretion * pigs surviving infection have depletion of lymphoid tissue and susceptible to concurrent infection

    Hog cholera/ classical swine fever

  • 14

    CLINICAL SIGNS * incubation period (5-10) or (2 - 20) days * anorexia, lethargy and fever (41c) * multifocal hyperaemia of skin * transient constipation, diarrhea, w/ vomiting

    Hog cholera/ classical swine fever

  • 15

    CLINICAL SIGNS * dyspaea * ataxia, paresis, and convulsion * pigs file up or huddle together

    Hog cholera/ classical swine fever

  • 16

    CLINICAL SIGNS * mortality in young (100%) * pre-terminal cyanosis of skin, especially ventrally base of ear and snout * transplacental infection

    Hog cholera/ classical swine fever

  • 17

    LESIONS * leukopenia * thrombocytopenia * turkey egg appearance of kidney * infarction of margin of spleen

    Hog cholera/ classical swine fever

  • 18

    LESIONS * button ulcers in large intestine * enlarge hemorrhagic lymph node * non-suppurative encephalitis w/ severe vasculitis

    Hog cholera/ classical swine fever

  • 19

    DIAGNOSIS * pneumonia (tonsils lymph node, spleen, kidney, distal ileum * immunofluorescence * immunoperoxidase * neutralization * ELISA

    Hog cholera/ classical swine fever

  • 20

    TREATMENT * hyperimmune serum

    Hog cholera/ classical swine fever

  • 21

    CONTROL * vaccination * slaughter and disposal of carcass * disinfection * waste-food feeding management

    Hog cholera/ classical swine fever

  • 22

    * highly contagious disease with signs and lesion resembling HC, but it was restricted to Africa

    African swine fever

  • 23

    ETIOLOGY * iridovirus, w/ some properties of poxvirus/ asfarviridae

    African swine fever

  • 24

    TRANSMISSION * Ornithodoros spp. (Tick act as vector) Including O. Coriaceus and O. Turicata from USA * Fomites, horizontal

    African swine fever

  • 25

    CLINICAL SIGNS * Ist sign is fever (40.5 - 42°C) * Leukopenia and thrombocytopenia * Anorexia, listlessness, incoordination, and cyanosis

    African swine fever

  • 26

    CLINICAL SIGNS * Vomiting, diarrhea, conjunctivitis * Abortion in pregnant animal * Survivors are usually carriers for life, although virus is not continuously present in the exertion

    African swine fever

  • 27

    LESIONS * Hemorrhage of lymph nodes and kidneys * Splenomegaly * Edematous areas of cyanosis in hairless portion * Pleural, pericardial and peritoneal fluid are excessive * Focal,caseous necrosis and mineralization of lungs

    African swine fever

  • 28

    DIAGNOSIS * hemadsorption * immunofluorescence * immunoperoxidase * ELISA, PCR

    African swine fever

  • 29

    TREATMENT * No treatment or vaccines available

    African swine fever

  • 30

    CONTROL * Control movement of animal * Control vectors * Quarantine and slaughter

    African swine fever

  • 31

    An acute and highly contagious, viral infection of domestic and wild cloven-footed animals

    Food and mouth disease

  • 32

    ETIOLOGY • Enterovirus of the picornaviridae family or Aphthosvirus
Family:  A      south African Territory 1
              O       SAT 2
              C       SAT 3
                       Asia 1 • Horse are resistant

    Food and mouth disease

  • 33

    ETIOLOGY • Rapidly inactivated by increase or decrease pH, sunlight and increase temp. • Lacks liquid containing envelope resistant to ether and chloroform • Most commonly used disinfectants (Na hydroxide, Na carbonate, acetic acid, methylene blue, gentian violet, formalin and dye)

    Food and mouth disease

  • 34

    TRANSMISSION  • Most common transmission is aerosol (50km.) • When man inhale the respiratory aerosol of FMD, virus persist in the respiratory tract for 24hrs • Esophageal fluid may contain the virus, even before and after the lesion appear • Cattle may retain the virus in tonsillar cells for as long as 3yrs after recovery

    Food and mouth disease

  • 35

    TRANSMISSION • Virus is also present in milk, pasteurization does not kill the virus, because they are protected by cell debris and fats. • Source of infection: Al, meat, bone,; garbage food, contaminated vaccine • Pigs tend to excrete more virus than ruminants • The disease is difficult to detect in sheep, but they can readily transmit the virus

    Food and mouth disease

  • 36

    CLINICAL SIGNS • Morbidity and mortality is high in young • Initial signs: dullness, in appetence, fever and shivering • Following by: smacking of lips, drooling, shackling, and kicking of the feet Vesicle formation: nares, buccal cavity, claws, mammary gland

    Food and mouth disease

  • 37

    CLINICAL SIGNS • Pronounced salivation and lameness • Abortion in pregnant, death young • Deformed claw • Mammary and involvement may result to mastitis and permanent impairment of milk production • Prolonged unthriftiness and failure to gain weight in

    Food and mouth disease

  • 38

    LESIONS • Vesicles • In sheep, dental pad is the most common site • Lesion in rumen pillars, myocardium in skeletal muscle • Type C have predilection for heart membrane

    Food and mouth disease

  • 39

    DIAGNOSIS • Complement fixation • Virus neutralization • Agar-gel precipitation • ELISA, PCR • DNA probes, labeled with avidin-biotin (fingerprinting/ PCR) in products form infected animals

    Food and mouth disease

  • 40

    TREATMENT • No specific cure, soft beddings • Antibiotics-to prevent secondary treatment • Wound Antiseptic

    Food and mouth disease

  • 41

    CONTROL • Alleviate sign, avoid feeding waste • Vitamins and minerals • Isolation and quarantine

    Food and mouth disease

  • 42

    CONTROL • Slaughter and disposal of affected animals • Hygiene and sanitation • Vaccination program ◦ Sow: once/twice ◦ Piglets: 5-1 week before farrow ◦ Gilts: 1-2 a year

    Food and mouth disease

  • 43

    • Transient disease of pigs in which vesicular lesions appear in mouth and feet. • Lesion is similar to FMD, but swine do not lose condition and the lesions heal rapidly • Do not cause severe production losses. • Pigs are the natural host, although the virus is present in sheep and cattle.

    Swine vesicular disease (SVD)

  • 44

    ETIOLOGY • Enterovirus of Picornaviridae/ or Vesiculoviridae

    Swine vesicular disease (SVD)

  • 45

    TRANSMISSION  • Direct and indirect contact • Contaminated pork and pork products

    Swine vesicular disease (SVD)

  • 46

    CLINICAL SIGNS • Vesicles in mouth, lips and snout, feet • Lesions are mild or inapparent, especially when pigs are kept in soft bedding

    Swine vesicular disease (SVD)

  • 47

    DIAGNOSIS • Complement Fixation test • ELISA, PCR • Require passage in tissue culture • Serum neutralization • Agar-gel precipitation

    Swine vesicular disease (SVD)

  • 48

    CONTROL • Cooking pork and pork products • Control pig movement • Disinfection (strong alkalies, iodophores, acids, hypochlorites, iodine)

    Swine vesicular disease (SVD)

  • 49

    An acute, highly infectious disease, characterized by fever a formation of blister

    Swine vesicular disease (SVD)

  • 50

    ETIOLOGY • Calicivirus or Vesivirus from caliciviridae • 13 types of VESV •  > 20 of SMSV • Isolated virus from marine, are capable of producing VES in Swine

    Swine vesicular disease (SVD)

  • 51

    CLINICAL SIGNS • Vesicular on the snout, oral mucosa and feet • Fever, lameness, anorexia, vesicle in mouth and hoof

    Swine vesicular disease (SVD)

  • 52

    DIAGNOSIS • Fever and vesicle w/c break w/in 24-48 hrs • Complement fixation test • Electron microscopy • Serum neutralization • ELISA

    Swine vesicular disease (SVD)

  • 53

    TREATMENT • No specific treatment

    Swine vesicular disease (SVD)

  • 54

    CONTROL • Prevent pig movement • Strict hygiene • No implement vaccination program

    Swine vesicular disease (SVD)

  • 55

    ETIOLOGY • Streptococcus suis

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 56

    TRANSMISSION  • Contact • Oral • Navel • Skin breaks • Knee breaks

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 57

    CLINICAL SIGNS • Subacute ◦ Lameness (3 to 5 days) • Chronic ◦ Joint distension (7-15 days) ◦ Fever, lameness, swelling joints

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 58

    LESIONS •  Subacute – joint capsule are filled with necrotic materials, fibrin and flecks of pus ◦ synovial membrane are hyperaemic • Chronic – necrosis – fibrosis of surroundings muscles pale-green pus o joint-capsule

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 59

    DIAGNOSIS • Bacterial Isolation • Necrotic debris

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 60

    TREATMENT • Long action Penicillin, amoxicillin, penicillin streptomycin, aminoglycoside, and cephalexin • Antibiotic sensitivity of causative agent

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 61

    CONTROL • Colostral immunity/intake • Hygiene and sanitation/ use povidone iodine • Provide non-abrasive floors

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 62

    • It affects mostly growers • Acute • Weanling and growers • Respiratory

    Type 2. Bronchopneumonia

  • 63

    CLINICAL SIGNS • Fever • Tremor • Depression • Incoordination/pneumonia arthritis and abortion

    Type 2. Bronchopneumonia

  • 64

    LESIONS • Red skin patches • Thick joint capsule • Excess cerebrospinal fluid and meningitis • Endocarditis

    Type 2. Bronchopneumonia

  • 65

    DIAGNOSIS • Bacterial isolation

    Type 2. Bronchopneumonia

  • 66

    TREATMENT • Tetracycline antibiotic • Amoxicillin develop resistance

    Type 2. Bronchopneumonia

  • 67

    CONTROL • Vaccination  • Hygiene and sanitation

    Type 2. Bronchopneumonia

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    問題一覧

  • 1

    * Mainly in growing pigs * common in many areas of the world

    Erysipelas

  • 2

    ETIOLOGY * Erysipelothrix rhusiopathiae * remain in carcass even after processing * carrier in pigs can cause re-infection

    Erysipelas

  • 3

    CLINICAL SIGNS * acute septicemia * fever (40 - 42°C) * walk stiffly

    Erysipelas

  • 4

    CLINICAL SIGNS * lie on sternum * erythema of ears, snout, and abdomen * diamond shaped skin lesion all over the body (lateral and dorsal part)

    Erysipelas

  • 5

    LESIONS * swollen spleen * congested lungs * arthritis

    Erysipelas

  • 6

    DIAGNOSIS * penicillin treatment within 24 hours * diamond shape lesion * staining (spleen/ kidney)

    Erysipelas

  • 7

    DIAGNOSIS * culture (blood agar) (tonsil/lymph nodes) * gram staining * bacterial isolation

    Erysipelas

  • 8

    TREATMENT * simple-acting penicillin

    Erysipelas

  • 9

    CONTROL * vaccination (4 - 6 months) * elimination of carrier * sanitation

    Erysipelas

  • 10

    * highly contagious viral disease of pigs * affects pigs of all ages * high morbidity and mortality

    Hog cholera/ classical swine fever

  • 11

    ETIOLOGY * pestivirus from togaviridae family * host specific * virus replicate in cell culture of pig origin * virus survive in bedding for days to weeks, depending on temp

    Hog cholera/ classical swine fever

  • 12

    ETIOLOGY * temperature remain in frozen pork (<4 yrs), chilled and preserve carcass (3 -6months ) * most common route infection is ingestion and replication occur in tonsil * viremia occurs within 24 hrs

    Hog cholera/ classical swine fever

  • 13

    ETIOLOGY * direct contact (most common mode of transmission) * infected pigs shed virus in body excretion/ secretion * pigs surviving infection have depletion of lymphoid tissue and susceptible to concurrent infection

    Hog cholera/ classical swine fever

  • 14

    CLINICAL SIGNS * incubation period (5-10) or (2 - 20) days * anorexia, lethargy and fever (41c) * multifocal hyperaemia of skin * transient constipation, diarrhea, w/ vomiting

    Hog cholera/ classical swine fever

  • 15

    CLINICAL SIGNS * dyspaea * ataxia, paresis, and convulsion * pigs file up or huddle together

    Hog cholera/ classical swine fever

  • 16

    CLINICAL SIGNS * mortality in young (100%) * pre-terminal cyanosis of skin, especially ventrally base of ear and snout * transplacental infection

    Hog cholera/ classical swine fever

  • 17

    LESIONS * leukopenia * thrombocytopenia * turkey egg appearance of kidney * infarction of margin of spleen

    Hog cholera/ classical swine fever

  • 18

    LESIONS * button ulcers in large intestine * enlarge hemorrhagic lymph node * non-suppurative encephalitis w/ severe vasculitis

    Hog cholera/ classical swine fever

  • 19

    DIAGNOSIS * pneumonia (tonsils lymph node, spleen, kidney, distal ileum * immunofluorescence * immunoperoxidase * neutralization * ELISA

    Hog cholera/ classical swine fever

  • 20

    TREATMENT * hyperimmune serum

    Hog cholera/ classical swine fever

  • 21

    CONTROL * vaccination * slaughter and disposal of carcass * disinfection * waste-food feeding management

    Hog cholera/ classical swine fever

  • 22

    * highly contagious disease with signs and lesion resembling HC, but it was restricted to Africa

    African swine fever

  • 23

    ETIOLOGY * iridovirus, w/ some properties of poxvirus/ asfarviridae

    African swine fever

  • 24

    TRANSMISSION * Ornithodoros spp. (Tick act as vector) Including O. Coriaceus and O. Turicata from USA * Fomites, horizontal

    African swine fever

  • 25

    CLINICAL SIGNS * Ist sign is fever (40.5 - 42°C) * Leukopenia and thrombocytopenia * Anorexia, listlessness, incoordination, and cyanosis

    African swine fever

  • 26

    CLINICAL SIGNS * Vomiting, diarrhea, conjunctivitis * Abortion in pregnant animal * Survivors are usually carriers for life, although virus is not continuously present in the exertion

    African swine fever

  • 27

    LESIONS * Hemorrhage of lymph nodes and kidneys * Splenomegaly * Edematous areas of cyanosis in hairless portion * Pleural, pericardial and peritoneal fluid are excessive * Focal,caseous necrosis and mineralization of lungs

    African swine fever

  • 28

    DIAGNOSIS * hemadsorption * immunofluorescence * immunoperoxidase * ELISA, PCR

    African swine fever

  • 29

    TREATMENT * No treatment or vaccines available

    African swine fever

  • 30

    CONTROL * Control movement of animal * Control vectors * Quarantine and slaughter

    African swine fever

  • 31

    An acute and highly contagious, viral infection of domestic and wild cloven-footed animals

    Food and mouth disease

  • 32

    ETIOLOGY • Enterovirus of the picornaviridae family or Aphthosvirus
Family:  A      south African Territory 1
              O       SAT 2
              C       SAT 3
                       Asia 1 • Horse are resistant

    Food and mouth disease

  • 33

    ETIOLOGY • Rapidly inactivated by increase or decrease pH, sunlight and increase temp. • Lacks liquid containing envelope resistant to ether and chloroform • Most commonly used disinfectants (Na hydroxide, Na carbonate, acetic acid, methylene blue, gentian violet, formalin and dye)

    Food and mouth disease

  • 34

    TRANSMISSION  • Most common transmission is aerosol (50km.) • When man inhale the respiratory aerosol of FMD, virus persist in the respiratory tract for 24hrs • Esophageal fluid may contain the virus, even before and after the lesion appear • Cattle may retain the virus in tonsillar cells for as long as 3yrs after recovery

    Food and mouth disease

  • 35

    TRANSMISSION • Virus is also present in milk, pasteurization does not kill the virus, because they are protected by cell debris and fats. • Source of infection: Al, meat, bone,; garbage food, contaminated vaccine • Pigs tend to excrete more virus than ruminants • The disease is difficult to detect in sheep, but they can readily transmit the virus

    Food and mouth disease

  • 36

    CLINICAL SIGNS • Morbidity and mortality is high in young • Initial signs: dullness, in appetence, fever and shivering • Following by: smacking of lips, drooling, shackling, and kicking of the feet Vesicle formation: nares, buccal cavity, claws, mammary gland

    Food and mouth disease

  • 37

    CLINICAL SIGNS • Pronounced salivation and lameness • Abortion in pregnant, death young • Deformed claw • Mammary and involvement may result to mastitis and permanent impairment of milk production • Prolonged unthriftiness and failure to gain weight in

    Food and mouth disease

  • 38

    LESIONS • Vesicles • In sheep, dental pad is the most common site • Lesion in rumen pillars, myocardium in skeletal muscle • Type C have predilection for heart membrane

    Food and mouth disease

  • 39

    DIAGNOSIS • Complement fixation • Virus neutralization • Agar-gel precipitation • ELISA, PCR • DNA probes, labeled with avidin-biotin (fingerprinting/ PCR) in products form infected animals

    Food and mouth disease

  • 40

    TREATMENT • No specific cure, soft beddings • Antibiotics-to prevent secondary treatment • Wound Antiseptic

    Food and mouth disease

  • 41

    CONTROL • Alleviate sign, avoid feeding waste • Vitamins and minerals • Isolation and quarantine

    Food and mouth disease

  • 42

    CONTROL • Slaughter and disposal of affected animals • Hygiene and sanitation • Vaccination program ◦ Sow: once/twice ◦ Piglets: 5-1 week before farrow ◦ Gilts: 1-2 a year

    Food and mouth disease

  • 43

    • Transient disease of pigs in which vesicular lesions appear in mouth and feet. • Lesion is similar to FMD, but swine do not lose condition and the lesions heal rapidly • Do not cause severe production losses. • Pigs are the natural host, although the virus is present in sheep and cattle.

    Swine vesicular disease (SVD)

  • 44

    ETIOLOGY • Enterovirus of Picornaviridae/ or Vesiculoviridae

    Swine vesicular disease (SVD)

  • 45

    TRANSMISSION  • Direct and indirect contact • Contaminated pork and pork products

    Swine vesicular disease (SVD)

  • 46

    CLINICAL SIGNS • Vesicles in mouth, lips and snout, feet • Lesions are mild or inapparent, especially when pigs are kept in soft bedding

    Swine vesicular disease (SVD)

  • 47

    DIAGNOSIS • Complement Fixation test • ELISA, PCR • Require passage in tissue culture • Serum neutralization • Agar-gel precipitation

    Swine vesicular disease (SVD)

  • 48

    CONTROL • Cooking pork and pork products • Control pig movement • Disinfection (strong alkalies, iodophores, acids, hypochlorites, iodine)

    Swine vesicular disease (SVD)

  • 49

    An acute, highly infectious disease, characterized by fever a formation of blister

    Swine vesicular disease (SVD)

  • 50

    ETIOLOGY • Calicivirus or Vesivirus from caliciviridae • 13 types of VESV •  > 20 of SMSV • Isolated virus from marine, are capable of producing VES in Swine

    Swine vesicular disease (SVD)

  • 51

    CLINICAL SIGNS • Vesicular on the snout, oral mucosa and feet • Fever, lameness, anorexia, vesicle in mouth and hoof

    Swine vesicular disease (SVD)

  • 52

    DIAGNOSIS • Fever and vesicle w/c break w/in 24-48 hrs • Complement fixation test • Electron microscopy • Serum neutralization • ELISA

    Swine vesicular disease (SVD)

  • 53

    TREATMENT • No specific treatment

    Swine vesicular disease (SVD)

  • 54

    CONTROL • Prevent pig movement • Strict hygiene • No implement vaccination program

    Swine vesicular disease (SVD)

  • 55

    ETIOLOGY • Streptococcus suis

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 56

    TRANSMISSION  • Contact • Oral • Navel • Skin breaks • Knee breaks

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 57

    CLINICAL SIGNS • Subacute ◦ Lameness (3 to 5 days) • Chronic ◦ Joint distension (7-15 days) ◦ Fever, lameness, swelling joints

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 58

    LESIONS •  Subacute – joint capsule are filled with necrotic materials, fibrin and flecks of pus ◦ synovial membrane are hyperaemic • Chronic – necrosis – fibrosis of surroundings muscles pale-green pus o joint-capsule

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 59

    DIAGNOSIS • Bacterial Isolation • Necrotic debris

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 60

    TREATMENT • Long action Penicillin, amoxicillin, penicillin streptomycin, aminoglycoside, and cephalexin • Antibiotic sensitivity of causative agent

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 61

    CONTROL • Colostral immunity/intake • Hygiene and sanitation/ use povidone iodine • Provide non-abrasive floors

    Type 1. Joint-ill (neonatal) septic Polyarthritis

  • 62

    • It affects mostly growers • Acute • Weanling and growers • Respiratory

    Type 2. Bronchopneumonia

  • 63

    CLINICAL SIGNS • Fever • Tremor • Depression • Incoordination/pneumonia arthritis and abortion

    Type 2. Bronchopneumonia

  • 64

    LESIONS • Red skin patches • Thick joint capsule • Excess cerebrospinal fluid and meningitis • Endocarditis

    Type 2. Bronchopneumonia

  • 65

    DIAGNOSIS • Bacterial isolation

    Type 2. Bronchopneumonia

  • 66

    TREATMENT • Tetracycline antibiotic • Amoxicillin develop resistance

    Type 2. Bronchopneumonia

  • 67

    CONTROL • Vaccination  • Hygiene and sanitation

    Type 2. Bronchopneumonia