Encephalomalacia (crazy chick disease)
Eneephalomalacia in birds (usually in good condition) up to the age of 5 weeks or so (commonly weeks 2 and 3). Clinical signs are of muscular weakness, progressive ataxia with frequent falling, spasmodic violent incoordination, head retraction and/or rorticollis, paralysis and death.
Vascular lesions give rise to oedema and peteehial and larger haemorrhages in the cerebellum, with ensuing neurone degeneration. Such gross lesions, seen in fresh brains in association with appropriate clinical signs and history, are virtually pathognomonic. That the cerebellum constitutes the target organ, while the cerebrum is not affected, is perhaps related to increased polyunsaturated fatty acid levels, which appear to occur in the second and third weeks in the cerebellum but not in the cerebrum.
On gross examination it may be necessary to examine numerous birds for typical ‘diagnostic’ cerebellar lesions to be found.
The condition is prevented by adequate vitamin E; selenium is said to have some prophylactic effect. The usual treatment is vitamin E given via drinking water.
Exudative diathesis
Capillary wall lesions lead to increased vascular permeability, with resulting blood and plasma leakage; this accumulates subcutaneously, particularly over the breast and under the wings, also intermuseularly and in the pericardial sac.
The condition is ptevented by and responsive to vitamin E and selenium. The usual treatment is vitamin E via drinking water.
Nutritional muscular dystrophy
Nutritional muscular dystrophy frequently occurs with exudative diathesis and tends to occur when vitamin E deficiency is accompanied by a deficiency of sulphur-containing amino acids (methionine and cysteine) in chicks, turkey poulrs and ducklings.
Microthrombosis of arterioles and smaller capillaries causes occlusion, which gives rise to degeneration and necrosis of muscle fibres, seen as pale streaks mainly in breast and thigh muscles (hence the reference to white muscle disease). Prevention and treatment ate by vitamin E supply, as previously described.
VITAMIN K
The antihaemorrhagic vitamin K occurs in a number of forms as derivatives of naphthoquinone. The most important, vitamin K1, is present in green plants, fruits and liver oils; vitamin K2 is present in animal and microbial materials. The essential structure in all vitamin K analogues is menadione (known also as vitamin K3), which has vitamin K activity. Vitamin K3 is qualitatively different in that it is not an antagonist of the anticoagulant drugs (e.g. dicoumarol, warfario) and is water-soluble, whereas vitamins K1 and K2 are fat-soluble.
Vitamin K3 or menadione acts as a provitamin and must be converted in the liver to menaquinone before it can exert a biological effect; however, since it is more readily manufactured than the other forms it is the basis for most commercial preparations. The various forms used tend to incorporate a bisulphite substiruent and this confers greater potency than menadione. The forms used include menadinne sodium bisulphite (MSB), menadione sodium bisulphirc complex (MSBC), menadionc dimerhylpyrimidol bisulphire (MPB) and menadione nicotinamidc bisulphite (MNB). These forms are also more stable, which is an important factor when considering feed processing conditions. Even then there are considerable losses, which have to be accommodated for by higher allowances.
Key function
Vitamin K is indispensable for blood coagulation, and participates in prothrombin formation. It also plays a role in calcium metabolism. Vitamin-K-dependent proteins are found in bones, shell gland and eggshell.
Deficiency
Microbial synthesis occurs in the caecum and large intestine and as a result deficiency is very rare, especially in adult birds, although the supply of vitamin derived from microbial synthesis
is thought only to be of benefit if faeces are consumed.
• Chicks can exhibit delayed blood clotting as a result of deficiency.
• Oral administration of antibacterial drugs such as sulfaquinoxaline and some other sulpha drugs are stared to be antagonistic to vitamin K activity.
The only real measurement of activity is the biological response in prorhrombin production (by chick assay).