intracranial lipoma?

[johnsonfarm]

So in trying to find answers for my duckling that I thought had a B deficiency, I ran across info on ducklings with intracranial lipoma on PoultryDVM, and the symptoms match!
Smaller than normal eyes
Walking in circles
Head tremors
I'll post a video in a second, but my question is, the info I found just talked about this happening in crested breeds... could it occur in a non crested breed too?

 

[johnsonfarm]

PoultryDVM doesn't mention the circling, but I found a research paper that did.

 

[Miss Lydia]

@casportpony may have some info. She is pretty knowledgeable on diseases.

 

[casportpony]

. could it occur in a non crested breed too?

I think ducks without crests can get them. Let me see if I can find the article I read.

 

[chickens really]

What are you feeding it?

 

[casportpony]

So in trying to find answers for my duckling that I thought had a B deficiency, I ran across info on ducklings with intracranial lipoma on PoultryDVM, and the symptoms match!
Smaller than normal eyes
Walking in circles
Head tremors
I'll post a video in a second, but my question is, the info I found just talked about this happening in crested breeds... could it occur in a non crested breed too?

To rule out the B and E deficiencies may I suggest that you give some vitamin B complex for cattle by injection or orally, and some vitamin E?

 

[johnsonfarm]

I have been with no results yet, They started on 20% unmedicated chick feed with brewers yeast and peas, then switched to an 18% duckling specific pelleted feed. I've also been giving this one liquid B complex, and I just bought livestock vitamins (for their water).

It's been like this since day 2 when I picked them up (perhaps since hatching?) No loss of appetite, growing well, one of the biggest. The strange eyes are what make me wonder, smaller than the rest and kind of sunken in. But not dehydrated.

 

[chickens really]

I have been with no results yet, They started on 20% unmedicated chick feed with brewers yeast and peas, then switched to an 18% duckling specific pelleted feed. I've also been giving this one liquid B complex, and I just bought livestock vitamins (for their water).

It's been like this since day 2 when I picked them up (perhaps since hatching?) No loss of appetite, growing well, one of the biggest. The strange eyes are what make me wonder, smaller than the rest and kind of sunken in. But not dehydrated.

Neurological issues I'm thinking and putting it down might be an option?...

 

[casportpony]

If it were mine I would try giving the 1/4 ml of the B complex for cattle orally or by injection 3 days in a row and I would try giving it some vitamin E too.

Vitamin E deficiency can cause this too. Not the eyes, but can cause the tremors and spinning. Look up "crazy chick disease" I have seen this twice and both times I was able to correct it with one or two doses of vitamin E

This is in the spoiler below:
"Signs of exudative diathesis and muscular dystrophy due to vitamin E deficiency can be reversed if treatment is begun early by administering vitamin E through the feed or drinking water. Oral administration of a single dose of vitamin E (300 IU per bird) usually causes remission."

Spoiler: Merck's

Vitamin E Deficiency
The three main disorders seen in chicks deficient in vitamin E are encephalomalacia, exudative diathesis, and muscular dystrophy. The occurrence of these conditions depends on various other dietary and environmental factors.

Encephalomalacia is seen in commercial flocks if diets are very low in vitamin E, if an antioxidant is either omitted or is not present in sufficient quantities, or if the diet contains a reasonably high level of an unstable and unsaturated fat. For exudative diathesis to occur, the diet must be deficient in both vitamin E and selenium. Signs of muscular dystrophy are rare in chicks, because the diet must be deficient in both sulfur amino acids and vitamin E. Because the sulfur amino acids are necessary for growth, a deficiency severe enough to induce muscular dystrophy is unlikely to occur under commercial conditions. Signs of exudative diathesis and muscular dystrophy can be reversed in chicks by supplementing the diet with liberal amounts of vitamin E, assuming the deficiency is not too advanced. Encephalomalacia may respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum.

The classic sign of encephalomalacia is ataxia. The results from hemorrhage and edema within the granular layers of the cerebellum, with pyknosis and eventual disappearance of the Purkinje cells and separation of the granular layers of the cerebellar folia. Because of its inherently low level of vitamin E, the cerebellum is particularly susceptible to lipid peroxidation. In prevention of encephalomalacia, vitamin E functions as a biologic antioxidant. The quantitative need for vitamin E for this function depends on the amount of linoleic acid and polyunsaturated fatty acids in the diet. Over prolonged periods, antioxidants have been shown to prevent encephalomalacia in chicks when added to diets with very low levels of vitamin E or in chicks fed vitamin E–depleted purified diets. Chicks hatched from breeders that are given additional dietary vitamin E seem less susceptible to lipid peroxidation in the brain. The fact that antioxidants can help prevent encephalomalacia, but fail to prevent exudative diathesis or muscular dystrophy in chicks, strongly suggests that vitamin E is acting as an antioxidant in this situation. Exudative diathesis results in a severe edema caused by a marked increase in capillary permeability. Electrophoretic patterns of the blood show a decrease in albumin levels, whereas exudative fluids contained a protein pattern similar to that of normal blood plasma.

Vitamin E deficiency accompanied by sulfur amino acid deficiency results in severe muscular dystrophy in chicks by ~4 wk of age. This condition is characterized by degeneration of the muscle fibers, usually in the breast but sometimes also in the leg muscles. Histologic examination shows Zenker’s degeneration, with perivascular infiltration and marked accumulation of infiltrated eosinophils, lymphocytes, and histocytes. Accumulation of these cells in dystrophic tissue results in an increase in lysosomal enzymes, which appear to function in the breakdown and removal of the products of dystrophic degeneration. Initial studies involving the effects of dietary vitamin E on muscular dystrophy show that the addition of selenium at 1–5 mg/kg diet reduced the incidence of muscular dystrophy in chicks receiving a vitamin E–deficient diet that was also low in methionine and cysteine, but did not completely prevent the disease. However, selenium was completely effective in preventing muscular dystrophy in chicks when the diet contained a low level of vitamin E, which alone had been shown to have no effect on the disease. Throughout the past few years, the incidence of “muscular dystrophy–type” lesions in the breast muscle of older (>35 day) broilers has increased. Characteristic parallel white striations on the muscle are similar to those seen in chicks with muscular dystrophy, yet on analysis the diet of these birds seems adequate in vitamin E as well as selenium.

Studies with chicks on the interrelationships between antioxidants, linoleic acid, selenium, and sulfur amino acids have shown that selenium and vitamin E play supportive roles in several processes, one of which involves cysteine metabolism and its role in prevention of muscular dystrophy in chickens. Glutathione peroxidase is soluble and located in the aqueous portions of the cell, whereas vitamin E is located mainly in the hydrophobic environments of membranes and in adipose tissue and other lipid storage cells. The overlapping manner in which vitamin E and selenium function in the cellular antioxidant system suggest that they spare one another in prevention of deficiency signs.

Only stabilized fat should be used in feeds. Adequate levels of stabilized vitamin E should be used in conjunction with a commercial antioxidant and at least 0.3 ppm selenium. Signs of exudative diathesis and muscular dystrophy due to vitamin E deficiency can be reversed if treatment is begun early by administering vitamin E through the feed or drinking water. Oral administration of a single dose of vitamin E (300 IU per bird) usually causes remission.

https://www.merckvetmanual.com/poul...ement-poultry/vitamin-deficiencies-in-poultry

 

[casportpony]

I've also been giving this one liquid B complex, and I just bought livestock vitamins (for their water).

I would give it orally or by injection ASAP.