Evolution of diseases in the intensive livestock industries : is the poultry industry a viable model?

Abstract

EVOLUTION OF DISEASES IN THE INTENSIVE LIVESTOCK INDUSTRIES. IS THE POULTRY INDUSTRY A VIABLE MODEL? R. J. COULTER SUMMARY The occurrence of disease is a direct manifestation of the failure of a production brn to provide adequate compensation for increased physiological demands on the ,iock in that system. The long term control of disease requires an holistic approach to the 'ecopathology' he biosystem. The development of this approach typically follows an evolutionary cess including a number of phases that are conceptually distinct. This paper contends f the evolutionary process is sufficiently generic that empirical evidence from the lltry industry may used as a model for other intensive industries. INTRODUCTION The concepts advanced in this paper are derived from observations on the incidence .d initiation of disease syndromes as they occur in various animal production systems. le chronological sequence of disease syndromes in intensively reared broiler poultry is aesented as a model for other intensively reared animal species. Central concepts The central concepts of this model are:1. The emergence of new disease syndromes is simply a manifestation of a failure to adequately compensate for changes to the total animal production system. 2. To achieve long term control of disease syndromes in intensive animal systems an holistic approach to the entire biosystem is essential. This is conceptually distinct from traditional veterinary medicine where the primary focus is on the individual animal and the pathogen(s). Inv&ig&ive tools The relevance of the symptoms of clinical disease observed in individual animals is directly related to the degree to which those individuals reflect the herd/flock/system status. Further to this point, clinical and pathological evidence of disease obtained from individual birds/animals should be reconciled with the data from the flock/herd history before making a diagnosis. The flock/herd history is the primary diagnostic tool for the investigation of disease syndromes in intensive animal production systems. As the complexity of the syndrome increases there is a greater need to augment the primary information with additional data (microbiology, gross/histo/clinical pathology), however, the clinical history remains the basic focus. Rhone-Poulenc Animal Nutrition Pty. Ltd, 19-23 Paramount Road, West Footscray, VIC 3012 154 TRADITIONAL PRODUCTION SYSTEMS Environmental agents of change Prior to domestication by man, changes to animal and their associated ecosystem occurred under a self regulating process of biological optimisation that Charles Darwin referred to as natural selection. The pressure of natural selection ensured that following a structural disruption to the ecosystem, only those individuals capable of compensating for the change were able to thrive. This process was all encompassing covering diverse inter-relationships between the animal and its natural food sources, physical environment, internal and external parasites, environmental pathogens and microflora. For all these inter-relationships the rate of the occurrence of the catalysing changes was slow and resulted in selection/adaption at all nodes of the biological matrix. Modified environments and domestication In the most basic form the 'farming' of animals for food may be little more than shepherding, that is, protecting from predators and preventing escapes. Even at this unsophisticated level, farmers were aware that the selection of breeding animals on the basis of particular desirable traits would result in progeny which accentuated these selected traits. Operating with small populations of animals, and in the absence of pharmacological aids, the selective breeding process slowly resulted in the evolution of many regional breeds of livestock. These animals, while purposefully selected for particular morphological traits, also benefited from the processes of natural selection with respect to adaption to the presence of biological stressors in their environment. As was the case under natural selection, the rate and quantitative increment of change to the population means and production systems was low, thus providing the livestock with ample potential for natural adaption. Uncompensated change: earlv intensification V By the middle of the twentieth century the rising cost of land, labour and energy, combined with the emergence of the more aggressive business philosophies of a post-war industrialised world, the result was a generalised drive towards improving economic efficiencies in all fields including livestock production, in essence more output from the same (or fewer) resources. Given that the generic cost equation for animal products consists of a numerator composed of the costs (livestock value, land cost and area, labour, feed, overheads and energy) and a denominator composed of the outputs (weight, number of animals) and the multipliers (dressing yield, batch rate), it is implicitly obvious that to reduce the cost of decrease the costs, or production one has to either:i) .. increase the outputs/multipliers. 11) Equally obvious is that the variables most amenable to rapid and independent manipulation are the land area and the number of animals, ergo: the birth of the intensive animal industry! The chicken meat industry is demonstrably the most intensified of the three major intensive meat industries (chicken, pigs, feedlot cattle). This is illustrated by the comparative industry statistics in the following table. (Table I). 155 Intensive Animal Industry - Selected Statistics (1991-92)* ANIMAL HEALTH IN THE INTENSIVE INDUSTRIES Intensive animal health programmes should all have the following core objectives:1. To achieve complete and continuous freedom from both subclinical and clinical disease. This will require control of disease syndromes involving both primary and secondary pathogens. a) Primarv pathogens must be controlled by either:genetic selection (eg Lymphoid leucosis) i ii eradication (eg Pullorum disease) iii vaccination (eg Avian encephalomyelitis) b) I The control of disease syndromes involving opportunist or secondary1 pathogens must focus principally on the environmental factors In these situations a narrow approach based on chasing pathogens rather than ameliorating the environmental stressors will only achieve disease suppression at best. 2 l To always keep long and short term strategies in their correct perspective the use of antimicrobial therapy should be regarded as an interim measure to effect some control over a dysfunctional production system while the appropriate long term control strategies based on a) or b) are formulated and enacted. Examples of where this approach may be required could include outbreaks of Fowl Cholera (Pasteurella multocida) or Infections Coryza (Haemophilus paragallinarum). Swine dysentery (Serpulina hvodvsenteriae) would be a V typical porcine example. 156 The I>oultrlv industrv At the outset, intensive poultry rearing was approached in a similar fashion to traditional farming, that is, the rearing of 5,000 chickens was regarded in the same way as the rearing of one chicken multiplied 5,000 times. This approach is seriously flawed from a disease pathogenesis perspective- The placement of one chicken in a small barn does little to change the biological environment of the barn, however, the placement of 5,000 chickens in the same barn will effect considerable changes. For example, in the absence of modifications to the ventilation system there will be a considerable increase in the concentration of: airborne bacteria viruses, desquama ted epithelial cells, dust from dried faeces, ammonia gas from the breakdown of uric acid, vaporised moisture. Also oxygen tension could theoretically decrease, CO2 may rise and barn temperature may become elevated. Most of the aforementioned changes are manifestations of a substantial reduction in the dilution effect of the 'natural' air environment of extensive agriculture. In addition to these changes, close inter-bird contact increases the potential for the spread of fragile pathogens such as Mvcoplasma gallisepticum, while the increased w* V a number of birds in close proximity to each other provide a substantially enhanced 'pathogen catchment and excretion system' for agents such as Infectious Laryngotracheitis (ILT) virus. High density rearing also leads to spectacular increases in the availability of the infections stages of the high fecundity internal parasites (particularly coccidia) and facilitates the transmission of ectoparasites. Intuitively one can see the inherent danger in assuming intensive animal husbandry is the same as extensive husbandry with the excess space removed. The new environment of the intensive system clearly has the potential to produce uncompensated change and, therefore, the emergence of an array of new disease syndromes. History tells us that is precisely what has occurred and that typically it was the bacterial agents, both primary and opportunist pathogens that rose to early prominence. THE PHASES OF DISEASE CONTROL IN INTENSIVELY REARED POULTRY The following empirical model divides the disease control history of intensive poultry rearing into a sequence of phases. The accompanying analysis attempts to determine why the sequence flows the way it does by describing the driving forces of each phase. Throughout the analysis attention is repeatedly drawn to the use of antimicrobial therapy as an indicator of the conceptual approach to disease control during each phase. The use of antimicrobials to control disease reflects a 'killing pathogens' approach which is generally more consistent with traditional single animal medicine with treatment directed at primary diseases, then it is for flock/herd medicine and diseases of complex aetiology. In addition, the use of antimicrobials in itself is not a permanent solution, in that it does not provide a long term correction for uncompensated changes to the production system. 157 Antimicrobial therapy may be contrasted with more long lived disease control .nethods including:Environmental engineering 11) Eradication of primary pathogens iii) Vaccination (potentially) The processes of each phase of intensification are sufficiently generic that the model may be used as a predictive tool across other species, principally intensively reared pigs and cattle. A diagrammatic representation of the model is presented in Figure 1. This figure depicts relative changes, in some key indicators, of the evolution and control of diseases in an intensive animal production system. This model uses existing diseases/industry practices/control procedures as practical examples of each stage of the model. This is not done in an attempt to suggest substandard practices in any industries, merely to demonstrate that greater intensification and economies of scale tend to drive the evolution of control to greater efficiency. It is hoped that these processes will provide an insight into the future for the newer industries. Phase 0: Sporadic disease in extensive svstems I * The cycle begins with the production system balanced and 'disease' occurring as single animal infections with a primary pathogen as the case. Common examples are seen today in the extensive dairy industry and could include Staphloccocal mastitis and Bloat. While hygiene management may play a role in these conditions they are not classic communicable diseases and are largely controlled by individual animal therapy. Phase 1: Primarv apathogens aided bv intensification I As greater numbers of animals are brought closer together the potential for larger and more rapidly spreading epizootics increases, as does the potential for the transmission of primary pathogens that are sensitive to inactivation in the environment. A typical example is the poultry disease Infections Coryza caused by the bacterium Haemophilus paragallinarum. First isolated in 1932 by de Blieck (1933) the causal agent is * quite delicate and suffers rapid inactivation outside the host, surviving only 4 hours in tap water at ambient temperature (Page 1962). The main reservoir of infection is the asymptomatic carrier occurring as a result of a previous outbreak. Clinical disease usually follows environmental stress (eg. increased humidity, ammonia and cold stress), the introduction of young susceptible stock or both of these factors. The control of Infections Coryza (IC) as it occurs in 'evolutionary Phase 1' is interest as it highlights the impact of the short to medium term focus on control that is typically seen in newly intensified industries. Eradication of the disease is simply a matter of logistics, that is depopulation and effective quarantine. In Australia, all primary breeders are free of I.C., in addition the disease is not vertically transmitted. Depopulation and basic disinfection followed by restocking with 'clean' stock will successfully remove the disease. Quarantine will keep a site clean. Despite these facts the modern egg laying industry continues to incur losses due to IC primarily because of the entrenched multi-age flock structure encouraged by the legislative supply regulation mechanisms and the carry over systems that still exist. Contrasting this situation is the broiler breeder industry in which the disease has been eradicated by following suitable epizootiological control procedures. Occasional outbreaks do occur, these will be discussed under Phase 3. . 1). . 160 At the same conference Janzen presented a paper (Van Donkersgood, 1990) in which he cited the following reason for treatment failure with respect to Bovine Respiratory Disease I. 2. 3. 4. 5. `Wrong diagnosis Pathology too advanced Insufficient duration of treatment Inadequate dose rate Drug insensitivity (occasional) The combination of the above presentations suggests that, at least in part, the North American feedlot industry is operating in Phase 2. Ironically, by the time a production system reaches Phase 2, many of the primary pathogens of Phase 1 may have been eradication through good epidemiological practise. Further to this, the obvious preclusions to eradicating opportunist pathogens from the normal flora may be used to rationalise the use of prophylactic treatment. Phase 3: The envidnment as a factor in disease control As the financial analyses of intensive animal production become more sophisticated, the full cost of disease (losses, treatment and prevention) become identified in a more formal fashion and invariably the conclusion is drawn that it is more economical to eradicate than live with a disease. The limiting factor is then available technology. Although there is no comparable reference for the poultry industry, Cutler and Gardner (1988) carried out a detailed review of the Australian Pig Industry. This paper identifies the high cost of 'living with' diseases such as Swine Dysentery ($99/saw/year) and colibacillosis ($75~$85/saw/year). Costs expressed per sow actually relate to the entire piggery but are calculated per breeding sow to allow easy interpretation. Financial pressures such as these have encouraged producers to re-assess their philosophies of disease control to include many environmental and husbandry factors as part of the process. Research on this subject is plentiful as exemplified by a recent local paper (Skirrow et al 1991) in which the authors assess the risk factors associated with post- 161 ning diarrhoea in pigs using a French 'Ecopathology' model in which the only disease at listed as risk factor is 'a recent episode of Transmissible Gastroenteritis (TGE)', an tic disease to Australia. All other risk factors relate to the physiological status of the iet and environmental stressors. Not surprisingly the sequelae to this approach tends to be a focus on correcting Dpathological' imbalances, that is, attempting to re-stabilise the complete biosystem. During Phase 3 it is not uncommon for some diseases caused by primary pathogens Bccur. It is also possible that these diseases may be treated using antimicrobial therapy in Phase 1 (eg Fowl, Cholera, Infections Coryza). The essential difference between .ases 1 and 3 is the recognition of the role environmental stressors in the pathogenesis of ;ease. In Phase 3 the rational use of medicants as temporary suppressants to control jizootic spread prior to eradication is regarded as a compromise, rather than the primary cus of the control strategy as it was in earlier Phases. Figure 3 is an expanded version of .gure 2 and depicts the evolution of the control strategy. In the more advanced form (Figure 3) of the model the objective is to remain out of the original (Figure 2) loop, although partial entry for a single pass may occur as the result of an economic or biological compromise. The 'Modified Medicated Early Weaning and Off-Site Production' system described by Conner (1992) is a good example of a rational compromise strategy designed to gain control over internal and external parasites and as many as ten infections disease agents:Mycoplasma hypneumoniae Actinobacillus pleuropneumoniae Haemophilus perasuis Streptococcus suis Treponema (Serpuline) hyodysentariae Pasteurella Mu1 tocida Bordetella broncloseptica Leptospira spp T.G.E. virus Pseudorabies 162 It is important to note that in Phase 3 the perpetual prophylaxis loop has been deleted. This was the primary focus in Phase 2. Phase 4: Highly developed svstems - complex svndromes * w -. This stage is essentially a late - Phase 3, the major difference occurring not in the approach to control, but the type of breakdown. Disease syndromes become increasingly more complex with immunosuppressive viruses playing a major role in de-stabilising the physiological balance of the system. Commonly, long term control strategies involving extremely detailed knowledge of the pathogenesis of the syndrome are required. Runting Stunting Syndrome (RSS) of poultry is an example, as possibly is Porcine Reproductive and Respiratory Syndrome (PRRS). Because of the multifactorial nature of the disease agents involvedand the pathophysiological processes that occur, the control of diseases typified by this phase requires the use of increasingly complex diagnostic aids. The procedures include the traditional histopathology and virology, progressing to immunological diagnostic aids such as the ELISA and Immunohistology through to gene probes and the polymerase chain reaction (PCR) multiplication of nuclear material. In Phase 4 the use of advanced diagnostic tools to identify specific pathogens tends not to be driven by the desire for a narrowly focussed quick-fix treatment programme, but rather to elucidate a complex pathogenesis. This allows for the implementation of a multifactorial control programme commensurate with the complexity of the disease syndrome. . Ultimately, it is hoped that projects of this type will lead to a conquering of sophisticated pathogens such as the coccidia and complex disease entities involving immunosuppressive agents and a multitude of physical and biological stressors. CONCLUSIONS This paper has presented a sequential view of the disease challenges that have arisen in the broiler poultry industry. The industry responses to these challenges have been discussed in an attempt to analyse the reasoning processes that have produced this evolutionary cycle. The author believes that both the environmental trigger factors leading to new disease syndromes and the industry reponses are not species dependent and may, therefore, serve as a useful insight to other intensive livestock industries. REFERENCES CONNOR, J. F.(1992). Modified Medicated Early Weaning and Off-Site Production, pp 97, Proceedings of AAPV Annual Conference, Adelaide, Upjohn. CUTLER, R. and GARDNER, I. (1988). A Blue Print for Pig Health Research, A.P.R.C. DEBLIECK (1933). cited in 'Diseases of Poultry', 7th ed, p 225, editors M.S. Hofstad, B.W. Calnek, C.F. Helmboldt, W.M. Reid and H.W.Jr. Yoder. (Iowa State University Press). JANZEN, E. D. (1990). Management of Disease in Feedlots - General Principles Proceedings No. 137, Post-Graduate Foundation in Veterinary Science, Uni of Sydney. MALDEC, F. and TILLON, JR (1985). cited in Proceedinrrs of the AAPV Conference, pp 99-101, editors S.Z. Skirrow, A.R. Merch and J.R. Buddle . Sydney, Upjohn. SKIRROW, S. Z., MERCY, A.R. and BUDDLE, J.R., (1991). Proceedings of AAPV Conference, pp 99-101, Sydney, Upjohn. VAN DONKERSGOOD, J., (1990) Bovine Respiratoy Diseases Proceeding No. 37 PostGraduate Foundation in Veterinary Science, (University of Sydney, Sydney).