THE POLAND (The Royalty of Poultry)
I have written many articles over the past few years on The Poland the breed I consider to be the Royalty of the poultry world, but to our friends they are referred to affectionately as the feather dusters.
The breed itself I am pleased to say has grown in immensely in popularity, but it is unfortunate that it is now being sold by inexperienced breeders with not enough knowledge or interest on keeping and looking after the welfare of these birds.
The Poland is what we would class as a very high maintenance breed, this in the most part being due to its crowning glory the Crest, this is the main area for concern and I cannot stress enough how important looking after this is. Keeping the eyes clear and clean, washing the crest feathers on a regular basis to avoid the black crest mite is the main issue, the use of ivomec (does not prevent crest mite). Routine checking for mite which is very visible and the use of anti mite spray (Johnson's Cage Bird) or a good louse powder does help as prevention is better than cure.
The breed itself has no other major problems other than the normal ailments and problems we associate with keeping poultry.
Most Poland's today are kept purely for exhibition or just by fanciers for there appearance and beauty, we have a lot of response from people who comment on what good pets they make, they usually have a very good temperament and are easy to handle. They do lay a very good white egg and do so on a pretty regular basis, but they are a non-sitting breed so if you want chicks turn on the incubator.
There is an amazing choice when it comes to colours in this breed, these total 14 basic colours and several non standard colours, these are as follows.
These are the standard colours recognised by the Poultry Club of GB and The Poland Club.
There are then the following colours, which are recognised in Europe but as yet not in the UK.
All these are available in both Large and Bantam and all in the Frizzle Feather Variety (Again the frizzles are quite rare) The main difference in the breed is that the White Crested varieties are all non-Bearded and the self and laced all carry a beard, although there has been a non-bearded self-variety created. The non-bearded carry long wattles as with the bearded they should have no wattles but some do tend to have very small wattles, which although this is not as standard has to be accepted.
White crested black and self black should always be a good solid black with a good green sheen, the White Crested Blue and Self Blue should be a solid blue which is a sort of pigeon blue and really almost lavender.
The cuckoo both white crested and self should be of an even medium shade but the hackles and tail in the cocks tend to be a little pale, it is best to have no solid white or black feathers but this is difficult to achieve and the self cuckoo does have a tendency to have some white feathers in the crest. When exhibiting the White Crested Varieties they must have the colour in front of the crest this applies to all the Black - Blue - Cuckoo, an article in a magazine in February 2000 Fancy Fowl shows a German bred White Crested Black hen with a large crest and no colour in the front this caused concern as to I was approached by a relative newcomer to the show circuit who had prepared his bird as the picture (big mistake) the result was no prize and a wait until the next moult for it to be corrected, so unfortunately the picture sent out the wrong message. The White Crested must carry the colour in the front of the crest and the best way to describe this is it should look like a butterfly stuck on the front.
The laced varieties which are bearded should have a good even lacing with no tipping (lacing just on the end of the feathers) this is normally far better in the hens as again there is fading in the males. The blue/gold and the blue/silver, which are non-standard, are very stunning if they can be found.
Black Crested Whites, these are as I said earlier are the oldest recorded colour, and although a lot of work over the past years has been done to recreate this variety they still need to be improved, but I must add they are very close to there objective, the crests are still to small and there is smuttiness in the white, but luckily there are several breeders in Europe and the US who will keep going until the goal is reached, we are among those breeders and I must admit we seem to be having a reasonable success at this time, but lets not count our chickens.
As to the colour variations there are many countries including ourselves who have spent time creating even more colours but I believe that concentration is needed on the present colours and the standardised types to improve these even more, although most of the birds exhibited properly are very, very good.
When buying birds always check for any eye infections, knock knees, white in feathers (other than the obvious with the white crested), split crests and lob sided crests, this covers most of the faults other than the normal faults you get with all breeds of poultry. I would also like to add that Poland's sold in auction are usually of a poor standard but will make good pets, but if you like good quality stock go to a specialized breeder as with any breed you will breed good from good. One of the most usually neglected faults which is nearly always ignored is the presence of a comb in the front of the crest, we call them horns, these are usually in the very front of the crest and although in my opinion you should cull the affected birds they are accepted by some judges.
DRINKING & FEEDING
Drinkers need to be of the very narrow lipped type, never use open drinkers, again the reason is commonsense, the bird gets the crest wet and vision is impaired, during freezing weather this can be terminal, but under normal circumstances causes unnecessary suffering. The use of Vaseline on the wattles of the non-bearded varieties prevents damage just as with standard breeds. Feeding is the same as with all poultry, but my own preference is to use pellets & wheat, I never use mash because the water and the dust do not mix and can get into the eyes and crust under the crest, the results are obvious and if not spotted in time will cause serious eye infections and blindness.
Poland's are not suitable birds to run with non-crested breeds as they are at an obvious disadvantage and cannot be expected to compete with other breeds that have an unobstructed vision.
Again we have our own preferences which are a nice shed with loads of ventilation (no draught) with run to the outside, which is covered therefore giving fresh air but keeping the birds dry all the time. We have large sheds with internal runs and concrete floors (rodent proof) and the floor is covered with dust free shavings (the dust free for the same reason as described with the food)
THE POLAND CLUB.
There is now a very good breed club in the UK know as The Poland Club and with a membership in excess of 80 is growing steadily, the members come from all walks of life and in general are dedicated people to the breed. There is a regular newsletter; the club show is in November at the Federation Poultry Show. Membership is cheap at £5 for the year single membership and £10 the year for family membership.
It is official that we are the largest breeders of Poland's in Europe and possibly the largest breeder anywhere, I think madness springs to mind but the rewards are tremendous. I am very lucky to have my wife Clare who has the same passion for these birds and I must admit she is like a beauty therapist when it comes to show time, she does all the show preparation which takes hours, but I love the breeding and rearing side so it works well and we are a good team.
We are also joint secretaries and treasurers of the UK Poland Club, and also one of the founder members of the International Poland Club a club that brings breeders and fanciers together from all over the globe. We will be pleased to help any genuine breeders to sort out problems etc with this breed; it only takes a phone call or e-mail.
Terry & Clare Beebe.
Breeders of fowls the world over has reported a condition that seems peculiar to crested breeds, particularly birds with heavier crests than others. The onset of the condition is described as a wobble in the head which can increase in severity to the point where the head twists right around and that bird in some cases looses its balance and mobility altogether. This is commonly called ‘cerebral hernia’. The Victorian Institute of Animal Science has conducted post mortems on breeds such a polish and silkies over the years and confirms the existence of a mutation connected with the gene for a dominant crest. A mutation is a genetic copying error or mistake that occurs when the DNA from the parent bird’s meet and divide incorrectly in what is known as meiosis. The skull of a crested fowl is unique. Unlike other breeds, it is dome like in structure and in heavily crested chicks; there is a tendency for the skull to be underdeveloped. Like the fontanels of a human baby, the skull of crested fowls has openings. These are supposed to fuse in the normal way and usually do. However, this does not always occur and the result is exposure of the cerebellum (brain). Subsequently, a bird’s brain space remains venerable to the environment. Certain bloodlines seem more predisposed to this condition, whereas other are seldom affected. Unsurprisingly, it is rare in adult birds, as their skulls have had the time to grow and fuse over. It is more prevalent with young birds between 1 and 4 months of age.
Conditions observed and possible causal factors.
There are a variety of causal factors and distinct conditions each of which can display the symptoms described above.
Cerebral trauma or brain damage can actually happen to any young bird of any breed. It involves direct impact (ie a peck on the head) resulting in brain damage. Crested breeds could fare worse in such a situation. The brain is forced by the pressure of the impact and can ‘herniated’, swell or ooze out through the cranium.
Cerebral oedema or swelling of the cerebellum is an internal reaction to the environment and can occur in at least two ways. Firstly, as a response to hot weather and change, an excess of fluid builds up as in the brain cavity, placing pressure on the centers of the brain, which govern mobility. The bird experiences vertigo (spinning sensation) and consequently loses its sense of balance. If left untreated this can lead to permanent brain damage. On occasion birds may recover and live with a permanent, but slight head wobble, continuing to eat and live with certain normality.
Secondly, same symptoms can occur with a respiratory condition. The immune system can respond to the invasion of bacteria or a virus by producing more fluid with similar results.
A) Prevention is better than cure. By ensuring that your birds are vaccinated and well managed the breeder can keep disease challenge to a minimum and avoid the third scenario. Identifying bloodlines that have this propensity and breeding away will help avoid heartbreak. Controlling temperature in extremes of weather can prevent this condition to some degree and ensuring that no foreign objects pose a threat to the birds’ welfare (ie checking perches, feeders etc are secure are all good preventative measures). B) Cure - there is no guaranteed cure if you have a bird with the condition. However, a vet friend administered an intramuscularly injection of cortisone with positive results. In this case the drug reduced the inflammation/swelling and the bird recovered. Other breeders have found that administering broad -based antibiotics have worked. The problem is that without a postmortem, you cant always isolates the cause. By then it is probably too late anyway. At the earliest detection of the condition I would use both cortisone and Baytril (antibiotic) to cover my bases. The longer a bird is left untreated, the harder it is to achieve recovery. Fortunately, the problem is not common. Edan Montgomery claimed that out of over 600 birds bred last year, about 5-6 developed the condition. Sadly, it is usually the heavily crested ‘potential champs’. By hatching in large numbers, line breeding rather than close in breeding and practicing good management techniques, this condition is largely avoidable. Every breed has its hiccups. For crested breeds, this is one of them. On a positive note, the rewards of producing a champion far outweigh the occasional disappointment linked with this condition. It also goes to show the largely detrimental nature of mutations. They are rarely if ever an advantage!
By Peter Jones
THE SIZE AND STRUCTURE OF THE CREST OF POLANDS:
VIEW ON VISION
Polands have a large crest. This can hinder the vision of these birds, which should be prevented. In the last decades the size of the crests has been bred larger and larger by the fanciers, encouraged by the prizes which could be won at exhibitions. Even more so the structure of the crests became more loose, which went to the detriment of visibility of the Polands. Not only fanciers became more critical but also the public discussion on well-being of animals made some Poland Clubs in Europe, notably in Germany, Switzerland and the Netherlands, aware of the necessity to agree on the maximum size of the crests of Polands. Within the Dutch Poland Club a lengthy discussion took place on the size and structure of the crest and the required amendments to the Standard description of Polands. In 1999 this led to a booklet of the Dutch Poland Club "View on Vision". In 2000 the Standard has been changed in line with the proposals of the Dutch Poland Club. Below a small summary of this booklet with illustrative pictures of poultry judge and Poland breeder Henk Timmer.
The discussion focusses on three topics:
the size and the structure of the crest in relation to the sight of the Polands
The size and structure of the crest
The size should be in harmony with the body of the bird. Also it must be densely feathered with good visisbility for the bird. This means that Polands must be able to look straight ahead and at both sides, to be judged at eye level.
Pictures 1 to 4 illustrate the relationship between skull and crest. If the skull is too wide and too low the crest falls for the eyes, and can even cause inflammation on the eyes. Ideally the skull is high, with the form of a cylinder. In general one can say, the higher the better. The basis of the skull should be as broad as the top. Breeders should exclude Polands with a small basis of the skull.
Breeders of Polands are advised to breed only with Polands with the right skull. Furthermore the feathering of the skull should be dense. Illustration 6 shows a good skull and 7 a poor skull.
Preparing Polands for shows
In the Netherlands it used to be common practise to cut the coloured feathers of the crests of Polands (see picture 8). In that way the crests seemed fully white. However, the coloured feathers (mostly black) are important for the sight of the birds. These coloured feathers are socalled supporting feathers; they support the other feathers to keep the crest upright. The same applies to the coloured feathers above the eyes. So, for these reasons the Dutch breeders changed the rules, i.e. the coloured feathers should stay, but may be cut modestly.
How should it be conditioned?
When cutting the coloured feathers we work from the back of the crest to the front. Coloured feathers in the middle of the crest can be cut close to the skin. In the front of the crest the feathers can also be cut, apart from the last rows. In that way a nicely cut crest will appear.
See illustrations 8 to 10.
As you may understand implementing changes takes time. This applies to the way the crests are cut for shows, but certainly for breeding Polands with the right skull and crests to get the necessary natural sight of our Polands. The Dutch Poland Club hopes to achieve this in 5 years time. The last things we want is birds which can not see. After all we all want the best for our Polands!
By Luuk Hans
We have searched the archives yet again and come up with a selection of articles from a 1959 laboratory series, although this is more recent than I would prefer I think they are very informative and interesting. No doubt like ourselves you will have come up against this disease which is devastating if not treated and handled properly.
Infectious bronchitis is an acute, highly contagious, respiratory disease of poultry caused by a virus, having the most serious effect in young chicks, although serious losses in egg production may occur in an outbreak in adult stock. Following its discovery in the US in 1931, it was soon found to be prevalent in many parts of the country, particularly in those areas where birds are reared intensively. It ranks as a major cause of financial loss and is classed as serious as fowl pest. It is now reported to exist in most parts of the world. Infectious bronchitis was first met in the UK in 1948 and in somewhat fortuitous circumstances. It was during a Newcastle decease investigation that a worker engaged in tracing fowls sold by dealers observed that some of them developed a respiratory disorder of a much milder type than the virulent form common to Newcastle infections then giving trouble.
INCIDENCE NOT CLEAR.
Further careful laboratory investigations revealed that the disease from which the birds were suffering was not Newcastle but infectious bronchitis.
The exact incidence in Britain is unknown, but experts are of the opinion that it is more common than is generally thought. There are two reasons for this point of view.
The virus responsible remains alive for several months at refrigeration temperatures, but usually dies within 14 days at the ordinary atmospheric temperatures experienced in this country. It is also killed by the commonly used disinfectants at their recommended strengths. American research workers have found that ultra violet lamps will not destroy airborne infectious bronchitis virus and have concluded that under field conditions of air sterilization would have little or no effect as a control measure. There are several ways in which I.B. may gain entry to a farm, chief cause is the import of fresh stock, which may have suffered from the disease previously and as a consequence are now carriers. It is generally believed that birds may remain such carriers for longer periods of time than is the case with Newcastle disease. Some research workers, for example were able to isolate infectious bronchitis virus from the nasal discharge of a bird which had contracted the infection for as long as 8 weeks. Other methods of spread are similar to those described for Newcastle disease which include contaminated humans, crates and other equipment.
SPREADS WITHOUT CONTACT.
The disease has been know to spread from flock to flock in the same neighbourhood without they're being any type of contact. This makes it apparent that the virus is in fact airborne. Once infection has been introduced it will spread regardless of all practical measures taken to prevent it. There is no evidence to indicate that infection will be passed on to the offspring via an infected egg. In young chicks the onset of I.B. is sudden. The first symtoms9 noted being coughing, sneezing and noisy breathing. As it develops, the chicks huddle together and become lethargic; they lose their appetite and diarrhoea may occur. In some outbreaks a copious discharge of mucus issues from the nostrils, but this symptom is by no means constant. Deaths may commence within a few days, while the death rate among young chicks is usually between 40% - 90%, although mortality may vary considerably from flock to flock, this being influenced by the standard of general health and cleanliness, the older the chick the better its chances of survival.
Main symptoms in older chicks and growers are some disturbance in breathing, general inactivity and loss of appetite. Some mortality may occur, but not usually in birds over six weeks of age. In any case, retarded growth will definitely occur, and this, although of minor importance only in chicks destined for egg production, is regarded as a matter of great economical concern in the broiler industry. One curious aspect is that an unexpectedly high proportion of birds suffering from I.B. when chicks do not come into egg production when adult because of abnormalities of their oviducts. The older the chick when it contracts the infection the greater the chances of this abnormality occurring.
On the other hand, if the chicks or embryos exhibit the characteristics signs of I.B. it can be assumed that the serum samples did not contain any antibodies to I.B. virus, and, consequently, that the chickens from which they have been obtained were suffering from some other sort of respiratory disease. Owing to the highly infectious nature, there is little that can be done to modify the course of I.B. once it appears in the flock. Despite all efforts to arrest its course, it will usually spread until all the birds on the premises have contracted it.
Certain palliative measures, such as increasing brooder temperature and feeding diets containing high levels of antibiotics, may have some effect in moderating the severity of the disease and combating the secondary infection, but anti bio tics have no effect on I. B. virus itself. Ultimate policy to be adopted must depend on the extent of the disease in the neighbourhood in which the outbreak occurs. In areas where it is not prevalent the best policy is one of eradication. This implies complete de-population of infected flocks, when convenient followed by cleaning and disinfected and then leaving the houses empty of poultry for a suitable period of time before re stocking. In heavily congested poultry areas where the disease is widespread, eradication methods applied to any particular premises usually fail because of the ease of re infection occurs from without. In such areas, as illustrated by many parts of the US, the best approach is live vaccines. Chicks are usually vaccinated when two to three days old by spraying live vaccines into the atmosphere around them.
These vaccines contain the actual virus that causes the disease modified by laboratory methods, so that the virulence is reduced. Even so, it is still too dangerous to use in younger chicks, so that they go through a susceptible period without any protection. Some American poultry men, particularly those engaged in broiler production, have overcome this disadvantage by purchasing their chicks from flocks which have suffered from, or been immunised against, I.B. Hens from thes3e flocks pass on sufficient immunity on to their chicks through the egg to enable them to withstand vaccination when a few days old. These chicks are thus protected from birth. If vaccinated chicks are kept for egg production then they are usually re vaccinated as growers.
I am sure that with todays medicines and antibiotics the problems are not as severe as when this article was put together, culling the whole flock is not an option as I have never had a full blown attack of respiratory disease, but being on the show circuit for most of the year these things are bound to arise. We do not segregate birds because I was informed by a very long served poultry man to breed it out and I am sure he is correct in his advice.I am no vet but we all learn by experience - so if anyone out there has some good advice on any type of poultry disease/problems please share it with us all.
Why the Hatching Failures ?
Chilled Eggs - in the Nest, in Transport and Storage - are one of the prime Sources of Loss
I have decided on this article for two reasons one is obvious as it is that time of the year the other is a comment made about the purchase of a trio last summer stating that the cock purchased is not fertile.
This article again is a bit older than I would have liked but very useful and informative.
About this time of the year there occur those troublesome failures in incubation which are often puzzling. In general, however, the explanation is usually relatively simple and one of several allied factors can be cited as the culprit.
Care in Handling
Chilled eggs are one of the principle causes of failure to hatch. Chilled in the nests, in transport, in storage. Avoid these troubles by exercising care in handling the eggs from the minute they are laid.
Heavy losses during the early period of incubation are not always immediately noticed. Many operators candle only once, at the change over from incubator to hatcher on the 19th day.
Look to the Stock
If over 15 per cent of all eggs set candle "clear", or as early dead germs, attention to the condition of the breeding stock, as well as the storage, is called for.
It could also mean deficiency; particular of vitamin A, in a breeder's ration and checking this is valuable. Long of faulty storage of vitamin supplements cam lower the vitamin A potential in the ration as a whole.
Inadequate turning in cabinet incubators can cause some early losses, as can any sort of jolting or jarring. In still air machines over cooling in the turning periods can spoil a hatch in its early stages.
The Worst Killer
The worst killer, however, is not temperature drop, but temperature rise, Once the eggs begin to generate some of there own heat - within a week or so - they can take a certain amount of heat loss. This resistance increases as the embryo progresses.
High Humidity Desirable
A high humidity at actual hatching is desirable, or the chicks may be small, and dry, and some will stick to the shells.
Humidity does not soften the shells, but it does lubricate the membranes inside the shell, when air reaches them as the chick breaks through at hatching time.
Until that point there is no need for high humidity and the chick has, during the final stages, the greatest need for oxygen, which can be reduced to a dangerous level, if the humidity is too high.
Compromise Called For
When mass production is the rule, and time is at a premium-and generally it is, then there has to be a compromise. Make the change when most embryos are in or about the recommended stage. The twenty-fifth day for turkeys and the nineteenth for chicks.
Sticky and stuck up dead in shell chicks indicate insufficient oxygen, too much humidity, inadequate ventilation in the hatcher and, possibly, mechanical errors in turning.
"Dead" Air Spots
It has been found occasionally that some machines have "dead" air spots in the setter where air fails to circulate. So it always as well to know precisely where in the setter any chicks that fail to hatch were located.
This article although based on one written 45 years ago stands very true today, this years experiences with the change in temperature etc have been a bit mind boggling, but my own results are now very good.
WARNING As far as the use of chemicals in incubators always check with the manufacturer first before using any chemical substance, personally I use the sterilizing solution used for babies bottles etc this works perfectly well with no risk to both eggs and machine alike, it is easily available both in liquid and dissolvable tablet form. The latest machines come with digital readouts and humidity units so a lot of the real problems are now easier to sort, but we have no control over the elements and the dreaded power cuts.
Coccidiosis - Symptoms, Treatment and Control
Coccidiosis is one of the least understood of all Avian Diseases. The key to controlling Coccidiosis is to be on a control program that will keep the disease under control, yet allow sufficient natural immunity to develop. Because the oocysts that cause Coccidiosis are present everywhere, it is virtually impossible to be free of this disease.
Coccidiosis is caused by a Protozoan which is a single celled animal. When the Protozoa multiply in the bird's intestine, infection takes place causing intestinal damage. Cells that line the intestine that are used for digestion and conversion of feed into Amino Acids and other nutrients are destroyed by the ever multiplying Coccidia. Some species of Coccidia can and do cause severe damage to the Intestinal lining and therefore make it difficult for the bird to absorb the necessary nutrients to nourish its body.
There are at least nine species of Coccidia known to infect Chickens. Every animal is affected by some species of Coccidia. All species of Coccidia are host specific. This means that Coccidia that are capable of infecting Chickens will not infect Turkeys and vice versa. Five of the nine species of Coccidia that infect Chickens can be very aggressive and cause permanent Intestinal damage if not properly controlled. Each of these species resides in a particular section of the Intestines. Emeria acervulina resides in the upper part of the small intestine and is usually found in birds that are eight weeks of age and older. EIrieria necatrix usually found in the middle areas of the small intestine and is usually responsible for the intestinal bleeding often seen with Coccidiosis and it usually attacks young birds. Emeria tenell resides in the Cecal tonsil or blind pouches of the Intestine and usually causes what is called Cecal bloody Coccidiosis and is usually found in birds that are between five to eight weeks of age. Emeria brunetti does its damage in the in the lower small intestine and the Cloaca or rectum of the bird. Emeria maxima causes Intestinal damage in the middle to lower portions of the small Intestine.
Coccidiosis is spread by contaminated feed and droppings from infected birds. The infectious oocysts that cause Coccidiosis can be carried by man, litter, contaminated equipment and free' flying birds. The main source of Infection is the Chicken itself. Birds that are infected with Coccidiosis will pass great numbers of Infectious oocysts in their droppings. Even a bird that has recovered from a Coccidiosis outbreak will remain Infectious as they are never really free of the disease. The oocysts are capable under the right conditions of surviving in the soil for periods of one year or longer. The oocysts that cause Coccidiosis thrive in wet surroundings and are easier to control if litter and or the ground is in a drier condition. It takes approximately four to seven days for an Infection to take place in the Intestines. It takes constan t fe-exposure to the Infectious oocysts in order for Immunity to Coccidiosis to develop. Immunity is not permenent nor is it guaranteed for the life of the bird. Immunity depends on constant re-exposure to the Infectious oocysts , if re-exposure is not accomplished then Immunity will be lost. There is no cross Immunity among the different species of Coccidia. This means that in order for birds to develop Immunity to all nine species of Coccidia they would have to be exposed to sufficient numbers of oocysts from all nine species. They would then have to be constantly re-exposed to all nine species of Cocci in order for Immunity to be maintained. The severity of a Cocci outbreak will depend upon the numbers of oocysts that are ingested by the birds and their overall health and conditioning.
Controlling Coccidiosis and still allowing immunity to build is accomplished in the following way. Use Amprol/Corid powder in the bird's drinking water at the rate of one teaspoon per gallon of water for seven days and 1/8 teaspoon of 3-Nitro-W as well. Then skip twenty one days and then begin treating with Sulfadimethoxine at the rate of one ounce per two gallons of drinking water for five days. Then skip twenty one days again and start the treatment allover again beginning with the AmproI/Corid and the 3-Nitro- W powder. Continue this program until all birds are five to six months old or until the hens begin laying eggs and then discontinue the program and treat on an as needed basis. It is important to start the Amprol/Corid powder first and then use the Sulfadimethoxine as some species of Cocci cause intestinal bleeding and the' use of Sulfa drugs first, will contribute to the bleeding before it makes the situation better. It is also advisable to add 1/4 teaspoon of VITAMIN E to the water as research shows that VITAMIN E can help shorten the course of a Coccidiosis outbreak. When starting baby chicks it is important to start this program no later than ten days of age as this disease will kill baby chicks very quickly. Newly developed technology has produced a. new Coccidiosis vaccine that is effective, safe and affordable. It is really simple to use just mix the vaccine according to the directions that are provided with the vaccine and spray the vaccine on the birds feed that you are feeding for that day. It's that simple. If vaccination was done properly the birds will show mild symptoms of Cocci but should not be 'overwhelmed by the vaccine and immunity will build from there. No medication should be necessary for the life of the birds.
Some of the symptoms that you may observe during an outbreak of Coccidiosis are as follows: Ruffled feathers, droopy or sleepy eyed appearance, birds may drop one or both wings, birds may become lethargic and reluctant to move even when prodded. Some birds may show an uncoordinated gate or appear to stagger or walk as: though they are trying to step over something when there is nothing in front of them. Some birds may have a chilled appearance as well. There mayor may not be blood in the droppings depending upon the species of Cocci that is affecting the birds. Weight loss as well as loss of appetite and mortality may also be observed.
Just a word of caution when using Sulfa drugs. Never use Sulfa drugs for longer than the suggested period of time. Never use two Sulfa drugs at the same time. Always use the proper dose for the drug being used. Always allow three weeks between the use of different Sulfa drugs, never use them back to back, The overuse of Sulfa drugs can and will if not properly used cause permanent and irreversible KIDNEY DAMAGE and RENAL SHUTDOWN (kidney Failure). Use Sulfa drugs with confidence but with a sense of caution. It can be of value to use Some 3-nitro- W in with the Corid/ Amprol powders when treating for Cocci. There is a synergistic effect when the two are used together. Synergistic just means that the ability of the Corid/ Amprol powder to fight Coccidiosis will be improved if the two are used together.
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