Continued from page 2The Host
The host's primary protective factor is resistance, which can originate from natural resistance, age, immunologic or nutritional resistance.
Natural resistance means that the agent may enter the host but not become established. Even if it does not become established, the agent causes no ill effects. Also, the agent may not be able to survive or replicate in the host, or those agents may enter and replicate but not cause disease. The particular vulnerability of penguins to Aspergillus infections most likely originates in part from a lack of natural resistance to that organism.
Age resistance means that a particular agent may infect a young animal and cause disease but be comparatively harmless in the older animals of the same species. The reverse may also occur. The predominance of Polyomavirus infection as a pediatric problem, or Paceco's disease being diagnosed in primarily adults may fall into this resistance category.
Immunologic resistance is usually acquired through maternal egg yolk transfer, previous natural exposure, or immunization. If the agent or its products will be overcome before a foothold can be secured, disease will be confined. Numerous examples of immunological deficiencies would be representative of a breakdown in this particular type of resistance.
Nutritional resistance implies that an animal in good nutritional condition is more resistant to disease than one in poor nutritional condition.. Though this point seems to be just 'common sense', it is very difficult to substantiate scientifically. Variation among the effects of different specific nutrition deficiencies in different species and with different infectious agents. The end result, at present time, is inconclusive, but still remains 'common sense'. It also seems that over nutrition, including the overfeeding of exaggerated intakes of protein, minerals or vitamins is usually not more advantageous for prevention of infectious disease than the required optimum. Nutrition most likely has a very real influence on disease prevalence in aviculture.
The Agent
The ability of the agent to cause disease is influenced by its virulence or tropism. Virulence implies the ability to invade an cause lesions. The destructive agent may cause death of cells by its own presence or by the presence of its secretions, or the destruction may be in large part caused by the reaction of the host to the agent via the host's immune response. Tropism is a characteristic of the agent that may allow it to strike as a preferential site within the host. Many pathogens have preferred sites that they will strike most characteristically within a host, as well as more classic group patterns of behavior in the aviary. These patterns allow for astute, predictive managerial intervention by the avicultural veterinarian. The aggressive, disease causing ability of a 'hot' chlamydial organism is a classic example of a particularly virulent strain that is more capable of causing, disease than other chlamydial organisms. Obviously, not all chlamydial organisms have the same disease producing potential.
Latent infection, or the so-called 'inapparent carrier', is used to describe the situation where an individual harbors and releases a known pathogen to the environment, but has no identifiable clinical evidence of disease. The individual carrier may have an acute attack of a disease or may just disseminate their agent into the environment and potentially expose other susceptible hosts. This pathogen may vary significantly in virulence as well as tropism. Subclinical or latent infection may cause clinical disease in the individual bird only after variations in environmental conditions or immune status of the host. Subclinical or latent infections cause clinical disease in a flock following significant errors in husbandry or environmental management. The most commonly recognized errors in this category are basic violations of the Closed Aviary Concept, which has allowed not only the introduction of pathogens into a collections' environment, but has also allowed for transmission to others within that facility.
Conclusions
From an individual bird as well as a flock perspective, the combination of environmental, host and agent factors should make biological and epidemiological sense. Reduced productivity in the flock originates from a logical combination of these factors, rather than solely from the presence of an identified pathogen.
There are several sequences of events that must occur on a flock basis in order for infectious disease to become an epidemic - scale problem in the aviary:
1. Introduction of agent to the aviary or shedding from within the collection.
2. Communication of the agent to others within the collection.
3. Exposure of others to this agent.
4. Infection of others by the agent.
5. Generation of disease in others.
6. Amplification, or increase in amount of agent in the environment.
7. Communication of increased amounts of the agent to others within the collection.
8. Exposure of others to these increased numbers of agents.
9. Infection of others by these agents.
10. Generation of disease in others.
11. Amplification of agent in the environment, or continued pathogen buildup.
12. Epidemic - scale disease in the aviary.The astute aviculturist and veterinarian can realize that there is much greater potential to stop or prevent infectious disease from spreading within the aviary by seeking to 'blockade' the multiple events of this cycle. Any single approach or step, such as focusing on the pathogen itself, is far from a complete approach to the problem.
By making sure that aviary management incorporates pathogenesis management, rather than a pathogen - hunting approach, the future veterinary needs of aviculture can most correctly and completely be served.
Additional Reading
1. Thompson, RG. General Veterinary Pathology. Toronto, Canada: WB Saunders, 1978.
2. Speer, BL. Avicultural Medical Management: An introduction to basic principles of flock medicine and the closed aviary concept. In: Rosskopf WJ, Woerpel, FW. Pet Avian Medicine, Vol 21, No 6, Philadelphia, PA: WB Saunders, 1991.
Brian L Speer, DVM About Brian L Speer, DVM
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