Treatment of an intramammary bacterial infection with 25-hydroxyvitamin D(3)

Abstract

Deficiency of serum levels of 25-hydroxyvitamin D(3) has been correlated with increased risk of infectious diseases such as tuberculosis and influenza. A plausible reason for this association is that expression of genes encoding important antimicrobial proteins depends on concentrations of 1,25-dihydroxyvitamin D(3) produced by activated immune cells at sites of infection, and that synthesis of 1,25-dihydroxyvitamin D(3) is dependent on the availability of 25-hydroxyvitamin D(3). Thus, increasing the availability of 25(OH)D(3) for immune cell synthesis of 1,25-dihydroxyvitamin D(3) at sites of infection has been hypothesized to aid in clearance of the infection. This report details the treatment of an acute intramammary infection with infusion of 25-hydroxyvitamin D(3) to the site of infection. Ten lactating cows were infected with in one quarter of their mammary glands. Half of the animals were treated intramammary with 25-hydroxyvitamin D(3). The 25-hydroxyvitamin D(3) treated animal showed significantly lower bacterial counts in milk and showed reduced symptomatic affects of the mastitis. It is significant that treatment with 25-hydroxyvitamin D(3) reduced the severity of an acute bacterial infection. This finding suggested a significant non-antibiotic complimentary role for 25-hydroxyvitamin D(3) in the treatment of infections in compartments naturally low in 25-hydroxyvitamin D(3) such as the mammary gland and by extension, possibly upper respiratory tract infections.

Figure 1. Bacterial Counts in Control and 25(OH)D₃ Treated Animals.

Ten dairy cattle were infused with approximately 500 cfu of S. uberis in one quarter of their mammary gland. Five cows were immediately treated with 100 ug of 25(OH)D₃ in FBS and the remain five cows were treated with FBS alone. Cows were subsequently treated after each milking (twice daily) with 25(OH)D₃ or FBS for 10 milkings (5 days). Milk sample were isolated from each cow and serially diluted and plated on blood agar plates. Average bacterial counts were determined for 25(OH)D₃ treated (υ) and control animals(ν). Time points with statistically significant differences are indicated with (*).

Figure 2. Rectal Temperature in Control and 25(OH)D₃ Treated Animals.

Rectal temperature were taken twice daily, at each milking, and the average was determined for 25(OH)D₃ treated (υ) and control animals(ν).

Figure 3. Somatic Cell Counts in Control and 25(OH)D₃ Treated Animals.

Milk samples for somatic cells counts (SCC) were taken at each milking and sent to a DHIA facility for counting. The average SCC were determined for 25(OH)D₃ treated (υ) and control animals(ν).

Figure 4. Bovine Serum Albumin in Milk of Control and 25(OH)D₃ Treated Animals.

Milk samples were tested for BSA levels at each time point and the average was determined for 25(OH)D₃ treated (υ) and control animals(ν).

Figure 5. Feed Intake in Control and 25(OH)D₃ Treated Animals.

Daily feed intake was determined for each cow. Data are expressed as a percentage of the pre-infections (the average of the 4 days feed intake prior to infection). Each the average was determined for 25(OH)D₃ treated (υ) and control animals(ν).

Figure 6. Milk Production in Control and 25(OH)D₃ Treated Animals.

Daily milk production was determined for each cow. Data are expressed as a percentage of the pre-infections (the average of the 4 days milk production prior to infection). Each the average was determined for 25(OH)D₃ treated (υ) and control animals(ν). Repeated measures analysis showed a significant treatment x time effect.