of the SAVA
Musculoskeletal degeneration and skeletal
abnormalities are associated with manganese
deficiency, particularly in neonatal animals. A
deficiency of manganese causes decreased
production and increased degradation of cartilage in
neonates resulting in skeletal deformities including
congenital joint laxity, dwarfism (in-utero growth
retardation), congenital spinal defects and congenital
chondrodystrophy. Adult animals usually do not
show any external signs of manganese deficiency,
but neonates born to dams fed manganese deficient
rations during pregnancy, may show various degrees
of skeletal deformity.
Iron excesses are far more prevalent than iron
deficiencies. Excess dietary iron can induce iron
overload disorders as well as interfering with
copper absorption. Pathology is characterized by
accumulation of iron pigments predominantly in
the liver associated with hepatic degeneration and
Bone tissue is the tissue of choice for analysis of
calcium, phosphorus, magnesium and fluoride
levels at post-mortem. Buffered formalin contains
phosphate buffered saline and so interferes with the
phosphorus levels recorded on bone tissue preserved
in 10% buffered formalin. 10% formalin prepared
with de-ionized water is suitable for bone fixation
for mineral analysis, but is impractical in the field
for wildlife veterinarians. Therefore, collection of
fresh bone material (rib bone), which is transported
on ice is the more practical option. Fixation in de-
ionized water formalin can then be performed at the
laboratory on reception of the samples.
Bone ash analysis for calcium, phosphate and
magnesium is most commonly employed to
investigate metabollic bone disease, while bone
fluoride analysis is more commonly utilized to
investigate potential fluorosis or fluoride deficiency.
Metabolic bone diseases are characterised by failure
of production, mineralization or maintenance of
bone matrix. The classic osteodystrophies include
osteopaenia/osteoporosis, osteomalacia, rickets and
fibrous osteodystrophy. These conditions denote
a continuum of processes that occur due to dietary
Ca/P imbalances, hypovitaminosis D, other trace
mineral deficiencies (copper, manganese, fluoride)
glucocorticoid therapy or physical inactivity.
When investigating metabolic bone disease in young
animals it is always important to collect sections of
long bones, which include the growth plate, into 10%
buffered formalin for histological examination. These
various metabolic imbalances produce characteristic
changes in the ossification process at the growth plate
which facilitates the diagnosis.
1. Keneko et al - Clinical Biochemistry of Do-
mestic Animals 6th edn 2008.
2. Kincaid – Assesment of trace mineral status of ru-
minants: A review. Proceedings of the Ameri-
can Society of Animal Science. 1999; 1-8.
3. Last et al – VDX Laboratory Manual 2nd edn
2010. Vetlink Publications, Pretoria.
4. Maxie – Pathology of Domestic Animals 6th
edn 2016. Saunders-Elsevier, Edinburugh.
5. Njaa – Diagnosis of Abortion and Neonatal Loss 4th edn
2012; Wiley-Blackwell, Chichester, United Kingdom.
6. Orr et al – Investigation of the selenium status of aborted
calves with cardiac failure and myocardial necrosis. Journal
of Veterinary Diagnostic Investigation 1997; 9:172-179.
7. Plumblee – Clinical Veterinary Toxicol-
ogy 2004; Mosby, St Louis, USA.
8. Smith – The effect of preserving liver tissue on the concen-
tration of trace minerals in the liver. Masters Dissertation.
University of Pretoria. 9.
Van Saun et al - Maternal
and fetal selenium concentrations and their interrelation-
ships in dairy cattle. Journal of Nutrition 1989; 119:1128.
10. Waldner & Blakley - Evaluating micronutrient concentra-
tions in liver samples from abortions, stillbirths, and
neonatal and postnatal losses in beef calves. Journal of
Veterinary Diagnostic Investigation 2014 26: 376-389.