Figure 1 - Summary of possible mechanisms and outcomes of viral and bacterial infections of the respiratory tract.
Damage to the mucociliary apparatus
SIV, PCMV, PRCV, PCV2, PRV, , BORD
Virus Virus Virus OR
bacterium bacterium
Local viral
replication or bacterial growth
Mild transient respiratory disease Clearance of infection
Subclinical
Severe respiratory disease Cough, fever, lethargy,
decreased feed consumption
Clinical PRDC
Morbidity: 30-70%
Mortality: 4-6% and higher
Source: Opriessnig, 2011.
Initial Infection of reapiratory tract
Induce immune suppression
PCV2, PRRSV, PRV
Alter
cytokine responses
MHYO, PRRSV, SIV, PCV2
Affect
macrophage function
MHYO, PRRSV, PCV2
Enhanced local ±systemic viral replication or
bacterial growth
+
Concurrent bacterial or viral infection
bacterium
Virus Virus
Implementation of PCV2 vaccination in PRDC-affected herds substantially lowers the incidence of respiratory disease and pulmonary co-infections. A pig vaccinated against PCV2 from a fattening farm had only half the chance (OR 0.51) of pneumonia being detected at post-mortem than a non-vac- cinated pig from a farrow-to-finish farm (see Table 1). This study demonstrated the benefit of a vaccination pro- gramme against PCV2 as an important tool to reduce the risk of post-mortem pneumonia findings and the severity of pneumonia in pigs at slaughter.
Role of M. hyo in PRDC M. hyo is the primary pathogen of enzootic pneumonia and the most important bacterial primary agent involved in PRDC. M. hyo participates in lung damage by itself through the de- generation of bronchial cilia and over-reaction of the local
immune system in lungs, resulting in a strong inflammatory response. The destruction of cilia leads to the dysfunction of the mucociliary defence system. Loss of the mucociliary ap- paratus and ineffective mucosal clearance also allows in- creased colonisation by secondary bacteria such as P. multoci- da and others. It was also described that the efficiency of phagocytic cells in lungs can be suppressed during M. hyo in- fection. M. hyo diminishes the ability of the respiratory tract to respond to other pathogens and increases the severity and duration of respiratory disease induced by other pathogens. Although M. hyo infects different target cells, PCV2 and M. hyo co-infected pigs show more severe clinical respiratory disease and lung lesions, poorer growth performance, longer PCV2 viraemia and greater amounts of PCV2 antigen in serum, lym- phoid and lung tissues than pigs infected with only one path- ogen. The peribronchial lymphoid hyperplasia induced by
Figure 2 - Confirmation of PCV2 as the cause in submitted cases in ISU-VDL. PVC2 systemic disease (PCV2-SD)
100% 90% 80% 70% 60% 50% 40% 30% 20% 10% 0%
181 326 210 387 43 2016 Source: Pineyro, 2020. 103 2017 Positive 59
Negative 2018
163 2019
100% 90% 80% 70% 60% 50% 40% 30% 20% 10% 0%
119 142 PVC2 respiratory disease (PCV2-RD) 109 227
162
250
175
294
2016
2017
2018 Positive Negative
2019
▶ PIG PROGRESS | Volume 38, No. 4, 2022
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