Blood, 1951, Vol. 6, No. 10, pp. 867-891.
© 1951 American Society of Hematology, Inc.
Hematologic Manifestations of Vitamin B12 Deficiency
in Swine
BETTY TATTING B.S.1,
JEAN ROBINSON B.S.1,
N. M. FELLOWS M.D.1,
F. D. GUNN M.D.1, and
M. M. WINTROBE M.D.1
1 Departments of Medicine, Surgery and Pathology, College of Medicine, University of Utah, Salt Lake City, Utah.
In an effort to produce a deficiency of vitamin B12 a total of 70 pigs were fed
a purified diet containing soybean alpha protein in place of casein. One group of
animals was started on the diet at 2 to 7 days of age. A second group began at
21 to 28 days of age. Methionine, iodinate casein, desiccated thyroid and
pteroylglutamic acid were added to the diet of certain animals and! omitted from
the diet of other pigs. In addition, 9 pigs were gastrectomized. Forty-three of
the animals survived for a sufficiently long period of time for adequate evaluation of the results of the experiment.
Severe liver damage was observed in 24 of the 25 animals autopsied. The only
animal not showing liver damage received vitamin B12 from the beginning of
the experiment. Necrosis of the liver cells, fatty infiltration, or both, occurred in
the presence of a high fat diet containing apparently adequate amounts of
protein, choline, vitamin E and methionine. These pathologic changes were
apparently prevented but not reversed by the administration of vitamin B12.
Growth of the animals on the above diets without added vitamin B12 was
retarded as compared with the growth of animals on the same diet supplemented
with this vitamin. The administration of vitamin B12 to the deficient animals
resulted in rapid growth.
Of the 39 animals not receiving vitamin B12 13 failed to develop anemia, 16
developed a mild anemia and in 10 a moderately severe anemia was present.
When present the anemia was normocytic and in 24 pigs was accompanied by
a moderately severe neutropenia. Differential cell counts on the sternal marrow
were normal except for a slight increase in the proportion of normoblasts. These
hematologic alterations were neither consistently or completely corrected by
the administration of vitamin B12 in spite of the fact that definite and sometimes
marked reticulocyte increases followed.
When methionine deficiency was associated with vitamin B12 deficiency, anemia
appeared to be more severe.
The administration of aureomycin, an "animal protein factor," did not
stimulate growth and failed to induce a hemopoietic response.
There was no macrocytic anemia, the bone marrow was not megaloblastic,
and neurologic disturbances or morphologic alterations in the neutrophils were
not observed.
These results are in contrast to those obtained in pigs with an experimentally
produced deficiency of pteroylglutamic acid. Such animals develop macrocytic
anemia, leukopenia and a macronormoblastic type of bone marrow.
It is not possible to give with any assurance the reason why megaloblastic
anemia was not produced in the "B12-deficient" animals. This may have been
due to the fact that (1) the deficiency was not sufficiently severe to result in
such a change in the hemopoietic system; or (2) because pteroylglutamic acid
prevents the development of megaloblastic anemia even in the absence of
vitamin B12.
Submitted on March 5, 1951
Accepted on March 28, 1951
