At what point does the pursuit for identification of pathogens and their subsequent elimination become counterproductive in flock medicine? When is avicultural disease best controlled by minimizing the multiple aspects of pathogenesis rather than simply seeking to eliminate the pathogen?

These are some of the significant questions that are now beginning to emerge in the field of avicultural medicine. The answers to these questions are not easy to come by, however. The purpose of this paper is not to answer these questions specifically, but to forward some of the foundational principles from which veterinarians and aviculturists can develop individualized answers of a more specific nature.

Exotic bird species pose many diagnostic and therapeutic challenges for veterinarians who are providing their medical care. As valuable, endangered, beautiful animals or beloved pets, of course we should diagnose and treat on an individual basis when they develop illness. This task alone is certainly not an easy one. Even more significant challenges begin when we cross from individual bird disease to generalizations about group or flock disease. Sometimes there is no clear demarcation between the individual bird and the flock. Does the E coli isolate from one chick in the nursery warrant group testing or therapy to all of the others?. What are the true flock ramifications of this finding? Does the presence of aspergillosis in one individual in the breeding aviary warrant mass screening or therapy? Does the presence of gram negative bacteria in healthy appearing adults warrant group therapy? Does an increase in dead in shell embryos from one breeding pair warrant pathogen testing or treatment of the hen or both birds?

Most veterinarians currently providing medical care for birds are doing so from a companion animal orientation. This most likely represents the pet oriented training that most have pursued in their veterinary education or in their clinical practices. Comparatively few avian veterinarians have a solid base of education or experience in production-oriented medicine (such as herd health management) to apply those towards non domestic bird propagation or maintenance issues.

Most aviculturists perceive veterinarians as primary providers of clinical services only, and few work together to maintain a flock health program designed to meet the production goals of the collection. Veterinarians also view themselves in this role - primary care givers to those individual birds presented for examination and treatment. As such, pet birds as well as breeding birds are most commonly presented to veterinarians for examination and diagnosis based on a perceived need by the client. This need may be based on noted clinical signs of disease, or an individual bird preventative health program, such as annual physical examinations, etc. When diagnoses are made, individual bird prognosis and appropriate therapy is easily applied. Unfortunately, generalizations about the ramifications for the group are easily applied also.

In flock medicine, the aviary, or group, is viewed as the primary patient. Individual bird diagnoses are used as clinical signs of potential flock disease. A higher than expected gram negative bacterial load in a chick in the nursery, in the absence of clinical disease or suboptimal growth parameters, may have no flock implications at all. Aspergillosis, when diagnosed in a breeding adult, poses no communicable disease risk to others, but may represent the presence of predisposing management factors in the aviary. Gram negative bacteria, isolated from the majority of adults in the aviary, may indicate an imbalance in homeostasis or an excessive source of contamination. None of these circumstances on their own necessarily warrant group medication, unless other facts are brought forward about the aviary. The primary patient - THE AVIARY must be properly evaluated in order to most accurately address these questions.

The definition of flock disease is expanded in this article to also include subclinical disease or production inefficiencies, many of which cause no recognizable clinical signs in the individual birds. Causes of disease can be wider in scope than infectious pathogens alone, and these may include over nutrition, undernutrition, toxicities, environmental stressors, etc. Indeed, many forms of subclinical disease in a flock initially do not involve the presence of an infectious agent. Subclinical disease should be viewed as the most important contributor to reduced production in the psittacine aviary.

Diagnoses represent the “what” in medicine. They answer the questions “What is wrong?” and “What disease process does this patient have?”. These diagnoses may be clinical, morphological, or etiological. Suppose an individual bird has diarrhea. Diarrhea is the clinical sign, as might be anorexia (loss of appetite) or dehydration. The clinical signs are occurring for a specific functional reason. This reason is the lesion, which may be functional or morphological. The lesion is the “abnormality” in this bird's tissues that is causing the development of the clinical sign, diarrhea. The lesion may involve morphological changes such as the selective cellular destruction of a particular component of the bird's intestinal tract, or it may simply be a non-infectious factor causing alterations in transit time of the gastrointestinal system. The cause of this bird's diarrhea-producing lesion is the etiology, and might represent the pathogen involved in the clinical and morphological diagnosis of E coli infection, but this agent still only represents the “what” - not the important question “why”.

To put this all together: Clinical signs are explained by the diagnosed condition of the patient. That patient has specific lesions that are responsible for the generation of those clinical signs. One or more specific etiologies may be identified as the cause of the lesions that are producing the clinical signs of the patient.

Pathogenesis is the “how” or “why” of medicine - the step by step progression from the normal state through the abnormal structural or functional state. The sequence of events from the point at which disease began through its entire development is called the pathogenesis. It is absolutely necessary to know the pathogenesis of disease in order to make a rational judgment regarding proper treatment, control and prevention of flock disease.

The theory of pathology involves the description of lesions and their known or assumed pathogenesis and etiology. Based on the description of ”what”, treatment can easily be applied on an individual as well as a group basis; however, this poses risk of medical incompleteness.

Clinical flock medicine involves being able to describe lesions, to recognize the disease process, and explain how it might have occurred. Perhaps most importantly, clinical flock medicine combines theory with action directly or preventatively aimed at the multiple steps required for a flock to progress from a normal state to an abnormal one. This multifaceted action requires practical experience, exposure to clinical cases, and problem-solving ability of the veterinarian as well as the aviculturist. If we understand the causes of things (pathogenesis), we can have a better grasp on how to prevent them than if we only understand what kinds of things (diseases) were caused alone.

A sage colleague of mine of whom I have immense respect once told me that a good doctor will ask what disease the patient has; an excellent doctor will ask what kind of patient has the disease. It is time for more aviculturists as well as veterinarians to strive for this level of excellence.

The main roles of the avicultural veterinarian are to diagnose, treat, prevent and control bird disease to reduce losses or increase productivity in the aviary. The foundational key of these functions is to diagnose. The key to flock prognosis is the ability to recognize lesions in the live or dead animal (diagnose) and to understand their pathogenesis. Through this understanding, rational conclusions and recommendations for treatment, control, and most importantly, prevention are made.

Infectious disease results from the interaction of an infectious agent with the host in a particular environment. The actual cause may exist in the external environment or in a defect in host response, rather than only in the infectious agent alone. The significance of host and environment in the pathogenesis of disease becomes much greater when flock health issues are considered rather than the individual bird.

The factors that are perhaps of greatest importance in initiating or influencing disease are environmental, particularly among animals in which intensive husbandry practices are followed. This circumstances, in most cases, directly applies to aviculture. These factors may change subclinical, or latent infections into acute or chronic disease, or generate circumstances that allow for the actual development of subclinical or clinical disease itself. For example, high dust and ammonia levels in poultry houses increase the incidence of respiratory disease.

Many of these adverse environmental influences are well recognized, but in other circumstances, we still have significantly more to learn about environmental roles in the pathogenesis of disease. The significant problem in flock management is how to prevent disease from occurring. This problem is not one that is new to animal production industries. Antibiotics and vaccines, alone, cannot replace the significant preventative value of good management.

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 disease 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 immunologic 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. 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 ability of the agent to cause disease is influenced by its virulence or tropism. Virulence implies the ability to invade and 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.

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.

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.

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.