Principal diseases in industrial poultry. Part 1 TO 4.

PRINCIPAL DISEASES IN INDUSTRIAL POULTRY. PART 1.
Introduction:
The diseases in broilers and layers, from industrial breeding, are similar in all countries and regions due to the common base provided by genetics, equipments and feed they eat. Some microorganisms join this base which turn to pathogens because of the special birds anatomy and physiology, as well as the microbiane load produced by birds density and the pathogeny increase of these microorganisms, aggravated because of the many passes between birds.
The use of additives in food, the application of vaccines and the shortening of breeding period have reduced mortality produced in the 60s and 70s. Thus, nowadays it is being necessary to find those processes with low mortality, but with high morbidity, which influence on productivity and economics of poultry farms even to make unviable the farm, due to the increase of production costs, joined with the reduction of market prices because of trade internationalization.
Essentially, there are 5 main processes:
1.Initial body weight, vitellus relative weight and microbiology of 1 day chick.
2.Presence of mycotoxins and Clostridium in feed.
3.Digestive mycosis.
4.Bad quality of fats in feed.
5.Chronic respiratory disease.
6. Sinusitis-tracheitis-tendinitis-dermatitis.
Conclusions.
* Classic pathology has evolved according to the influence of genetics, equipments, feeding and shortness of breeding periods.
* Every pathologic study, nutritional and immunotherapeutical has to be focused to improve efficiency of breeding, and so the possibility of great epizooties must be previously removed.
* In the perfect measuring of the breeding process it has been improved the importance of initial weight and relative weight of vitellus in 1 day old chicks because of their incidence in the final meat production.
* They have acquired importance, because of their economic incidence, some processes with high morbidity: necrotizing mycotoxins, Clostridium, excess and bad quality of fats in feed, chronic respiratory disease and sinusitis-tracheitis-tendinitis-dermatitis syndrome.
* Analysis methods have been developed based on the anatomy of lymphatic system, physiological temperature, sampling systems and culture mediums. They allow to isolate microorganisms which cause chronic respiratory disease and sinusitis-tracheitis-tendinitis-dermatitis syndrome with almost enough days to previously stablish preventive chemotherapic treatments.
1.Initial Body Weight, vitellus relative weight and microbiology of 1 day chick.
According to different lineages, chicks weigh from 35 to 45 g when they arrive in the farm. It is considered that chick has poor vitality and low development capability between 32 and 35 g. It is recommended to refuse using it. Between 35 and 38 g chick has less growth capability. Statistical results show that each gram less of chick will produce 25-35 g less of meat with same days of age at the end of breeding.
The initial weight of 38 g is the inflexion point, and so each more gram does not produce an important increase of final weight; maximum of 4 to 7 g per each chick. It is possible that the chick had lost weight in the hatchery or during transport. In this case, the lack of weight wouldn’t have a genetic or maternal origin and, thus, it is possible to restore weight by nutritional ways.
It has been necessary the specific study of birds physiology as a base to develop poultry rehydratants. They must be administrated at the moment of chicks arrival; this way normal weight is restored and growing process is to begin, which had been naturally stopped until initial weight is reached.
At the same time as the weight, microbiological status of chick has to be taken into account. Although it is well known that breeders and hatcheries are procured to have a good sanitary level, it is necessary, as a checking process, to keep an eye on the immunological status of the chick, its microbiology and the relative weight of vitellus according to body weight.
From this point of view, we can emphazise that weight of vitellus relative to body weight it has to be about 6% beeing normal to reach the 8% (because of managing in hatchery) but when the percentage of vitellus reaches the 8% a loss in growing capability takes place from 4% to 6% in comparison to healthy birds. When a 10% of vitellus weight is reached, mortality increases up to the 3,5% in the first week and the loss in growing capability is from 8% to 12%, whereas if the 14% of vitellus is reached, mortality in the first week increases up to 6% and the loss in growing capability increases up to 12 and 14%. This way, there’s a linking among vertical infection by SH2 enterobacteria (infectious toxic hepatoenteritis), percentage weight of vitellus, mortality in the first week and the loss in growth when slaughter.
Study of 26905 vitellus in different farms and countries between 1995 and 2005.
PRINCIPAL DISEASES IN INDUSTRIAL POULTRY. PART 2
2.Mycotoxins and Clostridium in feed.
The economic cost in feeding is the main part in broilers meat production. Thus, every change of feed quality goes straight to the final efficiency of breeding.
Mycotoxins traditionally causing disease (aflatoxins), have lost importance in front of necrotizing toxins (tricotecenes), produced by Fusarium. Their existence en cereals of recent harvest guarantees feed contamination with no need to depend on storage or transport influence, even actually considered as key factors.
Tricotecenes affect local gut mucose, they cause necrosis and scalation and, in consequence, the loss in digestive capability and nutrients absorption (up to a 18% in feed conversion rate loss). Just because it is difficult to avoid their presence, the most times it is needed to detoxify using ammoniac or qualified mycotoxin binders.
Clostridium contamination has poor quantitative importance, but excessive protein levels or the difference between total protein and digestive protein makes it potentially dangerous. The germ survives the granulation process and grows in the intestine thanks to the proteic excess. Although germ lives in duodenal mucose injuries, it has a general toxic effect that in the end shows muscular flabbiness in neck region and haematic alterations. The use or organic acids or phenolic extracts from aromatic plants frequently added to feed is useful to control Clostridium in the intestine.
Effect of cimenol ring on Fusarium spp.
Effect of cimenol ring on Penicillium spp.
3.Digestive mycosis.
Colonization of digestive system in birds follows a territorial pattern, depending on physic-chemical conditions of each anatomic region. Thus, yeast they prefer to settle down in the higher part of digestive tract, favoured by alcaline condition of this region and the presence of non-hydrolizated carbohydrate remains.
Acidophil mold (Penicillium, Aspergillus and Fusarium) settle down in the most acid zone, like gizzard muscular inside part.
Some non-septed fungus (Mucor, Rizopus and Absidia) have affinity to lymphatic tissues of the intestine, specially duodenal Peyer patches and ileocecal ganglion. In the end, intestine conditions come back to alcalinity allowing yeast to settle down in its last part of the tract. 0 ppm 100 ppm 200 ppm 400 ppm.
This colonization flora keeps balanced with its guest, with bacteria flora and with microscopic fauna. This balance may break and go into diseases from following situations:
a) stress situations in birds which increase ACTH levels and decrease general defense and specially intestinal ones.
b) quantitative increase of contaminations coming from feed and cereals. Seasonal changes of contaminations also influence.
c) the use of antibiotics that eliminate bacteriane flora compiting with fungus. The most important digestive mycosis we find in birds are candidiasis in beak and crop, ulcers in gizzard and mucormycosis in duodenous or ileocecal valves.
PRINCIPAL DISEASES IN INDUSTRIAL POULTRY. PART 3
4. Bad quality of fats in feed.
Another fact that affects feeding efficiency is the fat contain in it. It is frequent to use big quantites of fat to increase its deposit and to gain weight. In other situations lots of fats are used to supply the lack of energy derived from the use of subproducts or bad quality cereals. In this last case, quality of this fat is bad cause the purpose is to produce cheap feed.
In poultry production, animal, vegetal, mixed fats are used, also soap extracts and fats with high levels in free fatty acids (FFA). We can classify animal fats in meat and visceral grease (fussion point higher than 40ºC and impurity and FFA contain lower than 1,5%); butter from animal adipous tissues; birds fats and fish oil.
Among the most used vegetal oils in poultry we find the ones from soya, palm, colze and sunflower which, from a nutritional point of view they differ in their contain of fatty acids.
In the end, among the extracts of soap and fats rich in FFA, oleins are so used (comestible refined oils with levels in FFA higher than 54%) and those called prison fats which come from kitchens, restaurants and fast-foods.
The diseases caused by the use of fats in feed are not related to fats origin but in relationship between feed intake and digestion capability (lack of lipases and galls); between feed intake and capability of metabolizing of the bird (combustion, intraorganic accumulate) and according to toxic presence because of their composition (FFA, Saturated and Insaturated FA) degradation (peroxides coming from the presence of heavy metals or temperature, FFA by temperature and lypolisis, aldehides and cetones by autooxydation), inclussion (dioxins, PCB, furanes or clorated insecticides of environmental origin and antioxidants of technological origin) or accumulate (antioxidants by the recycling of birds fats).
Environmental rules and increase of nutritional energy costs have rised the use of prison fats and oleines with the consequence of intestinal integrity loss (Insaturated FA, Saturated FA, peroxides), liver integrity (Dioxins, PCB, furanes, insecticides) kidney and lungs epithelia (Free FA, antioxidants) immunitary defficience (dioxins, PCB, furanes) and egg bad quality (dioxins, PCB, furanes).
The use of a well balanced mix of fats, toxin binders-filtrated, decreases the risk of contamination, may be joined with the use of antioxidants from natural origin (phenols coming from aromatic plants extracts) to reduce impact of this cause of productivity loss, poultry disease or transmission to human alimentary chain of toxic with capability to accumulate.
5. Chronic Respiratory Disease.
This pathologic entity has kept its ethiologic, pathogenic and sympthomatic pattern. It is a mycoplasmatic base complicated with enterobacteria.
Our research is focused to select the earliest diagnosis methods, they have bring as a result the capability to isolate causing germs, by sampling on the 18th day of life of the chick.
It is possible thanks to the own idiosyncrasy of the anatomy and physiology of the broiler; as they don’t have a ganglion lymphatic system and mantain high physiologig temperature up to 41-42º C, germs are able to easily produce septicaemia with larved character due to the high temperature.
This pathologic process usually shows itself in 28-30 days of life. It is possible to prevent with the administration of chomotherapy according to analysis results from day 18 samples oe to treate when mortality from day 28 gets over the 1/1000 during 3 consecutive days.
Difficulties of the treatment are because of withdrawal period of pharmacs and so it is suggested the preventive use until day 25 or the use of immunoboosters from natural origin from day 28 of age and on.
In the end, among the extracts of soap and fats rich in FFA, oleins are so used (comestible refined oils with levels in FFA higher than 54%) and those called prison fats which come from kitchens, restaurants and fast-foods.
The diseases caused by the use of fats in feed are not related to fats origin but in relationship between feed intake and digestion capability (lack of lipases and galls); between feed intake and capability of metabolizing of the bird (combustion, intraorganic accumulate) and according to toxic presence because of their composition (FFA, Saturated and Insaturated FA) degradation (peroxides coming from the presence of heavy metals or temperature, FFA by temperature and lypolisis, aldehides and cetones by autooxydation), inclussion (dioxins, PCB, furanes or clorated insecticides of environmental origin and antioxidants of technological origin) or accumulate (antioxidants by the recycling of birds fats).
Environmental rules and increase of nutritional energy costs have rised the use of prison fats and oleines with the consequence of intestinal integrity loss (Insaturated FA, Saturated FA, peroxides), liver integrity (Dioxins, PCB, furanes, insecticides) kidney and lungs epithelia (Free FA, antioxidants) immunitary defficience (dioxins, PCB, furanes) and egg bad quality (dioxins, PCB, furanes).
The use of a well balanced mix of fats, toxin binders-filtrated, decreases the risk of contamination, may be joined with the use of antioxidants from natural origin (phenols coming from aromatic plants extracts) to reduce impact of this cause of productivity loss, poultry disease or transmission to human alimentary chain of toxic with capability to accumulate.
PRINCIPAL DISEASES IN INDUSTRIAL POULTRY. PART 4.
6. Sinusitis-Tracheitis-Tendinitis-Dermatitis Syndrome.
The first descriptions of this syndrome are from latest 70s, although it was in 1982 when they acquire importance in broiler pathology. Essentially it is a primum-infection of the infraorbiraty sinus which is shown with petechias. It may affect first part of trachea, with also petechias.
The origin of infection is bacterial. It does not exist one only bacteria specie, but the isoled ones they commonly produce SH2: Alcaligenes (Achromobacter), E.coli, Citrobacter, Proteus and Salmonella. The only isolated microorganism that does not produce SH2 for the time being is Bordetella avium.
The disease evolves with periorbital imflamation (swollen head caused by reaction to SH2) and gravitational subcutaneous drop of pus. As a consequence of that we may find pus through all tendon and muscular masses of cranial iliotrocantheric muscle (it affects coxofemoral joint) and perforated flexor muscles (it affects knee and heel joints). This tendinitis runs with fever and lameness in birds of 40-45 days of life.
Our research, has linked initial processes of sinusitis-tracheitis with next tendinitis and allows us to identify causing agent at 21 days of life.
When microorganism is also a dermotoxins producer (Alcaligenes group: Achromobacter or Bordetella) bad quality of the skin may appear in farms and specially in slaughterhouses, beacause every mechanic pressure may cause injuries, mainly with geometrical patterns, and loss of epithelium caused by abrasion.