|By goGreen | November 22, 2011|
Common drugs in poultry
- drinking water 1-2 g/ltr (lower concentration give no therapeutic bloodlevel); feed 4 g/kg
- rapid absorption, half-life time 80 minutes (in man 4 hours)
- layers: results in residues in the eggs
- chloramphenicol is rather insoluble (1:400); the palmitate form is to be used, is quite soluble and less bitter
- toxicity: is toxic for the bloodcell producing tissues (bone marrow)
2 Flumequine (Flumic contains 3% flumequine)
- 12 mg/kg bodyweight 20 g/50 kg b.w. Gives a good therapeutic bloodlevel
- good absorption, half-life time 1 hour; good therapeutic blood levels
- indications: E. coli, Salmonella, Pasteurella
- resistance: difficult to develop and is of the more-steps type; no cross-resistance with tetracycline, chloramphenicol, neomycin, sulfas, trimethoprim, furazolidone
- no growth depression
- oral application is not to be advised:
- no absorption
- easily creating multi-resistance
- decreasing colonisation-resistance to Salmonella, increased period of Salmo- nella excretion
- do not combine with synthetic amino-acid cystin/cysteïn
- no (or a very low) absorption, no therapeutic blood levels, no use for systematic diseases
furoxone } in feed 100-200 ppm
in water – 2 ml of a 3% suspension per ltr
- the absorption is influenced by the particle size (crystal size)
- nitrofuranes can be toxic for ducks, turkeys, guinea fowls and quails
All waterbirds receive the half dose. In all birds they decrease leucocyte production. Can lower the hatching percentage.
- growth depression
- the absorption is generally very low
- not soluble in water
- the absorption is better than furoxone but the renal excretion is so rapid that no measurable blood level exists
- the taste is bitter
- only synthetic products can be used orally, the biological products are destroyed in the stomach by HCI
- drinking water 1.1 g/ltr (lower dose gives no therapeutic blood level) e.g. against E. coli; for intestinal action 55 mg/ltr water
- rapid absorption; half-life time 15 minutes (in man 5 hours)
6 Sulfa drugs
- sulfadimidine – Na: 2 g/ltr water 3-2-2 (5 days with an interruption of 3 days); good therapeutic blood levels against E. coli
- Es B 3 (can be used in layers) 30% mixture: 1 g/ltr water; good therapentic blood levels e.g. against E. coli
- toxicity: kidney damage, haemorrhages, blood in faeces; in layers decreased production, eggs with thin shells or no shells
- chlortetracycline (aereomycin)
- oxytetracycline (terramycin)
Drinking water 1 g/ltr gives a therapeutic bloodlevel, e.g. against E. coli; for intestinal action 0.2 g/ltr water. Rapid absorption. Tetracycline gives the highest blood-level
- the watertroughs and tubes have to be clean. Tetracyclines adhere to proteins giving loss of drugs and formation of sediment
- quite soluble with exeption of chlortetracycline
- they are not stable in watery solutions
- they form insoluble complexes with calcium and magnesium, reducing strongly the activity. The same happens with hard water producing a brown sediment plugging the drinking nipples. They accumulate in the bones.
9 Diseases caused by parasites
Coccidiosis is the most common contagious disease in chicken farming. It is caused by several coccidium species which generally affect the intestinal tract of the chickens. The symptoms vary from acute death mainly in young birds, to suboptimal production in all ages (that is to say, production is not what it should be). Coccidiosis is caused by coccidia (singular coccidium) which are protozoa, one-celled parasites. Where there are chickens there are coccidia!
Economic losses can be enormous. Large-scale chicken farming only became possible after the discovery of coccidial drugs. Wire floors (or slatted) were mainly introduced to prevent coccidiosis. Coccidiosis is the main single reason for suboptimal production. Already slight infection of the small intestine in broilers reduces their growth. The preventive use of anti-coccidiosis drugs in broilers and rearing stock represents quite a lot of money.
Coccidiosis is not only a disease of chickens, it occurs in all types of poultry. And, for instance, it can also affect goats kept under intensive husbandry in goat houses. However, chickens have their own specific coccidia types which do not cross-infect other (bird) species.
In the chicken are nine species of coccidia, of which five are important. They are:
1 Eimeria (E.) acervulina very common, often subclinical
2 E.maxima mainly subclinical
3 E.necatrix together with tenella the most pathogenic species
4 E.tenella very common and pathogenic
The coccidium life-cycle is complicated and not exactly the same for the five species. There are three stages in the cycle. The first stage is an enormous, non-sexual multiplication inside the host. After that there is formation and fertilization of so-called oocysts, also inside the host. The oocysts are expelled with the faeces. Under favourable conditions the oocysts then sporulate (they form so-called sporozoites) and become infective for chickens. Only sporulated oocysts cause infection. The period of the cycle inside the host lasts 4-5 days (minimum) and the sporulation time under favourable conditions is 1-2 days. The total of the cycle is therefore 5-7 days, under favourable conditions.
Sporulation time depends on the factors (a) temperature, (b) humidity and (c) oxygen availability:
The optimum temperature is about 28 °C and about 90% of the oocysts will then sporulate in 1-2 days (if moisture conditions are right). Each coccidium species has its own range of temperature for oocyst development, e.g. E.tenella = 12 to 33 °C. Temperatures lower than the minimum temperature conserve the oocysts and there is no development.
Too dry means ‘no development’. Good litter contains 17-35% moisture. Ideal conditions for the development of immunity in the chickens is litter with 30-35% moisture. When it is too dry for sporulation the oocysts slowly die.
There is seldom a lack of oxygen and 10% of air oxygen pressure is already sufficient for sporulation.
Oocysts are difficult to kill. Their resistance is high, especially in a humid and cool environment. In litter oocysts are affected by dryness, high temperatures, ammonia, lack of oxygen and bacterial toxins.
Disinfectants in general have little influence, but ammonia kills in high concentration (5-10%); a combination of lime + ammonium sulphate (fertilizer quality) is effective in this respect.
Direct contact cannot infect the birds.
The chickens ingest the sporulated oocysts by eating and drinking. The infection is carried by contaminated buildings, the farm yard, litter, dust, contaminated feed and water, objects and persons. Also insects can transmit oocysts. Introducing new chickens always means introducing coccidia.
The ‘infection pressure’ of coccidia depends on several factors, indicated as follows:
- whether the birds are kept on litter or on wire (slatted) floors
- stocking density
- hygiene in general
- moisture content of the litter which in itself is related to water spillage, ventilation and air humidity
- during dry, cool conditions unsporulated oocysts can accumulate; by a change to warm, humid weather or by diarrhoea, water leakage and lack of ventilation, these accumulated oocysts sporulate and can cause an acute outbreak of coccidiosis
- the environmental temperature; an increase in humidity and temperature often precedes an outbreak
- the number of sporulated oocysts ingested by the birds; one oocyst can already start the infection of a flock, later on resulting in a disease outbreak; in bacterial infections one bacterium can do nothing and in most bacterial infections 1,000 to 1,000,000 bacteria are needed to cause infection.
The ‘pressure’ also depends on the species: acute disease results after infection with 500,000 sporulated oocysts of E.acervulina but with only 10,000 oocysts of E.tenella.
Within the coccidia species there are differences in pathogenicity. Mixed infections are common but generally one species strongly predominates.
Infections are often farm-linked; coccidiosis is a management disease!
The disease process
Acute outbreaks with rapid deaths are possible. In that case a large number of sporulated oocysts have been taken up (ingested) by the flock, in a short time.
The coccidia cause damage to the tissue forming the outer layer (= epithelium) of mucous membrane in the wall of the intestines of the chickens. The damage is mainly mechanical although there is production of toxins.
Tenella and necatrix cause haemorrhages, inflammation and epithelial loss; tenella in the caeca, necatrix in the small intestine (middle third part). Maxima and brunetti cause epithelial loss and sometimes small haemorrhages; maxima in small intestine, brunetti in colon, cloaca, last part of small intestine and first part of caeca. Acervulina cause epithelial destruction without haemorrhages.
The pathological effects are:
- loss of resistance
- loss of many mucosa cells resulting in poor digestion
- loss of blood serum or blood to the intestinal content (6 anaemia)
- inflammation of intestinal wall
- production of toxins
- secondary infections and absorption of toxins by loss of epithelial cells
The result is that even subclinical infections already have a distinctive negative effect on appetite, condition, production, feed conversion and health. In more severe cases the result is sick animals, rough feathers, diarrhoea by enteritis and mortality.
Immunity and resistance
Immunity is important and is more present in older birds. Because of the establishment of immunity, coccidiosis is mainly a problem in young chickens. The immunity to coccidiosis is so-called species-specific; this means that a chicken can suffer from coccidiosis as often as five times (because there are five E.species).
The development of immunity depends on several factors:
- breed and age of the chickens
- the overall resistance of the flock
- the species of coccidium; the immunogenic property of the species decreases in the following order: maxima > brunetti > acervulina > tenella > necatrix;
as illustration: a mild infection of maxima gives good immunity but necatrix requires several reinfections to obtain good immunity
- drugs can interfere with the development of immunity depending on where and how the drug acts in the life-cycle of the coccidium
Older birds without immunity are more susceptible than young birds. Outbreaks of coccidiosis in broilers of a certain age cause more growth depression than in young birds. Immunity can stop the cycle of development of a coccidium; with strong immunity there is no development at all. Other infections e.g. Gumboro, worms, management errors, stress, etc., lower the overall resistance of the birds and often initiate an outbreak of coccidiosis.
0ocyst excretion in a flock often lasts only a few weeks because of the development of immunity. Large differences in oocyst production exist between species; it decreases in the following order: acervulina > tenella > brunetti > maxima > necatrix.
In an acute outbreak of disease, especially of necatrix and tenella, severe symptoms can precede the production of oocysts.
9.1.1 A brief discussion of the five Eimeria species affecting chickens
Eimeria acervulina: chronic, subclinical, low mortality
Affects first half of small intestine. The cycle is completely performed in the epithelial cells; here oocysts can often be seen with the naked eye. Lesions are caused mainly by the huge number of oocysts of which more than one can develop in the same cell. Relapses are no exception because of the enormous contamination of the environment with oocysts, and the weak immunity.
Symptoms: in all ages, but often in older broilers and young layers. Many infections are subclinical or chronic (name: chronical coccidiosis). In severe cases there is poor feed conversion, suboptimal growth and production, slightly increased mortality, pale and thin birds.
Organ damage: thickening of the wall of first part of small intestine, flaky turbid content, never haemorrhages. In severe cases white striations (= linear marks) can be seen which are accumulations of oocysts and other stages, in the intestinal wall. In mild cases red mucous membranes.
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