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Pathogenetic observations on pleural effusion disease in rabbits
Abstract:
A pathogenetic study of pleural effusion disease (PED) in rabbits was made, using the virulent PED agent or virus (PEDV) and an avirulent derivate of this isolate. Independent of infective dose within the range examined, the virulent isolate caused fatal clinical disease, whereas the avirulent isolate caused subclinical infection. The two isolates differed in rapidity of initial spread of infection and in the maximum virus titres in serum, but they both resulted in a similar low level persisting viraemia. Circulating virulent virus gradually became avirulent during the viraemia. Avirulent infection induced protective immunity to virulent challenge during the first week after primary infection, but full clinical protection was not established until after the fourth week. The findings, corrobated with other closely comparable observations, suggest that the emergence of PED as an intercurrent mortality problem during rabbit passage of pathogenic Treponema pallidum is the result of a specific selective pressure on a benign passenger virus. The expression of virulence of PEDV appears to be dependent on length of interval between passages.
Insights
A study on rabbit pleural effusion disease (PED) found that virulent PED virus (PEDV) caused fatal illness, while avirulent strains caused mild infections. Virulent virus became less potent over time, and immunity developed gradually.
Area of Science:
- Veterinary Virology
- Pathogenesis Research
- Rabbit Disease Models
Background:
- Pleural effusion disease (PED) is a significant concern in rabbit populations.
- The etiological agent, PED virus (PEDV), has both virulent and avirulent forms.
- Understanding PEDV pathogenesis is crucial for disease management.
Purpose of the Study:
- To investigate the pathogenetic differences between virulent and avirulent PEDV isolates in rabbits.
- To elucidate the mechanisms of virulence and immune response to PEDV infection.
- To explore the potential role of selective pressure in PEDV virulence.
Main Methods:
- Infection of rabbits with virulent and avirulent PEDV isolates.
- Monitoring of clinical signs, virus titration in serum, and viraemia levels.
- Assessment of immune protection following virulent challenge.
Main Results:
- Virulent PEDV caused fatal disease, while avirulent PEDV resulted in subclinical infection, irrespective of dose.
- Virulent virus gradually lost virulence during viraemia.
- Protective immunity developed progressively, with full protection achieved by week four.
Conclusions:
- PEDV virulence is influenced by factors such as the interval between rabbit passages.
- Benign passenger viruses can emerge as significant pathogens under specific selective pressures.
- PEDV pathogenesis involves a dynamic interplay between viral virulence and host immunity.
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Clinical Manifestations:

