The pathology of industrially-bred broilers is similar in all countries and regions, due to the uniform base provided by genetics, facilities and food supplied to them. To this base are added the various organisms that become pathogens due to the microbial load caused by the birds’ density and the unique avian anatomy and physiology.
The use of coccidiostatics, the massive application of vaccines and shortening of the brooding period have reduced the mortality that was common in the 50’s and 60’s.
From 70’s to the present, the economic factors resulting from the increased production costs and the fall in market prices due to the internationalisation of trade are acquiring increasing importance.
Consequently, it is necessary to locate that low-mortality but high morbidity conditions that have a considerable influence on productivity and economics.
Basically there are four main processes:
1. Baseline weight and microbiology of the 1-day chick
2. Presence of mycotoxins, Clostridium and fat in feed.
3. Chronic respiratory disease.
4. Sinusitis-tracheitis-tendinitis syndrome
1. Baseline weight and microbiology of the 1-day chick
Depending on their strain, the chick weighs 35-45 g upon arrival at the farm. It is considered that between 32 and 35 gr, the chick has little vitality and low growth capacity. It is advisable to reject their use. Between 35 and 38 gr, the chick has reduced growth capacity.
The statistical results indicate that each gr less of chick produces 25-35 grs less of meat with the same days of final age of brooding.
The initial weight of 38 gr is the turning point so that any additional gr does not cause any significant increase in the final weight. Maximum 4 to 7 grs per gr of chick.
It is possible that chick has lost weight in hatchery or during transportation. In this case, the underweight would not be caused by maternal or genetic reasons and, therefore, it is possible to recover the weight by pharmacological means. It has become necessary to specifically study avian physiology as a basis for the development of avian rehydrating agents.
These would be given upon the chick’s arrival. By this means, the normal weight is recovered and the growth process –which, obviously, had been locked- is started until the original is obtained. Together with the weight, the chick’s microbiological status should be taken into account. Although it is true that it is attempted to ensure high hygiene level in breeder mothers and hatcheries, it is necessary, as an unconditional check, to monitor the chick’s immune status and vitellus microbiology.
In our quarterly information bulletins, we provide data on the results of these controls. A particularly common finding is the presence of maternal antibodies against mycoplasma and the isolation of several enterobacteria. The study of the evolution of antimycoplasma antibodies and antibiograms against enterobacteria, enable us to determine which drug treatment should be used in the chicks. By this means, we prevent deaths during the first days and the introduction of the mycoplasmal base of the future respiratory disease.
2. Mycotoxins, Clostridium and fat in feed
The economic cost of feed is the largest item in broiler production. Therefore, any change in its quality affects the final yield of the brooding.
The mycotoxins traditionally causing disease (aflatoxins) have lost ground to the new necrotising toxins (trichothecenes) produced by Fusarium. Their presence in recently harvested cereals guarantees contamination of food without requiring the influence of storage and transportation factors, considered determinant until today.
The trichothecenes affect locally the digestive mucosa, causing necrosis and desquamation, and, as a result, loss of ability to digest and absorb food. As it is difficult to avoid their presence, in most cases it is necessary to resort to detoxification using ammonia or aluminium silicates.
Contamination by Clostridium has little quantitative importance but excess protein or an excessive difference between total and digestible protein makesit potentially dangerous. The germ survives the granulation process and proliferates in the intestine thanks to the excess of protein. Although the germ lives in the lesions of duodenal mucosa, it has a general toxic effect that finally appears as muscular flaccidity of the neck. The regular use of organic acids added to the food is effective in controlling Clostridium in the intestine.
Finally another factor that affects nutritional yield is the food’s fat content. Large quantities of fat are used to increase fat deposits and gain weight. On other occasions, people resort to using large quantities of fat to make up for the energy shortfall caused by the use of byproducts or poor quality cereals.
In the latter case, the quality of this fat is poor as the aim is to produce cheap food.
3. Chronic respiratory disease
The disease entity has kept its etiologic, pathogenic and symptomatic structure. It has a mycoplasmal base complicated with enterobacteria. Our quarterly information bulletins provide the statistical results of the isolates and susceptibilities to antibiotics.
Our research aimed at selecting the earliest diagnostic methods has provided the ability to isolate causal germs by sampling when the chicken is 21 days old.
This is possible thanks to the idiosyncrasy of the chicken’s anatomy and physiology in that it has no nodular lymphatic system and has a high physiological temperature (41-42ºC). Therefore, the germs readily produce septicaemia but this of a larvate nature due to the high temperature.
This disease process normally appears after 30-35 years. It is possible to prevent it by administering chemotherapeutic agents on the basis of the analytic results obtained from the samples taken on day 21.
4. Sinusitis-Tracheitis-Tendinitis syndrome
The first signs of this syndrome may date from the end of the 70’s although it was in 1982 when they became important in broiler pathology.
Basically, this is a primoinfection of the infraorbital sinuses which appears as petechiae. It may affect the first segment of the trachea, which also shows petechiae.
The cause of the infection is bacterial. There is no single bacterial species but those that have been isolated share in common the fact that they produce SH2: Alcaligenes, Citrobacter, Proteus, Salmonella and E.Coli.
The disease progresses with periorbital inflammation (swollen head) and subcutaneous gravitational descent. As a result of the latter process, pus is found along the tendons and muscle masses of the cranial iliotrochanteric muscle (affecting the coxofemoral joint) and the perforated flexor muscles (affecting the knee and heel joints). This tendinitis is accompanied by fever and limping in chickens aged 40-45 days.
Our research has linked the initial sinusitis-tracheitis conditions with the subsequent tendinitis and enables the causative agent to be identified at the age of 21 days. Our quarterly information bulletins provide the statistical results of the isolates and susceptibilities to antibiotics.
• The classic pathology has evolved as a result of the influence of genetics, facilities, food and shortening of the brooding periods.
• Any pathological, nutritional, treatment or immunological programme study should be aimed at improving the efficiency of brooding and, therefore, the possibility of major enzootics must be ruled out beforehand.
• Within the perfect gauging of the brooding process, the importance of the chick’s baseline weight has increased due to its effect on meat production.
• High morbidity conditions have become important due to their economic effects: necrotising mycotoxins, Clostridium excess or poor quality fat in feed, chronic respiratory disease and sinusitis-tracheitis-tendinitis syndrome.
• Analytic techniques based on the anatomy of the lymphatic system, physiological temperature, sampling systems and culture mediums have been developed. They enable the organisms causing the chronic respiratory disease or the sinusitis-tracheitis-tendinitis syndrome to be isolated enough days beforehand to establish preventive chemotherapeutic treatments.