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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 5  |  Issue : 1  |  Page : 94-97

Therapeutic management of hypovitaminosis A and zinc deficiency in a lactating cow from a small dairy herd in muranga county, Kenya


Department of Public Health, Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Nairobi, Nairobi, Kenya

Date of Submission21-Dec-2020
Date of Acceptance13-Feb-2021
Date of Web Publication13-Mar-2021

Correspondence Address:
Dr. Joseph Mwanzia Nguta
Department of Public Health, Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Nairobi, P.O Box: 29053-00625, Nairobi
Kenya
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/bbrj.bbrj_221_20

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  Abstract 


Background: Hypovitaminosis A and zinc deficiency were diagnosed in a 7-year-old Friesian cow from a small milking herd comprising of thirty Friesian cows in a zero grazing unit in Muranga County in Kenya, on Friday, November 15, 2019. The cow was weighing approximately 500 kilograms and had calved four months ago. The daily production of milk was tweny five litres. The cow had a history of sudden inappetance, reduced weight, sternal recumbency, convulsions and heavy lacrymation. Clinical examination revealed slight clouding of the cornea, and dilated pupils which did not respond to light. The menace response was almost absent but palperal and corneal reflexes were present. The cow was not apparently blind. Methods: The clinical examination of the skin revealed a fungal infection. Skin scrapings and hair from the lesions were examined for fungal species by direct microscopy in 10% KOH and lactophenol. Collected samples were inoculated on mycobiotic agar. The inoculum was incubated at 28°C for two to six weeks and examined for colony formation. Culture examination revealed Trichophyton verrucosum as the cause of dermatophytosis. Blood sample was taken from the cow into a vial containing heparin for spectrophotometric estimation of vitamin A and serum zinc concentrations. Results: Vitamin A and serum zinc concentrations were 5.12 μg/dl and 3.24 μg/L, respectively. The reference serum values for vitamin A are in the range of 15.4 to 32.3 μg/dl, while reference serum zinc levels are in the range of 6-12 μg/L for optimum physiologic functioning in dairy cattle. On the basis of history, clinical examination and significantly low serum vitamin A and zinc levels, the lactating friesian cow was diagnosed to be suffering from combined hypovitaminosis A and zinc deficiency. The dairy cow was therapeutically managed through administration of zinc sulphate orally, at a dosage rate of 1 gram per week for six weeks, administration of vitamin A at a dosage rate of 30,000 international units (IU), deep intramuscularly, once daily for seven days, and intramuscular administration of 3 mls of BelamylR, once daily for seven days. The body parts with lesions caused by T. verrucosum were treated through topical administration of zinc oxide ointment once daily for twenty one days. Following treatment of the lactating cow, significant improvement was observed in terms of disappearance of lachrymation, corneal clouding, sternal recumbency, skin lesions and convulsions. The appetite also returned to normal. All the other cows in the farm were supplemented with vitamin A and zinc. The client was also advised to include fresh napier and bermuda grass in the cattle diet, since they have been shown to contain adequate levels of beta carotene and zinc. Conclusion: In conclusion, zinc and vitamin A supplementation may be of benefit for recovery of cows from sternal recumbency and dermatophytosis.

Keywords: Dairy cows, dermatophytosis, Friesian, hypovitaminosis A, lactation, recumbency, zinc deficiency


How to cite this article:
Nguta JM. Therapeutic management of hypovitaminosis A and zinc deficiency in a lactating cow from a small dairy herd in muranga county, Kenya. Biomed Biotechnol Res J 2021;5:94-7

How to cite this URL:
Nguta JM. Therapeutic management of hypovitaminosis A and zinc deficiency in a lactating cow from a small dairy herd in muranga county, Kenya. Biomed Biotechnol Res J [serial online] 2021 [cited 2021 Apr 11];5:94-7. Available from: https://www.bmbtrj.org/text.asp?2021/5/1/94/311098




  Introduction Top


Vitamin A (retinol) is a fat-soluble, colorless, long chain unsaturated compound with five double bonds. Retinol can exist in different isomeric forms, since it contains double bonds. Oxygen, heat, acids, and light rapidly destroy both Vitamin A and its precursors and carotenoids. The activity of Vitamin A in feeds is substantially reduced by the presence of moisture and trace elements.[1]

The precursors of Vitamin A, the carotenes, occur in different forms in plants, but Vitamin A does not occur in plants. Provitamin A (carotenes) occurs mainly in the green leaves and to a lesser extent in the maize grain. Of particular importance are the four carotenes, alpha-carotene, beta-carotene, gamma-carotene, and cryptoxanthin (the main carotenoid of corn), because of their provitamin A activity. The Vitamin A activity of beta-carotene is significantly greater compared to that of the other carotenoids. As an example, both alpha-carotene and cryptoxanthin are about one-half the conversion rate of beta-carotene to Vitamin A.[2] Carotenoids can be enzymatically transformed to Vitamin A by most species, hence commonly referred to as “provitamin A”. The intestinal mucosa is the primary site of conversion of carotene to retinol. Beta-carotene is cleaved by the enzyme beta-carotene 15, 15′ dioxygenase,[3] yielding one molecule of retinaldehyde, which is enzymatically reduced to retinol. Some animal species, such as cats, are devoid of the enzyme and hence cannot convert carotenoids to retinol. Normal processes of fat digestion and absorption and adequate dietary fat content are required for the absorption and subsequent conversion of beta-carotene to retinol. Supplemental fat has been shown to elevate the plasma levels of beta-carotene in dairy cattle.[4]

Vitamin A is responsible for spermatogenesis and maintenance of pregnancy and supports osteoblastic activity, bone growth, maintenance of epithelial cells, vision, immune cell function, and gene regulation.[5] Pharmacokinetic parameters, such as absorption, distribution, metabolism, liver release, and tissue utilization of retinol, depend on adequate serum zinc levels. Zinc deficiency has been reported to predispose animals to vitamin A deficiency.[6] Trace element zinc plays a regulatory role on retinol distribution mediated through protein synthesis. Decreased synthesis of retinol-binding protein (RBP) in the liver due to zinc deficiency has been associated with low concentrations of RBP in the plasma.[7] It has been reported that retinol (Vitamin A) and zinc also interact through the ubiquitous, oxidative conversion of retinol to retinaldehyde (retinal), a crucial step in the metabolic pathway of retinol that is well described in the visual cycle in the retina of the eye, and requires the action of a zinc-dependent retinol dehydrogenase enzyme.[7]

Trace element zinc is also an essential part of the body's antioxidant defenses that play a critical role in the prevention of free radical-induced cellular and tissue damage.[8] Cattle susceptibility to both inflammatory and infectious conditions increases during zinc deficiency.[9] Both Vitamin A and zinc are important immune boosters in cattle. Vitamin A increases disease resistance and has stimulatory effects on cell-mediated immunity.[10] The prevalence of infectious diseases in cattle, such as fungal infections, as observed in the current case, increases in cattle with Vitamin A and zinc deficiency. Therefore, supplementation of zinc along with Vitamin A in Vitamin A and zinc animals is beneficial. A suspected case of Vitamin A and zinc deficiency in a 7-year-old Friesian cow, 4 months after calving in a herd of thirty dairy cows feeding on silage supplemented with dairy meal and mineral salt block, is reported. The case was reported by the client to the local veterinary personnel approximately 4 h after signs of convulsions and recumbency were noticed.

Methods

The current study was carried out in a small dairy farm in Muranga County, Kenya. Hypovitaminosis A and zinc deficiency were suspected in a 7-year-old Friesian cow from a small milking herd comprising thirty Friesian cows in a zero grazing unit in Muranga County in Kenya, on November 15, 2019. All the cows were fed on silage prepared off-farm and supplemented with HiyieldR dairy meal (Sigma feeds), fed dry at the rate of 4 kg/day, in combination with Josera Frumi PlusR mineral feed (Sigma Feeds) at the rate of 50 g/day. The silage was prepared from maize stalks in Kiambu and Nakuru counties in Kenya. All the cows had been vaccinated against foot and mouth disease, black quarter, and anthrax. Spraying was carried out in a spray race using BimatixR 10% EC (alpha-cypermethrin) regularly. All the cows were dewormed regularly with ValbazenR (albendazole), in accordance with the manufacturer's instructions. The farm reported abortions during the third to the 4th month after conception. A bull was used for breeding due to poor conception rates following artificial insemination. The reported cow was weighing approximately 500 kg and had calved 4 months ago. The daily production of milk was 25 l. The cow had a history of sudden inappetence, reduced weight, sternal recumbency, convulsions, and heavy lachrymation. Examination of the cow clinically revealed corneal clouding and dilated pupils, which, upon exposure to a light source, did not respond. The menace response was almost absent, but both corneal and palpebral reflexes were observed. Apparently, the lactating Friesian cow was not blind. On further examination, it was revealed that the body temperature and pulse rate were within the normal range, but respiration was slightly increased. Following cardiac auscultation, the intensity of the heart sound was found to be decreased. Clinical examination of the skin of the dairy cow revealed wrinkling at the neck and the head, rough dry hair coat, heavy deposition of scales, and alopecia. The lactating cow was not under any medication, either for the treatment of suspected fungal infection or any other condition.

A cotton swab that had been soaked in 70% ethyl alcohol was used for cleaning of the affected skin areas with suspected fungal lesions. Skin and hair scrappings from the lesions were obtained and examined for fungal pathogens by direct microscopy in 10% potassium hydroxide and lactophenol.[11] Samples collected from the cow were inoculated on mycobiotic agar. The inoculum (plates) was incubated at 28°C for 2–6 weeks and later examined for the formation of colonies. Microscopic and macroscopic examination were used to identify the fungal species. The growth characteristics, colony morphology, shape, color, and size were also observed. To remove contaminant fungal species and other agents, fungal colony reverse side morphology was examined, according to the standard protocols.[12] Blood samples for serum Vitamin A and zinc concentrations were aseptically withdrawn from the jugular vein. Blood samples for examination of zinc levels were taken twice, in the morning and also in the evening, whereas the samples for Vitamin A studies were taken once only in the morning. The collected blood samples were centrifuged at 1700 g for 5 min immediately after collection to separate the serum. The sera collected following blood sample centrifugation were stored in plastic tubes at -20°C until analysis. The concentration of zinc in the stored sera was analyzed on a spectrophotometer (Shimadzu 1601) using commercial kit (Randox, United Kingdom). Concentration of serum Vitamin A was determined spectrophotmeterically in accordance with the methodology of Suzuki.[13] Examination of the culture revealed Trichophyton verrucosum (T. verrucosum) as the fungal agent responsible for the observed skin fungal infection, dermatophytosis.


  Results Top


Serum Vitamin A (retinol) and zinc concentration were 5.12 μg/dl (reference values, 15.4–32.3) and 3.24 μg/L (reference values, 6–12), respectively. On the basis of history, clinical examination, and significantly low serum Vitamin A and zinc levels, the lactating Friesian cow was diagnosed to be suffering from combined hypovitaminosis A and zinc deficiency. The dairy cow was therapeutically managed through administration of zinc sulfate orally, at a dosage rate of 1 g/week for 6 weeks, administration of Vitamin A at a dosage rate of 30,000 international units, deep intramuscularly, once daily for 7 days, and intramuscular administration of 3 ml of BelamylR, once daily for 7 days.[14] The body parts with lesions caused by T. verrucosum were treated through topical administration of zinc oxide ointment once daily for 21 days. Following treatment of the lactating cow, significant improvement was observed in terms of disappearance of lachrymation, corneal clouding, sternal recumbency, skin lesions, and convulsions. The appetite also returned to normal. All the other cows in the farm were supplemented with Vitamin A and zinc. The client was also advised to include fresh Napier and Bermuda grass in the cattle diet, since they have been shown to contain adequate levels of beta-carotene and zinc.


  Discussion Top


Deficiency of Vitamin A (retinol) can partly be caused by pharmacokinetic interferences at the level of absorption, distribution, or metabolism to produce low bioavailable fractions and, consequently, low tissue levels of Vitamin A. Alternatively, hypovitaminosis A in dairy cattle can also be associated with absolute deficiency of either Vitamin A or its precursors, mainly beta-carotene in the animal's diet. Chronic hepatic or intestinal illnesses coupled with low serum levels of zinc can also cause secondary Vitamin A deficiency.[15] This observation is in agreement with the findings from the current study, where serum zinc levels were found to be significantly low. Concentration of Vitamin A tends to decrease with storage, and in particular if oxidizing compounds are present. To mitigate this phenomenon, additional amounts of vitamin E are usually added to the feed of dairy animals in an attempt to reduce excessive oxidation. Mineral mixes have been shown to immensely destroy fat-soluble vitamins, especially Vitamin A. Premixing vitamins and minerals may decrease the quantity of Vitamin A availability to dairy cattle. This could be the possible cause of low Vitamin A levels in the lactating cow in the current study, since it was fed on stored silage and supplemented with fifty grams of mineral and vitamin premixes on daily basis. The pharmacokinetics of Vitamin A, including absorption, distribution, metabolism, release from the liver cells, cellular, and tissue utilization, may in part depend on adequate serum zinc levels. Low serum levels of Vitamin A may interfere with absorption and lymphatic zinc transport by inducing changes in synthetic pathways of a zinc-dependent binding protein.[10] These observations are in agreement with the findings from the present study since serum Vitamin A and zinc levels were significantly low.

Dermatophytosis caused by a Trichophyton verrucosum, a filamentous fungi, is a superficial skin infection in cattle associated with huge losses and is widely distributed globally.[16] Increased cattle susceptibility to the fungal infection is associated with low serum levels of specific nutrients, which, in turn, lower immune responses with resultant increased susceptibility to infectious conditions.[17] The fungal infection in the reported case could have been caused by low serum zinc and Vitamin A levels, since therapeutic administration reversed the disease process.

Zinc is an important trace element and a key component of the body's antioxidant defense system that plays a crucial role in the prevention of cellular and tissue damage associated with free radicals.[18] The function of a number of inflammatory products in the regulation of balanced zinc concentrations has been discussed in detail.[12] Increased metallothionein synthesis in the liver and other tissues induces phagocytic activation, with consequent release of cytokines such as interleukins (IL) 1 and 2, causing decreased serum zinc concentrations.[13] Metallothionein synthesis has been shown to be an efficient mechanism for hepatic elimination of zinc.[13] The current study did not investigate hepatic metallothionein levels, but low serum zinc levels observed in the current study could be associated with increased hepatic synthesis of metallothionein.[6] Low circulating levels of the trace element zinc have been reported in a number of inflammatory and infectious disease conditions.[19] The current observation of a skin fungal infection caused by Trichophyton verrucosum in a lactating cow with significantly low zinc levels is in support of the previous observations in regard to the relationship between low serum zinc levels and susceptibility to infectious conditions in cattle. Low serum zinc levels have also been reported in dogs with skin dermatoses.[20] This observation is in consonance with the observations in the current study. The current study reported dermatophyte infection in a lactating cow with significantly low serum zinc levels, a finding which supports earlier observations.[21] The observed low serum zinc levels could negatively affect the normal functioning of the immune system in the lactating cow, facilitating skin lesions associated with dermatophyte infection.[21] Earlier reports have suggested that circulating zinc concentrations in a lactating cow could be related to the diet that the cow is being exposed to,[21] but the current study did not investigate zinc levels in the silage and supplemented feed, since it is the bioavailable zinc fraction that is responsible for maintenance of optimum physiologic functions in the cow.

Retinol (Vitamin A) is involved in maintenance of epithelial cells, vision, immune cell function, spermatogenesis, and maintenance of pregnancy and supports osteoblastic activity, bone growth, and gene regulation.[22] It has been reported that retinol serum concentrations are altered by different infections.[22] These changes are partly caused by released cytokines, such as IL-1 and IL-2, which are components of the defense strategies of the affected animal.[10] Vitamin A-deficient cattle have been found to be more prone to different types of infectious conditions.[23] The current study reported significantly low Vitamin A levels in a lactating cow with a fungal skin infection, thus supporting earlier observations. The observed low serum Vitamin A levels could in part be due to the dermatophyte infection. During infectious disease states, the combined release of IL-1 from macrophages and IL-2 from lymphocytes plays a central role in metallothionein release and, subsequently, decreased hepatic levels of Vitamin A.[22]

The potential dependence of Vitamin A on zinc levels has been explained by two mechanisms. The first mechanism, mediated through protein synthesis, postulates the regulatory role of zinc on the distribution of retinol (Vitamin A). The synthesis of RBP in the liver can be depressed by low serum levels of zinc, resulting in low RBP levels in the plasma, and, consequently, interferences in zinc transport and cellular and tissue deficiencies of Vitamin A. The second mechanism involves the role of zinc in the metabolic pathway of Vitamin A, in the ubiquitous, oxidative conversion of Vitamin A to retinaldehyde, a pathway well described in the visual cycle in the retina of the eye. This pathway requires catalysis by a zinc-dependent retinol dehydrogenase enzyme.[7]


  Conclusion Top


Zinc and Vitamin A supplementation may be of benefit for the recovery of dermatophytosis as well as antifungal therapy.

Acknowledgments

Special thanks are to the local veterinarian for his kindness and his input in this project.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Olson J. Vitamin A. In: Machlin L, editor. The Handbook of Vitamins. New York: Marcel Dekker; 1984. p. 1-43.  Back to cited text no. 1
    
2.
Tanumihardjo S. Vitamin A fortification efforts require accurate monitoring of population vitamin A status to prevent excessive intakes. Procedia Chem 2015;14:398-407.  Back to cited text no. 2
    
3.
Bauernfeind J. Carotenoids as Colorantsand Vitamin A Precursors. New York: Academic Press; 1981.  Back to cited text no. 3
    
4.
Weiss S, Lai K, Patel S. Retinyl ester hydrolysisand retinol efflux from BFC- 1B adipocytes. J Biol Chem 1997;272:1459-65.  Back to cited text no. 4
    
5.
Chew B. Vitamin A and β-carotene in host defence. J Dairy Sci 1983;70:2732.  Back to cited text no. 5
    
6.
Serdar P, Funda K. Serum zinc and vitamin A concentrations in calves with dermatophytosis. Kafkas Üniv Vet Fak Derg 2009;15:1.  Back to cited text no. 6
    
7.
Christian P, West K. Interaction between zinc and vitamin A: An update. Am J Clin Nutr 1998;68:435-41.  Back to cited text no. 7
    
8.
Anand K, Srinivas C, Dananjay S, Harsha K, Dhoolapas S. Zinc deficiency in two calves. Indian Vet J 2005;85:768-9.  Back to cited text no. 8
    
9.
Oteiza PI, Olin KL, Fraga CG, Keen CL. Zinc deficiency causes oxidative damage to proteins, lipids and DNA in rat testes. J Nutr 1995;125:823-9.  Back to cited text no. 9
    
10.
Bendich A. Physiological role of antioxidant in the immune system. J Dairy Sci 1993;76:2789-94.  Back to cited text no. 10
    
11.
Halley D, Standard P. Laboratory Methods in Medical Mycology. 3rd ed. Atlanta, USA: US Depeartment of Health, Education and Welfare Center of Disease Control; 1973. p. 41-57.  Back to cited text no. 11
    
12.
Klassing G. Nutritional aspects of leukocytic cytokins. J Nutr 1988;118:1435-43.  Back to cited text no. 12
    
13.
Swenson G, Hallgren R, Johansen E, Lindth U. Reduced zinc in peripheral blood cells from patients with inflammatory connective tissue disease. Inflammation 1985;9:189-99.  Back to cited text no. 13
    
14.
Quinn P, Carter M, Markey B, Carter G. Clinical Veterinary Microbiology. 1st ed.. London, UK: Wolfe Publishing; 1994. p. 1164-7.  Back to cited text no. 14
    
15.
Radostits O, Clive C, Gay C, Blood D, Kenneth W. Veterinary Medicine: A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses. Published by Saunders; 2000.  Back to cited text no. 15
    
16.
Piero D. Zoonotic dermatitides. Acta Clin Croatica 2003;42:139-49.  Back to cited text no. 16
    
17.
Beisel W. Single nutrients and immunity. Am J Clin Nutr 1982;35:417.  Back to cited text no. 17
    
18.
Evans P, Halliwell B. Micronutrients: oxidant/antioxidant status. Br J Nutr 2001;85 Suppl 2:S67-74.  Back to cited text no. 18
    
19.
Naresh R, Dwivedi S, Swarup D, Dey S. Zinc, copper, and cobalt concentrations in blood during inflammation of mammary gland in dairy cows. Asian Aust J Anim Sci 2001;14:564-6.  Back to cited text no. 19
    
20.
Van den Broek A, Stafford W. Diagnostic value of zinc concentrations in serum leucocytes and hair dogs with zinc-responsive dermatitis. Res Vet Sci 1988;44:414.  Back to cited text no. 20
    
21.
Nisbet C, Yarim GF, Ciftci G, Arslan HH, Ciftci A. Effects of trichophytosis on serum zinc levels in calves. Biol Trace Elem Res 2006;113:273-80.  Back to cited text no. 21
    
22.
Chew B. Vitamin A and β-carotene in host defence. J Dairy Sci 1987;70:2732-43.  Back to cited text no. 22
    
23.
Spears JW. Micronutrients and immune function in cattle. Proc Nutr Soc 2000;59:587-94.  Back to cited text no. 23
    




 

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