50. Porcine reproductive and respiratory syndrome.

Question 1

PRRS Nomenclature and history?

Answer 1

PRRS Porcine reproductive and respiratory syndrome

Nomenclature

• PRRS: porcine reproductive and respiratory syndrome
• SIRS: Swine infertility and respiratory syndrome
• PEARS: Porcine epidemic abortus and respiratory syndrome
• Mystery swine disease, Blue-ear disease

History

• 1980s ➝ USA: reproduction losses, post-weaning pneumonia, reduced growth performance, increased mortality
• 1990 ➝ Germany
• 2007 ➝ China: highly pathogenic PRRS

Question 2

Steps of cell infection?

Answer 2

Steps of cell infection

• 1. GP5/M complex binds to cell surface heparin sulfate
• 2. Sialic acid bound to GP5/M binds to sialo adhesin lektin
• 3. Activates clathrin mediated endocytosis(virus enters the cell, it is in endosomes)
• 4. pH drop (+protease and CD163) releases virus into cytoplasm
• 5. Replication starts: blocking of apoptosis, then induction of apoptosis at the end of replication,
• virus is released when the cells fall apart, virus proteins are not present on cellmembrane!

Question 3

Transmission/shedding?

Answer 3

Transmission/shedding

• Saliva, nasal secretion (urine, semen, feces)
• Can cross the placenta, replicates in fetus from the 14th day of fetal life
• But efficient transplacental migration only in the last trimester
• There is no sialoadhesine expression in early embryonic development
• Chronic, persistent infection (tonsils, lymph nodes)

Question 4

Pathogenesis?

Answer 4

Pathogenesis

• Inhalation (or other local, activated macrophages -> lymphoid organs, lungs (other tissues)
• Polyclonal B activation: only 1% of Ig-s are specific to PRRSV
• Alveolar macrophages: 2 weeks regeneration time needed after 2 weeks of destruction
• Viraemia at 12-24 hours pi, titers peak at 7-14 days in blood and lungs
• Apoptosis of (mainly macroph.) infected and bystander cells(GP5)

Question 5

Virus replication?

Answer 5

Virus replication

• In vivo: activated macrophages
• Intravascular macrophages of the respiratory tract and lymphoid organs
• Less efficiently in macrophages of other organs, microglia
• Detected in epithelium, endothelium, fibroblasts, spermatocytes
• In vitro: porcine alveolar macrophage, African green monkey kidney cells, cotton rat lung cells

Question 6

Immunity?

Answer 6

Immunity

• Protective humoral immunity directed to GP5
• IgM from 5-7 days, declines by week 3, IgG from 7-10 days, peaks at week 4
• VN from week 3, remains low
• Maternal antibodies also low only in 1/3 of pigs lasts up to 3 weeks

Question 7

Clinical signs?

Answer 7

Clinical signs

• Various clinical signs
• From asymptomatic to lethal
• Concurrent infections, virulence, immune status, bacterial LPS determine severity
• First phase
• For 2 or more weeks: anorexia (for 1-5 days), lethargy, quick spread, hyperpnea, dyspnea,
• high temperature, cutaneous hyperaemia
• Young: respiratory
• Sows: abort and return to estrus
• Second phase: Continues for 1-4 months: reproductive failure, high pre-weaning mortality
• Sows
• 1st phase
• Abortions, return to estrus, agalactia, incoordination
• Concurrent infections
• Low 1-3 % sow mortality (with pulmonary edema)
• 2nd phase: for up to 4 months, farrowing earlier (between 100-108 days); like SMEDI
• Boars: lack of libido, reduction in semen quality
• Suckling pigs: 2nd phase: high preweaning mortality (up to 60%)

Question 8

Pathology, Histopathology?

Answer 8

Pathology, histopathology

• Periocular edema, interstitial pneumonia, enlarged lymph nodes
• Edema of myo-and endometrium
• Macrophages, lymphocytes, plasma cells filling alveolar septa
• Necrotic macrophages in alveoli
• Lymphocytes around airways and blood vessels
• Enlarged germinal centers of lymph nodes - mild lymphoid necrosis and depletion
• Lymphohistiocytic vasculitis and perivascular myocarditis
• Clumped or absent cilia of upper respiratory tract
• Foetal lesions
• Perirenal and mesenteric
• edema, ascites, hydrothorax
• Arteritisin lungs, heart and kidneys
• Interstitial penumonia

Question 9

Diagnosis, Prevention and control and eradication?

Answer 9

Diagnosis:

• clinical signs, pathology + lab tests

Prevention & control

• General rules, expose gilts, give time
• to seroconversion
• Vaccinations: only limited cross
• protection between strains!
• MLV: protects better, but
• dangerous (reversion)
• Inactivated: very weak
• protection from clinicalsigns
• Eradication
• Possibility of spontaneous
• elimination, but rarely, only in
• closed herds
• Total or partial de-and repopulation, segregated
• early weaning
• Simian Haemorrhagic fever virus ʹ also caused by arteriviridae
• Patas, Verret, Baboon Macaque (acute severe disease with high mortality)
• Epidemic in labs in 60s
• Clinical signs: fever, anorexia, cyanosis, melena, facial edema, cutaneous hemorrhages, Macrophages killed but tissue damage not important
• Similar to EBOLA