MANGANESE DEFICIENCYA

Dietary deficiency of manganese (Mn) can cause skeletal deformities,

both congenitally and after birth, and infertility. Fig. 15-14 Degenerative

joint disease (arrow) affecting P2 to P3 of a calf.

(Reproducedwithpermission.6)

ETIOLOGYA

Primary deficiency occurs endemically in some areas because of a

geological deficiency of manganese in the local rock formations. Apart

from a primary dietary deficiency of manganese, the existence of factors

depressing the availability of ingested manganese is suspected. An excess

of calcium and/or phosphorus in the diet increases the requiremints of

manganese in the diet of calves and is considered to reduce the

availability of dietary manganese to cattle generally. Congenital

chondrodystrophy in calves has been associated with a manganese

deficiency, and there are outbreaks of congenital skeletal defects in calves

-suspected to be attributable to manganese deficiency.1

EPIDEMIOLOGY

Soils containing less than 3mg/kg of manganese are unlikely to be able to

support normal fertility in cattle. In areas where manganese responsive

infertility occurs, soils on farms with infertility problems have contained

less than 3mg/kg of manganese, whereas soils on neighboring farms with

no infertility problems have had levels of more than 9mg/kg. A secondary

soil deficiency is thought to occur, and one of the factors suspected of

reducing the availability of manganese in the soil to plants is high

alkalinity. Heavy liming is associated with manganese-responsive

infertility. There are three main soil types on which the disease

occurs:•Soils low in manganese, which have low output even when pH is

less than 5.5•Sandy soils, where availability starts to fall Heavy soils,

where availability starts to fall at a pH of 7.0Many other factors are

suggested as reducing the availability of soil manganese, but the evidence

is not conclusive. For example, heavy liming of soils to neutralize sulfur

dioxide emissions from a neighboring smelter is thought to have reduced

the manganese intake of grazing animals. Herbage on low-manganese

soils, or on marginal soils where availability is decreased (possibly even

soils with normal manganese content), is low in manganese. A number of

figures are given for critical levels. It is sug-gested that pasture containing

less than 80mg/kg of manganese is incapable of sup-porting normal

bovine fertility, and that herbage containing less than 50mg/kg is often

associated with infertility and anestrus. The Agricultural Research

Council believes that although definite figures are not avail-able, levels of

40mg/kg DM in the diet should be adequate. Other authors state that

rations containing less than 20mg/kg DM may cause anestrus and

reduction in conception rates in cows and the production of poor-quality

semen by bulls. Most pasture contains 50 to 100mg/kg DM. Skeletal

deformities in calves occur when the deficiency is much greater that just

noted; for example, a diet containing more than 200mg/kg DM is

considered to be sufficient to prevent them. Rations fed to pigs usually

contain more than 20mg/kg DM of manganese, and deficiency is unlikely

unless there is interference with manganese metabolism by other

substances. There are important variations in the manganese content of

seeds, an important matter in poultry nutrition. Maize and barley have the

lowest content. Wheat or oats have 3 to 5 times as much, and bran and

pollard are the richest natural sources, with 10 to 20 times the content of

maize or wheat. Cows’ milk is exceptionally low in manganese. Diets

high in iron reduce duodenal activity of manganese transporters in calves,

although the clinical importance of this finding is unclear.4

PATHOGENESIS

Manganese plays an active role in bone-matrix formation and in the

synthesis of chondroitin sulfate, which is responsible for maintaining the

rigidity of connective tissue. In manganese deficiency, these are affected

deleteriously, and skeletal abnormalities result. Only 1% of manganese is

absorbed from the diet, and the liver removes most of it, leaving very low

.blood levels of the element

CLINICAL FINDINGS

In cattle, the common syndromes in con-firmed or suspected manganese

deficiency are infertility, stillbirth, perinatal loss, calves with congenital

limb deformities, and calves that manifest poor growth, dry coat, and loss

of coat color.2,3 The deformities include knuckling over at the fetlocks,

enlarged joints, and, possibly, twisting of the legs. The bones of affected

lambs are shorter and weaker than normal, and there are signs of joint

pain, hopping gait, and reluctance to move.Heifers fed a low-manganese

diet (16mg Mn per kg DM of diet) during pregnancy had impaired fetal

growth and development evident as lower birth weight than calves from

heifers fed 50mg of Mn per kg DM, superior brachygnathism,

unsteadiness, dis-proportionate dwarfism, and swollen joints.5A severe

congenital chondrodystrophy in Charolais calves occurred on one farm.

The limbs were shortened and the joints enlarged. The pregnant cows

were fed on apple pulp and corn silage, both of which were low in

manganese.An outbreak of congenital skeletal mal-formations in Holstein

calves was character-ized clinically by small birth weights (average

15kg). Abnormalities included joint laxity, doming of the foreheads,

superior brachyg-nathia, and a dwarflike appearance as a result of the

short length of the long bones. The features of the head were similar to

those of the wildebeest. The majority of affected calves were dyspneic at

birth, and snorting and grunting respiratory sounds were common.

Affected calves failed to thrive, and most were culled because of poor

performance. A manganese-responsive infertility has been described in

ewes and is well known in cattle. In cattle, it is manifested by slowness to

exhibit estrus and failure to conceive, often accompanied by subnormal

size of one or both ovaries. Sub estrus and weak estrus have also been

observed. Functional infertility was once thought to occur in cattle on

diets with calcium-to-phosphorus ratios outside the range of 1:2 to 2:1.

This was not upheld on investigation but might have been correct if high

calcium-to-phosphorus intakes directly reduced manganese (or copper or

iodine) availability in diets marginally deficient in one or other of these

elements. In pigs, experimental diets low in manganese cause reduction in

skeletal growth; muscle weakness; obesity; irregular, diminished, or

absent estrus; agalactia; and desorption of fetuses or the birth of stillborn

pigs. Leg weakness, bowing of the front legs, and shortening of bones

.also occur

CLINICAL PATHOLOGY

The blood of normal cattle contains 18 to 19μg/dL (3.3 to 3.5μmol/L) of

Mn, although considerably lower levels are sometimes quoted. The livers

of normal cattle contain 12mg/kg (0.21mmol/kg) of Mn and down to

8mg/kg (0.15mmol/kg) in newborn calves, which also have a lower

content in hair. The Mn content of hair varies with intake. The normal

level is about 12mg/kg (0.21mmol/kg), and infertility is observed in

association with levels of less than 8mg/kg (0.15mmol/kg). In normal

cows, the Mn content of hair falls during pregnancy from normal levels

of 12mg/kg (0.21mmol/kg) in the first month of pregnancy to 4.5mg/kg

(0.08mmol/kg) at calving. All of these figures require much more critical

evaluation than they have received before they can be used as diagnostic

tests.Although tissue manganese levels in normal animals have been

described as being between 2 and 4mg/kg (0.04 and 0.07mmol/kg), in

most tissue there appears to be more variation between tissues than this.

However, tissue levels of manganese do not appear to be depressed in

deficient animals, except for in the ovaries, in which levels of 0.6mg/kg

(0.01mmol/kg) and 0.85mg/kg (0.02mmol/kg) are recorded in contrast to

a normal level of 2mg/kg (0.04mmol/kg).Thus, there is no simple, single

diagnostic test permitting detection of manganese deficiency in animals.

Reproductive functions, male and female, are most sensitive to

manganese deficiency and are affected before possible biochemical

criteria (e.g., blood and bone alkaline phosphatase, and liver arginase

levels) are significantly changed. The only certain way of detecting

moderate deficiency states is by measuring response to supplementation.

Clinical finings in response to treatment that may provide contributory

evidence of manganese deficiency