- Feb 6, 2007
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What? There are other birds that are sick? If you have others that are sick this should have been in with them, this chick is part of the whole.
Eye problem
- Thread starter siz8003
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- Jan 11, 2007
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It could be a nutritional/vit deficiency...Vitamin A deficiency can cause (sometimes severe) symptoms (see links below) ... it may be primary (and respiratory infection secondary to it)... if you have already given them a course of antibiotics then try a course of POLYVISOL (liquid childrens A-B-C vitamins) >give three drops a day for a week then taper off... if you have Avia Charge 2000 then mix this with their feed also.
Here are the links:
http://www.cipav.org.co/lrrd/lrrd16/10/bhui16083.htm
(excerpt)
"...Poultry are very rapidly affected by vitamin A (retinol) deficiency, which will seriously affect growth rate, feed utilization, development of bone, movements, vision, reproduction, resistance against diseases, and mortality. Deficiency symptoms occur usually within 3 to 4 weeks. Early signs of vitamin A deficiency are loss of appetite and decreased growth rate followed by general weakness, staggering gait, and ruffled plumage. Birds become more susceptible to infection, and both egg production and hatchability are markedly reduced. The eyes are affected with an abnormal exudate and epithelial keratinisation (for review see Olson 1991).
Vitamin A deficiency may be caused by several factors. In natural feedstuffs vitamin A is only present in animal products, notably liver, eggs, fish meal, and fish oil. Pro-vitamins A, of which â-carotene is the most common vitamin A source are only present in plants. According to NRC (1994) poultry are as efficient as the rat in converting â-carotene into vitamin A, and 1mg of â-carotene equals 1667 IU retinol. However, recent findings suggest that the vitamin A activity of â-carotene may be overestimated. In broiler chickens it was found that 1mg of â-carotene was equal to 400 IU retinol (Johannsen et al 1998), in older geese (3-4 months old) to 1200 IU and in young geese (1-3 weeks of age) only to 60 IU (Jamroz et al 2002). The commercial source of vitamin A is an ester of retinol, either retinol acetate or palmitate. These are susceptible to light, oxygen, heat, moisture and pressure during processing (Roche 1994; Barua and Olsen 2000). Thus, in tropical climate zones with high temperature and humidity, the storage stability of premix products containing vitamins may be limited. Feed ingredients may also indirectly induce oxidation. Soya-beans for example contain a lipoxidase that readily destroys the carotenoids present in the feed unless quickly inactivated (Roche 1994)..........
Results
Clinical findings, disease frequency and mortality
At the beginning of the experiment, no vitamin A was added to the diet of the control group, because the purpose of the planned experiment was to observe if the birds could thrive only on natural feedstuffs. However, the birds of this group showed deficiency symptoms from the middle of the third week in Farm1, at the beginning of week 5 in Farm 2 and at the end of week 6 in Farm 3. Initial symptoms were weight loss and inappetance, almost no feed in the crop, followed by ataxia, and some birds were unable to walk.
Figure 1. Vitamin A deficient chickens showing crooked tails
One feature was very common: swollen watery and white caseous mass in the eyes, and the tail was crooked to one side (Figure 1). Post mortem lesions were: swollen kidneys with white urate-like substances, excessive bile in the gall bladder, and epithelial metaplasia in the oesophagus and oropharynx when the birds survived for a few days after showing deficiency symptoms..........................The possible causes of mortality were evaluated at post mortem examination during the experiment. In the control group a total of 102 birds died from vitamin A deficiency, while no birds died from vitamin A deficiency in the VitA group. Coccidiosis was more profound in the dead birds of the control group than of the VitA group (32 vs 7) as was also yolk sac infection (13 vs 3). The cause of the death of the rest of the birds was not identified..............
The natural vitamin A content may have been destroyed during storage of the feed. Previous results have shown that day-old chickens, derived from hens with an adequate intake of vitamin A, but receiving a diet completely devoid of vitamin A, had marginally deficient levels of vitamin A from the third week (Nockels et al 1984) and showed signs of deficiency from the sixth week (Scott et al 1982; Nockels et al 1984). Turkey poults fed a diet without added vitamin A died between 18 and 22 days after hatching (Sklan et al 1995). Liver vitamin A level declined significantly after consumption of a low vitamin A diet for 3 weeks and were depleted after 5 weeks (Aye et al 2000). Similar findings were observed in the progeny of normal hens fed a diet without vitamin A (West et al 1992). We observed that early infection like coccidiosis, yolk sac infection or poor brooding condition may affect the onset of vitamin A deficiency symptoms. Coccidial infection may have disrupted the intestinal epithelium. Injury to the intestinal wall by the coccidia may therefore result in an impaired conversion of â-carotene to vitamin A or in an impairment of absorption of vitamin A per se, or both, which would, in either case, result in a decreased liver storage of vitamin A (Erasmaus et al 1960). Interference with the absorption of the vitamin or conversion of the pro-vitamin would increase the requirement of vitamin A. On the other hand, vitamin A exerts a specific action on the formation, maintenance and regeneration of epithelial tissues which may also increase the dietary demand of vitamin A (Erasmaus et al 1960).
Yolk sac infection and poor brooding condition might exert an increasing utilisation of the limited store of vitamin A in the yolk sac during early weeks of life. Factors like disease, gastrointestinal parasites, environmental stress due to temperature and/or humidity may increase the requirement of vitamin A, which is a relatively unstable vitamin under tropical conditions (Christensen 1983)...............................
In the present studies it was observed that mortality and morbidity were much higher, and the course of the disease was prolonged when vitamin A deficient chickens were affected with coccidiosis, and the response to the anti-coccidial drug was also very poor. These findings confirm that dietary inadequacy of vitamin A apparently increases susceptibility and severity of coccidiosis in chickens (Wilgus 1977). Birds on low vitamin A diets were not able to respond to this antigenic stimuli as quickly as birds on normal vitamin A rations, and consequently, the coccidial life cycle progressed for a longer period of time (Coles et al 1970). However, the reason for a poor response to this treatment is not clear.
It was observed that oral supplementation of water-soluble vitamin A to the severely deficient birds reduced the mortality within 2-3 days, and feed intake became normal within one week. However, a milder form of ataxic symptoms persisted in some cases even after three weeks. It has been reported that squamous metaplasia arising from vitamin A deficiency is reversed through intake of vitamin A (Biesalski and Seelert 1989).......................
It appears that one cannot rely on feed tables as to the content of vitamin A. The natural content of vitamin A is not stable under humid and warm conditions ...."
http://anscigallery.nal.usda.gov/search.php
(type in"the NAL number or "poultry" into the search box to see the photo) " [NAL 3666] Vitamin A deficiency, necrotic eye.
" Early in vitamin A deficiency, increased cerebrospinal fluid pressure can be observed. This causes bulging eyes or exophthalmia. The mucus membranes of the conjuntiva are also affected. When mucus is not secreted then keratinization of the tissues takes place leading eventually to secondary infection and necrosis. "
Here are the links:
http://www.cipav.org.co/lrrd/lrrd16/10/bhui16083.htm
(excerpt)
"...Poultry are very rapidly affected by vitamin A (retinol) deficiency, which will seriously affect growth rate, feed utilization, development of bone, movements, vision, reproduction, resistance against diseases, and mortality. Deficiency symptoms occur usually within 3 to 4 weeks. Early signs of vitamin A deficiency are loss of appetite and decreased growth rate followed by general weakness, staggering gait, and ruffled plumage. Birds become more susceptible to infection, and both egg production and hatchability are markedly reduced. The eyes are affected with an abnormal exudate and epithelial keratinisation (for review see Olson 1991).
Vitamin A deficiency may be caused by several factors. In natural feedstuffs vitamin A is only present in animal products, notably liver, eggs, fish meal, and fish oil. Pro-vitamins A, of which â-carotene is the most common vitamin A source are only present in plants. According to NRC (1994) poultry are as efficient as the rat in converting â-carotene into vitamin A, and 1mg of â-carotene equals 1667 IU retinol. However, recent findings suggest that the vitamin A activity of â-carotene may be overestimated. In broiler chickens it was found that 1mg of â-carotene was equal to 400 IU retinol (Johannsen et al 1998), in older geese (3-4 months old) to 1200 IU and in young geese (1-3 weeks of age) only to 60 IU (Jamroz et al 2002). The commercial source of vitamin A is an ester of retinol, either retinol acetate or palmitate. These are susceptible to light, oxygen, heat, moisture and pressure during processing (Roche 1994; Barua and Olsen 2000). Thus, in tropical climate zones with high temperature and humidity, the storage stability of premix products containing vitamins may be limited. Feed ingredients may also indirectly induce oxidation. Soya-beans for example contain a lipoxidase that readily destroys the carotenoids present in the feed unless quickly inactivated (Roche 1994)..........
Results
Clinical findings, disease frequency and mortality
At the beginning of the experiment, no vitamin A was added to the diet of the control group, because the purpose of the planned experiment was to observe if the birds could thrive only on natural feedstuffs. However, the birds of this group showed deficiency symptoms from the middle of the third week in Farm1, at the beginning of week 5 in Farm 2 and at the end of week 6 in Farm 3. Initial symptoms were weight loss and inappetance, almost no feed in the crop, followed by ataxia, and some birds were unable to walk.
Figure 1. Vitamin A deficient chickens showing crooked tails
One feature was very common: swollen watery and white caseous mass in the eyes, and the tail was crooked to one side (Figure 1). Post mortem lesions were: swollen kidneys with white urate-like substances, excessive bile in the gall bladder, and epithelial metaplasia in the oesophagus and oropharynx when the birds survived for a few days after showing deficiency symptoms..........................The possible causes of mortality were evaluated at post mortem examination during the experiment. In the control group a total of 102 birds died from vitamin A deficiency, while no birds died from vitamin A deficiency in the VitA group. Coccidiosis was more profound in the dead birds of the control group than of the VitA group (32 vs 7) as was also yolk sac infection (13 vs 3). The cause of the death of the rest of the birds was not identified..............
The natural vitamin A content may have been destroyed during storage of the feed. Previous results have shown that day-old chickens, derived from hens with an adequate intake of vitamin A, but receiving a diet completely devoid of vitamin A, had marginally deficient levels of vitamin A from the third week (Nockels et al 1984) and showed signs of deficiency from the sixth week (Scott et al 1982; Nockels et al 1984). Turkey poults fed a diet without added vitamin A died between 18 and 22 days after hatching (Sklan et al 1995). Liver vitamin A level declined significantly after consumption of a low vitamin A diet for 3 weeks and were depleted after 5 weeks (Aye et al 2000). Similar findings were observed in the progeny of normal hens fed a diet without vitamin A (West et al 1992). We observed that early infection like coccidiosis, yolk sac infection or poor brooding condition may affect the onset of vitamin A deficiency symptoms. Coccidial infection may have disrupted the intestinal epithelium. Injury to the intestinal wall by the coccidia may therefore result in an impaired conversion of â-carotene to vitamin A or in an impairment of absorption of vitamin A per se, or both, which would, in either case, result in a decreased liver storage of vitamin A (Erasmaus et al 1960). Interference with the absorption of the vitamin or conversion of the pro-vitamin would increase the requirement of vitamin A. On the other hand, vitamin A exerts a specific action on the formation, maintenance and regeneration of epithelial tissues which may also increase the dietary demand of vitamin A (Erasmaus et al 1960).
Yolk sac infection and poor brooding condition might exert an increasing utilisation of the limited store of vitamin A in the yolk sac during early weeks of life. Factors like disease, gastrointestinal parasites, environmental stress due to temperature and/or humidity may increase the requirement of vitamin A, which is a relatively unstable vitamin under tropical conditions (Christensen 1983)...............................
In the present studies it was observed that mortality and morbidity were much higher, and the course of the disease was prolonged when vitamin A deficient chickens were affected with coccidiosis, and the response to the anti-coccidial drug was also very poor. These findings confirm that dietary inadequacy of vitamin A apparently increases susceptibility and severity of coccidiosis in chickens (Wilgus 1977). Birds on low vitamin A diets were not able to respond to this antigenic stimuli as quickly as birds on normal vitamin A rations, and consequently, the coccidial life cycle progressed for a longer period of time (Coles et al 1970). However, the reason for a poor response to this treatment is not clear.
It was observed that oral supplementation of water-soluble vitamin A to the severely deficient birds reduced the mortality within 2-3 days, and feed intake became normal within one week. However, a milder form of ataxic symptoms persisted in some cases even after three weeks. It has been reported that squamous metaplasia arising from vitamin A deficiency is reversed through intake of vitamin A (Biesalski and Seelert 1989).......................
It appears that one cannot rely on feed tables as to the content of vitamin A. The natural content of vitamin A is not stable under humid and warm conditions ...."
http://anscigallery.nal.usda.gov/search.php
(type in"the NAL number or "poultry" into the search box to see the photo) " [NAL 3666] Vitamin A deficiency, necrotic eye.
" Early in vitamin A deficiency, increased cerebrospinal fluid pressure can be observed. This causes bulging eyes or exophthalmia. The mucus membranes of the conjuntiva are also affected. When mucus is not secreted then keratinization of the tissues takes place leading eventually to secondary infection and necrosis. "
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- #14
- Jan 11, 2007
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...if the symptoms persist or get worse, then it may be an indication of Coryza or MG and you will need a straonger antibiotic than the terramycin (which many feel is ineffectual except in a very few early stage instances)... keep an eye out...hopefully the vitamins will boost up their immune system and if not enough to "cure" them, then to help them get through the next round of antibiotics if you find that is necessary...you should also be offering them free choice live culture (not pasteurized) yogurt now also.
Last edited:
- Feb 6, 2007
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Diana, did you catch the inference that there are other birds also sick? I didn't know that until after I posted. This post being seperated makes it look like its an isolated problem and not a flock issue.
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the silkie is the only one with the eye problem none of the others are bad just sneezing and the 2 polish have watery poo but they are not snezzing so it could be something i gave them and other than the sneezing and an head scratch now and then they are fine so it is just the silkie i am trying to figure out
- Jan 11, 2007
- 4,870
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did you give the antibiotic to the rest of the flock?
In addition it would be a good idea to do a complete clean out and disinfection of their coop (with a bleach mixture>>>ensure the birds are well away while doing this as the fumes from bleach can be noxious)...
What is the weather currently like?
Are you giving the rest of the flock aviacharge (if not do so > this will help ensure no dietary issues to weaken their immune systems further)
Do you have any oxine???
In addition it would be a good idea to do a complete clean out and disinfection of their coop (with a bleach mixture>>>ensure the birds are well away while doing this as the fumes from bleach can be noxious)...
What is the weather currently like?
Are you giving the rest of the flock aviacharge (if not do so > this will help ensure no dietary issues to weaken their immune systems further)
Do you have any oxine???
- Thread starter
- #19
do i have a what? The coop was cleaned out last week and yes all the older chickens had the meds I am going now to find diff meds and the vits. Yesterday and today are hot but nice so I might open ALL doors and windows air it out some might help oh and they dont like the yoguart anything else i might try?
Coryza and ILT can have the exact same symptoms; so can Avian TB. We went to a huge amount of research, too, when our flock was sick. That is why I said earlier...you don't have a lot of time to do experimenting with a lot of different meds. However, dlhunicorn's advice about vitamins is good; it is always a good idea to make sure they are as healthy as possible, by pumping up vitamins, and making sure they have no parasites; deworm, delouse. And you won't hurt them keeping them on antibiotics, or switching to a stronger one; the antibiotic will help to keep any secondary infections away, even if they do have a virus, which isn't treatable with an antibiotic. Just make sure that when they are better you give them live culture yogurt, or something with probiotics. I don't think you have a vitamin deficiency; I think you have a highly contagious virus. Some chickens just develop an eye condition whenever they are sick...and some don't. It probably isn't two different things you're dealing with. Most of the information I gave you about treatment, etc, is information I passed on to you from the State of Ohio vet who helped us with our ILT problem. And, to me, that's what it sounds like it is. Or Coryza. We have some of the best livestock vets in the country here at Ohio State University, so I'm pretty confident with what they told me, especially since our flock recovered.
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