Test 2- Circoviridae

Question 1

2 genuses in Family: Circoviridae

Answer 1

Genus: Circovirus

 Psittacine beak and feather disease virus- we aren’t studying

 Porcine circovirus type-1 (Non-Pathogenic)- not studying

Porcine circovirus type-2 (Post-Weaning Multisystemic Wasting Syndrome [PMWS])

Genus: Gyrovirus

Chicken Infectious Anemia virus

Question 2

Family: Circoviridae

Answer 2

 Small viruses, 17-22nm in diameter.

 Viruses with circular single-stranded DNA genomes.
 Genus Circovirus has a circular, single-stranded ambisense( both positive and negative sense stretches) DNA
 Genus Gyrovirus has a circular, single-stranded negative sense DNA

 Virions are small (20–25 nm), non-enveloped, spherical in outline, with icosahedral symmetry (T=1).

 Chicken infectious anemia virus having 12 trumpet-like structures that are less obvious in the other circoviruses

Question 3

Circroviridae Replication

Answer 3

 Virus replication occur in actively dividing cell.
 Viral DNA replication occurs in the nucleus and requires cellular proteins and other components produced during the S phase of the cell cycle(only in actively dividing cell).
 Virions are very stable, resisting 60°C for 30 minutes and pH 3 to pH 9

Question 4

Answer 4

Post-Weaning Multisystemic Wasting Syndrome (PMWS)

Question 5

Post-Weaning Multisystemic Wasting Syndrome (PMWS)

Etiology

Host

Distribution

Answer 5

Etiology: Caused by Porcine circovirus 2 (PCV2).

1st reported Western Canada in 1991
Host: Pigs. Most common at 4-6 weeks of age or 2-3 weeks post-weaning.

Distribution: Worldwide

Question 6

Transmission of PWMW

Answer 6

 Transmission:
 Virus is wide-spread in most pig populations.
 Fecal-oral transmission appears to be most common method of spread.
 Virus is found in all secretions, such as feces, urine, nasal secretions, saliva, etc.

 Vertical transmission (Transplacental infection) occurs in swine.
 Virus is stable and can survive on fomites for long periods.

Question 7

Post-Weaning Multisystemic Wasting Syndrome (PMWS) Pathogenesis:

Answer 7

 The pathogenesis of PCV2 infection and the major cell types that support PCV2 replication are poorly understood.

 PMWS is characterized by individual to coalescing foci of granulomatous inflammation in lymphoid tissues, lungs, liver, kidney, heart, and intestines, sometimes with prominent “botryoid” (grape-like) intra-cytoplasmic inclusion bodies in virus infected macrophages.

 PCV2 targets mainly cardiomyocytes, hepatocytes, and macrophages during fetal life, and mainly monocytes in early post-natal life.

Question 8

Answer 8

Botryoid inclusion bodies in Macrophages

Question 9

Pathogeneisis of PWMW

Answer 9

Lymphoid depletion and lymphopenia in peripheral blood is a consistent feature in pigs that develop clinical PMWS.

 Loss of B-cells and T-cells. There appears to be no direct effect of PCV2 on lymphocytes and how this lymphopenia is caused is unknown.

 Inhibitory effect on interferon  production by porcine leukocytes.

Question 10

Answer 10

Granulomatous inflammation Langhans giant cells

Question 11

PMWS Transplacental infection:

Answer 11

Transplacental infection: Infection during the first and second trimesters results in fetal death and resorption or aborted fetuses with severe cardiac congestion. Infection during last trimester has minimal effect on fetuses.

Question 12

Answer 12

Fetal Resorption and Abortion (SMEDI)

Question 13

Post-Weaning Multisystemic Wasting Syndrome (PMWS)

 Clinical signs:

Answer 13

 Clinical signs:
 Subclinical infection is most common.  Morbidity rates vary from 10-30%.

 Common clinical signs are Lethargy, Progressive Weight Loss, Cough, Dyspnoea, Slow growth, Lymphadenopathy (Swollen inguinal lymph nodes), Diarrhea, Skin discoloration, Congenital tremors, Less commonly icterus

Question 14

Co-infection with PMWS

Answer 14

Co-infection with Porcine parvovirus (PPV), porcine reproductive and respiratory virus (PRRSV), SIV, Mycoplasma hyopneumoniae (M. hyopneumoniae), and/or a variety of opportunistic bacteria may cause severe disease and more pronounced lesions

Question 15

Answer 15

Normal lung on the right, circovirus-affected lung on the left. The infected lung looks rubbery.

Enlarged mandibular lymph nodes

PMWS

Question 16

Answer 16

Enlarged mandibular lymph nodes

PWMW

Question 17

Answer 17

Pneumonic Lung

PWMW

Question 18

Answer 18

Interstitial Pneumonia

PWMW

A. Lymphohistiocytic infiltrates

B. Immunoperoxidasestain

Question 19

Answer 19

PMWS

Kidney: Multifocal Liver:

Question 20

Answer 20

-Interstitial Pneumonia

Co-infection: Porcine Arterivirus (PRRS)

Question 21

Answer 21

Co-infection: Porcine Arterivirus (PRRS)

Aborted Fetuses

Left: Normal fetus Right: PRRS fetuses

Question 22

Answer 22

Co-Infection: Mycoplasma hyopneumoniae

• Enzooticpneumonia of swine

Chronic bronchopneu- monia

Question 23

Post-Weaning Multisystemic Wasting Syndrome (PMWS)

 Diagnosis:

Answer 23

 Clinical signs

 Samples: Blood, Tonsils, Lymph nodes, spleen, ileum

 Characteristic histopathology

 Serological assays: Most pigs are seropositive, therefore antigen detection is not of much value.

 Detection of PCV-2 nucleic acids by PCR

Question 24

Answer 24

Litter from a sow experimentally infected with PCV2 at the time of insemination. Note the small litter size and the presence of two mummified fetuses.

Post-Weaning Multisystemic Wasting Syndrome (PMWS)

Question 25

Post-Weaning Multisystemic Wasting Syndrome (PMWS) Vaccination

Answer 25

 Chimeric Vaccines: New generation chimeric vaccines have been developed that utilize the non-pathogenic porcine circovirus 1 (PCV-1) as a genetic backbone for expression of the immunogenic capsid protein of PCV-2.

 Inactivated or baculovirus-expressed vaccines: virus-like particles that include the capsid protein of PCV-2 are also available as vaccines.

 Vaccine schedules for piglets are either 1 or 2 doses with the 1st dose at 3 weeks of age, and second dose 3 weeks later.

 Sow vaccination: 2 and 5 weeks antepartum.

Question 26

Porcine Dermatitis and Nephropathy Syndrome (PDNS)

Answer 26

• Associated with PCV2
• Sporadic
• Reported in older piglets

• Findings

Necrotizing skin lesions
Necrotizing vasculitis
Necrotizing and fibrinous glomerulonephritis

Question 27

Answer 27

Porcine Dermatitis and Nephropathy Syndrome

Question 28

Answer 28

Porcine Dermatitis and Nephropathy Syndrome (PDNS)

Question 29

Chicken Infectious Anemia

Etiology and host

Answer 29

Genus: Gyrovirus

Etiology: Chicken Anemia Virus (CAV), member of genus Gyrovirus, family Circoviridae

First isolated in Japan in 1979

Host: Highly contagious disease of young chickens (2-4 weeks of age). Older chicken are more resistant to clinical disease.

Question 30

Answer 30

Chicken Infectious Anemia

Question 31

Answer 31

Chicken Infectious Anemia

Question 32

Transmission: of Chicken Infectious Anemia

Answer 32

 Transmission:
 Virus is shed in feces and feather dander.
 Horizontal transmission is through inhalation or oral exposure.
 Virus is also transmitted vertically through egg.
 Environmentally stable virus, remains in contaminated fomites for long periods

Question 33

Chicken Infectious Anemia

 Pathogenesis:

Answer 33

 The principal sites of CAV replication are hemocytoblasts in the bone marrow, precursor T cells in the cortex of the thymus, and dividing CD4 and CD8 cells in the spleen. Replication in the hemocytoblasts leads to anemia, while replication in the T cells causes immunosuppression. .

 The apoptin protein of CAV virus induce apoptosis and cause destruction of infected lymphocytes.

 Immunosuppression and aplastic anemia. Blood may be watery and clot slowly as a result of thrombocytopenia.

 Birds are vulnerable to secondary bacterial and fungal infections

 Virus replication in oviduct of chicken may be regulated by estrogen, allowing more efficient vertical transmission.

Question 34

Chicken Infectious Anemia

 Clinical Signs and Lesions:

Answer 34

 Chicks are anorectic, lethargic, depressed, reduced body weight gain, and pale.

 Blood may be watery and clot slowly as a result of thrombocytopenia.
 PCV is low (in chicks, anemia is defined as a PCV ≤27).
 Subcutaneous hemorrhages and skeletal hemorrhages, pale muscles.

Question 35

Answer 35

Hemorrhages on the Wing

Chicken Infectious Anemia

Question 36

Answer 36

Subcutaneous Hemorrhage

Chicken Infectious Anemia

Question 37

Answer 37

Top—Normal thymus

Bottom—CAV-induced thymic atrophy

Question 38

Answer 38

Top—Femur with normal dark red bone marrow

Bottom—Femur with pale aplastic bone marrow

Question 39

Chicken Infectious Anemia Signs

Answer 39

• Pale carcass
• Pale bone marrow and watery blood
• Atrophied Bursa

Question 40

Chicken Infectious Anemia

 Diagnosis:

Answer 40

Diagnosis:

• Clinical signs
• Examination of Blood: Low PCV, examination of blood for total erythrocytic count will reveal anemia, thrombocytopenia, blood watery and will clot slowly.
• Necropsy
• Histopathology
• Serology: ELISA, Neutralization test, FAT test
• Virus isolation
• PCR, Real-time PCR

Question 41

Chicken Infectious Anemia

 Vaccination:

Answer 41

Vaccination:

• Immunity to chicken anemia virus is complex.
• The presence of antibodies in breeders greatly reduces
• The aim of vaccination is to protect the progeny from vaccinated breeders from early infections by means of maternally derived antibodies.
• Live vaccines are available for vaccination of antibody-negative breeder flocks before the start of egg production.
• Administration is by injection or by addition to the drinking water depending on the type of vaccine
• Because of the synergism between CAV and other immunosuppressive viruses, such as Marek’s disease virus, control of the latter is also important.