Help! Corid dosage confusion

The sentence: Chickens will have a healthy parasite load, so if they keep getting it, likely there is a secondary thing going on.
is sooo very true. Chickens need to be allowed to obtain a immunity to many parasites. Cocci is definitely one of them. Older chickens should have been exposed to many things, especially free range birds.

Worm of course can be a problem and your chickies need a worming if you see a problem, otherwise I feel it unnecessary to do this.

Round worms are the most common worm a chicken will get.

Have you tried Sulmet ? This is not "off label" for chickens, corrid is.

The digestive tract of you chicken is pretty complex:

THE DIGESTIVE SYSTEM OF BIRDS

(This document helps expain how some diseases such as Enteritis, Diarrhoea, Crop Infection & Aspergillosis form, and what part of the bird is infected and covers some possible cures. See individuial diseases for other possible cures)
THE BEAK
The beak, in addition to being a vital organ for grasping food, is also important for investigating the bird's environment, for preening, carrying nesting and other material and as an offensive or defensive weapon. Hereditary defects of the beak are sometimes seen, although it is often impossible when presented with a young bird showing a deformity of the beak to establish whether its nature is hereditary. This is made less difficult when a breeder notices that some of his birds periodically produce chicks with abnormal beaks. It is not sufficient for him to destroy these freaks and carry on breeding as if nothing has happened, because he is liable to intensify the character in his stock, since it is liable to be a recessive factor. There are numerous other causes of beak deformity, In the nestlings, sticky food presented by the parents tends to coat the palate and lower jaw or accumulate under the tongue. Most parents clean the food material away at regular intervals, but if they are disturbed the young may be neglected and the food will then build up into thick plaques in the mouth. The constant pressure of the tongue on these plaques can slowly elevate, or deviate the position of the beak until the whole mechanism of its movement is deranged, resulting in uneven growth and distortion of both mandibles. Quiet, methodical methods of management, close attention to hygiene and diet, and regular checks on the cleanliness and progress of young stock help to prevent such deformities. Caking of food in the mouth may be complicated by secondary fungal infection in adult parrots and some "softbilled" birds. The primary cause is usually feeding soft and mushy scraps of food and is therefore most common in pet birds which are sometimes fed incorrectly in this way. The fungi Candida and Aspergillus are secondary or contributory causes. In such cases, a mass of hard material is found impacted under the tongue, firmly attached to the lower beak. Sometimes the tongue is ulcerated due to pressure or friction and infection, and slight distortion of the beak may occur. A lack of inclination or the disability to eat is the main sign, with a tendency to pick up and drop food as if playing with it. Dribbling from the beak is another sign, the odour from the mouth being sour or cheesy. Picking out the mass with a sharp-hooked instrument brings immediate relief, and no further treatment is usually necessary. Knemidocoptic mange of the cere of nestling budgerigars is common in some establishments. Often the early stages are missed and only when the thickened, spongy horn of the upper beak begins to spread over the face do some owners suspect abnormality. In this disease deformities occur in adults as well as in nestlings and growing stock, resulting in a wide range and degree of deformity. Injuries to the beak may occur when the bird flies into a door or snaps its beak in the framework of its cage. Soft-feeders can manage to eat if adequate supplies of food are available and if there is the minimum competition for food. Nut and grain-feeders, which shell or dehusk seed are less able to adapt to the resultant deformity, but can manage if a stump of beak is left, on which to crack the seed. However, repeated trimming of the unopposed beak is necessary to prevent its overgrowth.
THE MOUTH
Simple congestion of the mucous membranes in the mouth is difficult to see, because birds lack soft, fleshy gums and a soft palate comparable with that in mammals. Inflammations accompanied by exudates or discharges are more obvious. Excessive salivation can result from injury, ulceration, or an impacted foreign body in the buccal cavity. Infections of the upper respiratory tract may also sometimes over-stimulate the salivary glands. An excessive amount of bubbly saliva may indicate infestation with gapeworms. Thick, white or cream-coloured material adhering to the mucosa of the mouth, oesophagus, pharynx, larynx or trachea denote a possible deficiency of vitamin A. In pigeons, however, the most common cause of these lesions is trichomoniasis. The one-celled parasite, with flagellae or whip-like processes, is readily found by microscopical examination of fresh exudate. Other species may contract trichomoniasis, but the disease is most important in young birds when a high proportion of birds may become affected. Candida and less frequently Aspergillus may produce similar deposits in the mouth. In "sour crop", oesophageal or crop obstruction, or in general alimentary tract inflammations, a tenacious bubbly fluid may be produced in the throat and mouth, and this usually contaminates the face as well. Regurgitation of crop contents, especially in budgerigars during courtship display, leads to similar signs, so that care is needed before a diagnosis can be made.
THE OESOPHAGUS & CROP
Carnivorous birds, especially those which habitually swallow whole carcasses such as fish or the heads of rats and mice or other mammals, occasionally suffer from impaction of the cervical part of the oesophagus. Such obstructions can be gently manipulated into the mouth. The oesophageal walls of these birds are tough, but if tearing or other damage is to be avoided, the manipulation must be carefully and slowly carried out. Obstruction of the oesophagus beyond the crop will sometimes induce a bird to carry on eating until the greater part of the oesophagus is a dilated mass of food. This can sometimes be broken down by the fingers through the intact tissues of the neck and squeezed upwards in small quantities at a time through crop and oesophagus to the mouth, using intermittent pressure only, to obviate the danger of asphyxiation. Impaction of the crop is also a common occurrence in birds which eat an omnivorous diet, including hard shelled seeds. The impacted crop can assume the consistency and size of a golf ball or be even larger and almost as hard. In predominant seed-eaters, a less durable impaction may result from lack of sufficient saliva to lubricate and soften the seed, or when a highly, absorbent, glutinous material such as oatmeal is incorporated in the diet. Usually, however, only debilitated birds are affected by such crop impactions, which should be treated as previously described. It is sometimes necessary to operate in cases where starvation or other serious sequelae are imminent. It must not be assumed that every swelling at the base of the neck is an impacted crop or oesophagus, because tumours in this area and enlargements of the thyroid gland are easily confused with distended crops. Tumours and cysts of the thyroid, however, usually have the consistency of sponge rubber and are smooth in outline. If too great a pressure is applied to cysts of this type they may rupture and give rise to internal haemorrhage. Death then will occur fairly rapidly. If a skin incision is inadvertently made over such a cyst, the deep, red colour of the swelling should be sufficient to discourage further surgery and the skin wound should be sutured or the bird destroyed.
On rare occasions a concretion or stone develops in the crop of budgerigars but the cause is obscure. It has been suggested that when the primary constituent is urate the cause may be due to eating excreta from the floor of the cage: such a theory, however, would not account for the composition of the calculus illustrated here. Occasionally, the subcutaneous fat stored on the breast is displaced forward to the crop region and this hinders digital examination. Large fatty deposits of this type can also be easily mistaken for a full or impacted crop. Infected injuries of the crop wall occasionally develop into granulomas which appear as hard tumour-like masses and these may also affect the skin. Regurgitation, or vomiting as it is so often referred to by bird fanciers, is very common in many species. Caged budgerigars kept alone frequently regurgitate at their reflection in a mirror with apparent enjoyment, this probably being an abnormal form of courtship display. The regurgitation of crop contents may also indicate an inflamed or ulcerated crop, or so-called "sour crop". The crop contains evil smelling fluid, which may result from ingestion of poorly nutritious, stale or mouldy food. Irregular feeding, chilling, or some infection or other disturbance lower down the alimentary canal may also be contributory causes. "Sour-crop" may often be associated with vitamin or protein deficiencies, infections such as candidiasis and trichomoniasis, or with liver or kidney disease. Another possible cause is pressure from growths inside the body cavity which may hinder the flow of intestinal content, causing backflow into the proventriculus and crop. Sometimes it is possible that destruction of mucous or enzyme-producing glands in the proventriculus may stimulate the return flow of acid into the crop and in poor health this alone may be sufficient to cause "sour crop" with erosion of the crop epithelium. Sometimes the crop becomes flaccid, as a result of the muscles of the crop wall losing their tone or contractibility. This results in food being held up in the crop because of its inability to force the food further down the oesophagus into the proventriculus. There is often no actual obstruction, but when the crop becomes full the food material begins to overflow into the upper part of the oesophagus and this may eventually lead to true obstruction. The circumstances leading to crop obstruction and "sour crop" are similar. Mild inflammations may be checked by intermittent "milking out" of the crop contents or removing them with the aid of a wide-bored, hypodermic needle and syringe; the latter method being less likely to interfere with the breathing. An antifermentation liquid may then be given by dropper or by using the hypodermic syringe and drainage needle. A harmless antiseptic or an antibiotic should be added if infection is suspected. Gentian violet, hexamine, potassium permanganate, or one or two drops of 1 per cent formaldehyde are suitable to check fermentation. When irritation is suspected, a bland fluid such as liquid paraffin, lime water, egg albumen, barley water, kaolin or aluminium hydroxide may suffice. The diet should consist solely of liquids every hour or two for the first 24 to 36 hours after emptying the crop, gradually followed by semi-solids, finely chopped and softened solids, and finally the normal diet after 3 to 5 days. A multivitamin and mineral tonic should always be added to the drinking water during the recovery phase. If there is no response to such treatment in budgerigars, it will indicate the presence of a specific type of necrosis or ulceration of the crop. With this disease death often occurs within a few days. Early cases sometimes respond to treatment with oxytetracycline or chloramphenicol by mouth. Experiments have failed to prove that the disease is infectious, in spite of the fact that many birds in a flock may become affected. In addition to vomiting, greenish diarrhoea is usually present. Theories that allergic, deficiency or stress mechanisms produce the disease have not been supported so far by convincing evidence. At post-mortem examination the crop lining shows elevated, parallel ridges or finger-like projections, which are yellowish in colour and consist of necrotic material. Death is probably the result of impaired digestion, and loss of fluid due to vomiting and diarrhoea.
THE PROVENTRICULUS OR GLANULAR STOMACH
Food passes through the oesophagus and crop to reach the proventriculus, which it tends to traverse relatively easily. When the normal passage of food is interrupted by irregular feeding, it may interfere with the outflow of proventricular juices. The normal peristaltic or squeezing onward movements of the oesophagus and crop, may then be reversed (antiperistalsis) resulting in souring of the crop contents by proventricular secretions, and producing irritation of the crop lining and vomiting. Deficiencies in the diet, for example of vitamin A, and certain bacterial and possibly viral infections, may lead to ulceration of the epithelium of the proventriculus. Candidiasis is also capable of producing lesions in the proventriculus. Abnormal fermentation, as in the crop, can also result in distension of the proventriculus with gases.
THE GIZZARD
The gizzard is a tough structure and resistant to the enzymes and acids produced by the proventriculus. In the gizzard of omnivorous and seed-eating birds a great deal of pummelling and grinding of food occurs aided by grit which is normally present in this organ. The ingesta or partially digested food emerges as a pulp of fine particles of gruel-like consistency and is still strongly acid. In weak, debilitated birds the ingesta may be incompletely pulverised on entry into the duodenum, where it is then liable to irritate the openings of the bile and pancreatic ducts thus leading to digestive disturbances. If a foreign body, such as a coin, button, nail, staple or small piece of wire is swallowed, it may cause no trouble until it reaches the gizzard, where it tends to be retained, in the same way as grit. Round objects cause a mild, chronic "gastritis" or ventriculitis, which may not prevent the bird from living a relatively healthy life, but may cause occasional brief bouts of indigestion. Sharp or hooked objects tend to bury their ends into the gizzard wall during contraction of the organ, probably causing pain and perhaps resulting in loss of appetite and consequently weight. Sometimes a sharp object will perforate the gizzard wall and cause peritonitis and death. Unfortunately x-ray examination does not always differentiate between foreign bodies and the shadows cast by grit in the gizzard. When a foreign body is strongly suspected an operation for removal is not to be embarked on lightly, even by an experienced veterinarian, because this is usually very difficult and the chances of success are low. Erosion of the horny lining of the gizzard does not appear to be as common in cage and aviary birds as it is in poultry, but it may result from a lack of vitamins such as vitamin A. In waterfowl and occasionally other species, gizzard worms produce severe erosions. Gizzard erosion can be suspected in vague illnesses accompanied by indigestion and loose, greenish, mucoid and intermittently bloodstained droppings. Distension and flabbiness of the gizzard musculature occurs mostly in debilitated birds, specially when the exit into the small intestine is impacted with hard fibrous ingesta. Such an obstruction soon causes depression, loss of appetite, and soft droppings which rapidly become smaller in amount, and are passed progressively less frequently. If the condition is not relieved, death can result from toxaemia even before the effect of starvation is felt. Birds affected in this way are generally those kept in planted aviaries or where little food and an abundance of coarse fibrous material is present. Liquid paraffin given slowly by mouth in liberal amounts using a dropper (10-20 drops per 100 gram body weight) is the most effective and safest treatment. This tends to ease and soften the obstruction, and soothe the mucows membrane of the gut. Diagnosis is difficult and has to be based on careful observation, and consideration of all the circumstances.
THE DUODENDUM & SMALL INTESTINE
These organs are erroneously believed by many aviculturalists to be the seat of over half of the ills that affect birds because loose droppings are a common sign in digestive disorders and many diseases which are not confined to the digestive tract. These diseases are frequently lumped together, being referred to as "diarrhoea" or more often as "enteritis", the two words being used interchangeably by bird keepers. Diarrhoea , is not a disease but a clinical sign. It simply refers to the voiding of fluid faeces. It can be caused by irritation or infection of the gut resulting from eating unaccustomed or contaminated food and drinking excessive amounts of milk or oily liquids. The watery urate fraction of the droppings is often mistaken for diarrhoea. Excessive amounts, however, indicate urinary upset and not alimentary disease. Enteritis is the inflammation of part or all of the gut behind the gizzard. Although a specific gut infection or other localised inflammatory change may be responsible, much more likely causes of diarrhoea are the results of a septicaemia, pressure from a tumour of a gonad or kidney; liver damage; visceral gout; parasitism; a localised bacterial infection elsewhere, causing a toxaemia or even a change of environmental conditions or feeding routine. The first step towards a diagnosis is to establish that true diarrhoea and not watery urine is being excreted. Both fractions of the droppings, urinary and faecal, are often affected simultaneously when a generalised disease is present, but in the early stages one fraction usually alters before the other. In order to diagnose the cause and significance of diarrhoea many factors have to be considered, for example, whether or not the disease is contagious; the ages of those affected; the significance of other clinical signs; the diet; general management, and all factors known to influence disease. It is thus an exercise for the veterinarian. In an isolated pet bird, the cause of diarrhoea can be undiagnosable, when it is the only or main sign of illness, even with the full services of a laboratory at one's disposal.
Although post-mortem examinations do not always reveal the cause, carcases of any dead birds should always be submitted to a laboratory, as well as samples of excreta from live birds. In the case of illness in only one bird, factors such as impactions, foreign bodies, large abdominal tumours and abdominal rupture should be considered. When a bird suddenly becomes ill, and is well fleshed, but huddles, shivers, or pants, an acute infection or poisoning must be suspected. In such acute cases the administration of a broad-spectrum antibiotic to both the affected and the other birds may be indicated. A veterinarian should be consulted as soon as possible since unscientific treatment can merely mask deadly diseases until the cause is well and truly established in the premises and stock. Diarrhoea without significant depression or illness in one or several birds may have a dietary origin; so this possibility should be checked. When appetite is reduced, a multi-vitamin/mineral/amino-acid elixir given by dropper is most useful. It aids recovery in most diseases, increasing the appetite and vitality, especially if vitamin B., is included. It also temporarily alleviates most dietary upsets, including deficiency of various food factors. When marked loss of breast muscle and fat is noticed, this suggests a chronic type of disease. Aspergillosis , nephrosis, large tumours of internal organs and certain slowly developing bacterial infections such as tuberculosis come into this category. A true inflammation of the duodenum and/or small intestine can be a serious matter. An inflamed gut is more permeable than normal; it allows poisonous substances and bacteria to pass through more easily, even though its increased blood supply brings an army of defending white cells with it. The increased blood flow causes swelling of the gut wail, in particular its lining mucous membrane. Mucous outflow is increased, and digestive juices are unable to function properly because the increased gut movements hustle the ingesta on towards the cloaca before digestion is complete. The swelling of the mucous membrane may be so marked as to close the openings of glands, and also involve the bile or pancreatic ducts, causing damage to the liver and pancreas and leading to infection of these organs. An acute hepatitis or pancreatitis (the latter fortunately appears to be rare) causes more severe illness than an inflamed duodenum.
If the pancreas is damaged it tends to digest itself, and because its enzymes are so potent, it partly liquefies; this results in a local or generalised peritonitis with dire results. If the liver is infected first in a septicaemia, the flow of bile may cease and this in itself interferes with digestion, causing a duodenitis and enteritis. It can be appreciated therefore that little can happen in a single tissue or organ of the body without it having effects in the neighbouring or distant organs. Probably a further result of intestinal inflammation is the liberation of certain substances into the bloodstream which may produce shock. This results in lowered intake of food and weakness. The excessive loss of water, acids, enzymes and mineral salts also has a rapidly weakening and debilitating effect. In birds, with their high metabolic rate, this rundown is rapid and soon becomes serious. The type of treatment depends upon the cause but is usually a matter of trial and error.
THE LIVER
The liver features in many diseases, especially infections, mainly because it is a kind of sieve, a factory and a scrapyard for the various products reaching it via the bloodstream. Degenerations, especially of a fatty type, are common and usually associated with unsuitable food, lack of exercise or certain poisons. Fatty infiltration of the liver is common in otherwise healthy budgerigars, parrots and cockatoos. Later stages lead to fibrous replacement of liver tissue (cirrhosis) which, when advanced has widespread effects, especially on the heart, kidneys, and digestive functions. Tumours of liver tissue, and metastatic, multiple tumours originating from cancerous growths elsewhere, are quite common in budgerigars and seriously interfere with metabolism. Single, large, benign tumours and cysts of the liver produce effects mainly by pressure-destruction and replacement of liver substance as well as pressure on neighbouring organs. Clinical signs develop more slowly in these benign cases, and usually only when the lesion has reached a considerable size. It is usually impossible to diagnose liver disease in the live bird before it is too late in most cases but with todays technology most vets can detect problems by taking blood samples or by analyzing the droppings.
THE PANCREAS
This organ is remarkably free from localised inflammations and degenerations, although it can readily be inflamed or otherwise damaged in many generalised affections. Pancreatitis, either acute or chronic, is occasionally found at necropsy, but can rarely be diagnosed in life. Diabetes does not appear to have been reported in birds. Tumours of the pancreas are uncommon. Atrophy of the pancreas has recently been reported for the first time in budgerigars. An affected bird loses weight in spite of the fact that its appetite increases markedly. At the same time the amount of faeces produced also increases greatly. The general condition of the bird gradually deteriorates and the abdomen becomes distended. The faeces are a light grey in colour and a little greasy on the surface. Eventually the faeces become hard and chalky obscuring the white urate part of the excreta. The faeces stain dark blue with iodine owing to the presence of undigested starch. The cause of the disease is at present unknown and it is incurable.
THE CAECA OR BLIND GUT
Most birds have two caeca lying at the junction of the long, small intestine and the short, large bowel. In a few species, only one caecum is present. Large caeca occur mainly in species which eat bulky, vegetable food such as grain, but the organs are by no means vital and their surgical removal causes little or no departure from normal health. Only in the large, flightless birds, gallinaceous species, and some seabirds, do the caeca have a major function, and even in these species removal does not seriously impair health, although digestive processes are less efficient. The larger caeca of gallinaceous birds, like the appendix of human beings, can be the site of trouble and become infected by pathogenic bacteria such as Salmonella or Escherichia coli, causing inflammatory changes. In these species too, certain nematode worms, coccidia and Histomonas can flourish in the caeca. Most passerine birds have vestigial caeca which cause no trouble, while budgerigars and a few other species are without them. In those species possessing caeca fermentation may produce gas, causing marked distension if the exit into the large bowel is obstructed by swelling of the mucous membrane, or by solid ingesta. Such distension appears to cause pain, depression, and loss of appetite, and spread of the inflammatory process to neighbouring parts of the gut may cause diarrhoea. Caecal disease is not generally diagnosable in the living bird although specific bacterial infections or parasitic infestation of the gut, including the caeca, can be diagnosed on laboratory examination of faeces. An operation for the surgical removal of caeca in turkeys has been devised, but although this prevents certain diseases, mortality from the operation is high and it probably has no useful place in the surgery of cage birds.
THE RECTUM & CLOACA
The large bowel or rectum (colorectum) is a short, straight structure, whose main function is reabsorption of water and all useful digestive soluble materials; it is helped in this by the proctodeum of the cloaca. The useful materials include bile, mineral salts, used enzymes, sugars, fatty acids, amino acids and vitamins. If an inflammatory process occurs higher up the digestive tract, not only will the flow of ingesta be quicker than can adequately be dealt with by the absorptive powers of the rectum, but also the inflammation may eventually spread to the rectal wall itself. An enteritis seldom remains limited for long to a short portion of the tract. Both acute and chronic inflammations interfere with absorption from the rectum, and diarrhoea results. Tumours of the gut wall are not common in birds, abdominal tumours which press on the gut or liver being more frequently seen. These may cause irritation, increasing the flow of gut contents, or more usually causing partial obstruction. In the case of a large tumour, retained egg, or cyst of the oviduct or other structure in the posterior half of the abdomen, pressure on the rectum or cloaca results in partial or complete obstruction of the gut. When there is a slowly developing structure such as a tumour, the muscles of the gut above the growing obstruction tend to enlarge in response to the extra work. The obstruction to the lumen of the gut results in impaction with faeces anterior to the obstruction, and soon leads to general abdominal enlarge. When straining occurs, the abdominal wall is liable to rupture and the power of the abdominal contraction is lost. This stage usually causes obvious respiratory difficulty. The rate of breathing may increase, panting may occur, and abnormal, fluid-like clicking sounds may be heard in the chest on auscultation. Complete constipation may occur or faeces may be passed in small amounts and be infrequent, depending upon the severity of the obstruction. Sudden obstruction causes considerable straining and distress. Successful palpation of the obstruction is often impossible. Continuous pressure must be avoided because it will kill the bird by causing interference with respiration and blood circulation.
Sometimes the masses of faeces in the cloaca become very sticky owing to the absorption of moisture. The impaction then becomes difficult to void and may cause pressure on the gut, reproductive or urinary tracts. Liquid paraffin by mouth is the most useful simple remedy. "Pasting of the vent" is the result of a disease causing diarrhoea or excessive excretion of urates, and is not a disease in itself. The "paste" can be composed of abnormal faecal or urinary products. Excessive brooding, incubating in wet or dirty nests, poor diet and hygiene, can all play a part in producing this unpleasant condition. At best it is a sign of some defect in diet, hygiene, or other aspects of husbandry, but in most cases it is a portent of disease about to show-itself in some other way. First, one should eliminate the simpler and less harmful possibilities and then consider the various infections. In uncomplicated cloacal inflammations and diarrhoea due to dietetic disorders, all that may be necessary is simple bathing of the vent, liquid paraffin by mouth, the use of an enema (under professional advice only), and attention to diet and hygiene. In other cases, the casual agent must be found and appropriate treatment given. "Vent gleet" is a chronic inflammation of the vent or cloaca, particularly in the laying domestic fowl and occasionally in the male birds. It is characterised by necrosis of the mucous membrane which becomes covered with a yellowish layer of dead epithelium. The lesion gives rise to a very unpleasant odour and starts with swelling and reddening of the mucosa. The exact cause is not known, but since the greatest number of victims are laying birds, metabolic or stress factors may be involved. Although various bacteria may be isolated from affected vents, none are apparently capable of producing the disease without a predisposing cause. Only a few birds at a time usually become affected. Diarrhoea with "pasting of the vent" may occasionally be a contributory factor. Although this is primarily a disease of poultry, cage birds sometimes develop clinical signs which are indistinguishable. "Constipation" is the name given for the excessive dehydration of the faeces in the rectum and cloaca which causes partial or complete retention. Contrary to common belief, this seldom occurs to a serious extent, unless a mechanical obstruction has held up the faeces in the first place. In other cases the cause may be due to an excess of fibrous material or grit in the diet, poor tone of the muscles in the bowel wall due to inactivity or obesity, or "pasting of the vent". Prevention and treatment are self-evident, an oily laxative being most helpful .
 
Thanks very much for all the help and information!!!

I don't really understand why the chickens still have this. Their litter is dry and I clean out the coop every week. But they do free-range: could they be re-infecting themselves? Wouldn't they have more immunity? I don't think I can feasibly remove every dropping from their environment.....

One possibility is that it's only the one hen who has it, whose droppings were analyzed. Perhaps she's sick with something else, as silkiechicken suggested? I lost another hen to vibrionic hepatitis last summer and maybe she has it too (although I treated all the hens at the time...maybe her liver is damaged?).

The link to the Amprolium dosage on the fowlfacts site still listed two quantities: 2 cc/gal and 4 cc/gal. Does anyone know why there are two listed?

Thanks again!
 
I'm not sure if you said what your chickens have, but I'm guessing cocci?

If so, one treatment type does not kill all cocci types. You sometimes need to alternate drugs to be effective. I would suggest trying another if the problem persists.
 
Yes, a fecal analysis showed cocci. I'm thinking I'll try another round of Amprolium, wait, then try Sulmet. Does that make sense? They seemed to get better after the first Amprolium treatment, last summer, but I wasn't convinced they were cured.

I've started them on 4 cc/gal. Any ideas why there are also recommendations of only 2 cc/gal?
 
If I remember correctly, it's ~ 4cc for the first 5 days, then only 2 cc for a little bit after that... backing down the dosage.
 

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