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EXAM Q&A in animal internal medicine



Today, we have chosen an important niche of animal internal medicine to discuss.


Q&A in nutritional deficiency in different animal species, including: 



  1. Discuss the importance of  vitamin A & clinical findings of vitamin A deficiency in farm animals.


  1. Write briefly on general steps for diagnosis of trace mineral deficiency diseases in farm animals.


  1. Write on clinical signs of cobalt deficiency in sheep.


  1. What is the treatment of iodine deficiency in sheep?


  1. Enumerate clinical signs of thiamine deficiency in calves.




Q1: Discuss clinical findings of vitamin A deficiency in farm animals. 


Vitamin A is an essential micronutrient for many body functions, including:

  • Function of the immune system.


  • The health of epithelial tissues, mucous membrane reproduction and development.


  • Normal bone growth.


  • The functioning of the nervous system and vision, especially in growing animals.


Vitamin A levels in the animal body depend on dietary sources of β-carotene.


The synthesis of this micronutrient does not occur in vertebrates. 


Therefore, it has been reported that vitamin A deficiency could occur more often in winter or spring, when the animal diet might lack green plants which are the main source of β-carotene.


Vitamin A deficiency 


The clinical signs of hypovitaminosis A include:


In Sheep and Cattle: 


The sheep and cattle with vitamin A deficiency Show:


  • poor weight gain, convulsions, diarrhea, and blindness in calves.


  • Convulsions, ataxia, and blindness in adult cattle.


  • Keratinization, which breaks down the protective functions of epithelial cells in the digestive, respiratory, urinary, and reproductive tracts. This leads to a higher susceptibility to infections.


  • Nasal discharge and excess tears from the eyes.


  • Poor conception rates and infertility, due to low quality of semen in males, and the disability of females to conceive and maintain pregnancies.


  • Stillbirths, Abortions, Retained placentas.


  • Microphthalmia (small, incompletely developed eyes) in calves born to deficient mothers.


  • Calves and lambs that may be malformed or born weak and unable to stand. 


In poultry:


Loss of appetite and decreased growth rate followed by general weakness, staggering gait, nasal discharge, sneezing, periorbital swelling, conjunctivitis, dyspnea, polyuria and polydipsia, poor feather quality, feather picking, and anorexia.


Birds become more susceptible to infection, and both egg production and hatchability are markedly reduced.


In dogs:


Their skin and coat do not look healthy, or they may suffer from night blindness.  


Muscles will deteriorate, and your dog will feel weak. 


Vitamin A is especially important for pregnant females and puppies because growing puppies require it for growth, muscle, and neurological development.



Q2:Write briefly on general steps for diagnosis of trace mineral deficiency diseases in farm animals.


 

Appropriate diagnosis of mineral status involves:

  • Thorough evaluation of groups of animals. 

The evaluation should include a thorough health history, feeding history, supplementation history, and analysis of several animals for their mineral status.

  • Clinical signs that would lead you to suspect a mineral deficiency include the following:

    • Copper deficiency : rough coat, faded coat, poor growth, and diarrhea.

 

  • Selenium deficiency, including: stiff-legged gait, poor growth, and sudden death.

 

  • Cobalt deficiency: ill-thrift and emaciation.

 

  • Phosphorus deficiency: pica (eating bones and other rubbish), poor growth, soft bones and fractures, infertility, and post-calving red water.

 

  • Observing the response to nutritional therapy.


  • Live Animal Sampling:

 

A variety of samples are available from live animals that can be analyzed for mineral content. 

 

The most common samples from live animals are serum and whole blood.


  • Pasture samples and soil samples can also be useful in the diagnosis of mineral deficiencies. 


  • Post-Mortem Animal  Sampling:

A variety of post-mortem animal samples are available that can be analyzed for mineral content. 

 

The most common tissue analyzed for mineral content is the liver, as it is the primary storage organ for

many of the essential minerals. 

 

In addition, bone is used as the primary storage organ for calcium, phosphorus, and magnesium.  

 

Other post-mortem samples that can be beneficial in diagnosing mineral deficiencies include urine and ocular fluid.

 

 

 

Q3:Write on clinical signs of cobalt deficiency in sheep.



Cobalt is required by the ruminant for the synthesis of Vitamin B12 – Cobalamin – by the ruminal microflora. 


Vitamin B12 is an essential nutrient for carbohydrate metabolism and protein synthesis, and is important for the production of red blood cells and nervous system function.

 

Clinical signs of Cobalt deficiency :

Different clinical signs can be shown, including:


  • Lethargy, reduced appetite, poor quality wool with an open fleece, small size, and poor body condition despite adequate nutrition. 


  • There may be tear staining of the cheeks, and pale mucous membranes (eyes) develop after several months. 


  • In severe cases of cobalt deficiency (referred to as ovine white liver syndrome) lambs present with nervous signs including depression, head pressing, and aimless wandering.


  • Less common in adults but is reported to cause reduced fertility and poor mothering ability.


Q4:What is the treatment of iodine deficiency in sheep?

A severe deficiency of iodine causes a lack of essential thyroid hormone production and goiter.

Treatment of iodine deficiency in sheep:

  • Managerial Precautions:

If practical, avoid grazing pregnant livestock over (at risk areas) such as the sandier soil types, especially during the latter half of pregnancy.


  • Pasture iodine intake:


The iodine intake from pasture is lowest in winter, as the requirement of the pregnant animals is highest.

 

Iodine deficiency is likely to cause goitre in spring born lambs.

Because of the heavy autumn rains and lush pasture growth are in autumn and winter.

Goiter can be treated by painting the teats of cows, goats, ewes, and sows with tincture of iodine or an iodophor teat dip once daily for 2 weeks.

This will allow the suckling animals to obtain enough iodine to control the  goitres' development. In

As goats have a higher requirement for iodine, it has become a standard recommendation that pregnant does grazing in high rainfall areas receive a drench of supplementary iodine once or, in some cases twice, during the last two months of their pregnancy.

 

Iodine supplementation of ewes depends on the region and seasonal conditions.

 

Treatment of affected kids and lambs with iodine or thyroxine tablets is rarely useful, and it is far more effective to ensure adequate iodine nutrition of the foetus.

  • DRENCHES:

The drench is made up by dissolving 28 gm of potassium iodide in one litre of water. Each doe should receive 10 ml.

 

Iodine is highly volatile, and it is important to mix the drench just before use.

 

iodised salt licks and feed supplements containing iodine may not  prevent the problem because some animals avoid licks and it is impossible to accurately gauge intake with these systems.

 

Drenching is cheap and accurate and can even be combined with some worm drenches, although it is wise to check this with the manufacturer.

 

Q5:Enumerate clinical signs of thiamine deficiency in calves.

Thiamine, also known as vitamin B1, is normally produced by bacteria in the rumen of cattle and sheep on well-balanced roughage diets.

 

Thiamine deficiency reduces energy availability to the brain, which leads to a type of brain degeneration called polioencephalomalacia (PEM).

Thiamine deficiency in the young dairy calves is characterized by :

  • Weakness, incoordination of legs, convulsions and head retraction, and in some calves, by severe scouring, anorexia and dehydration.

Finally, follow DR.provet for more Q&A that support all veterinary students.


Written by: Dr. Mai Foda


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