Download RIBOFLAVIN DEFICIENCY IN BABY PIGS W. P. LEHRI,:R, JR. AND

RIBOFLAVIN D E F I C I E N C Y IN BABY PIGS ~
W. P. LEHRI,:R,JR. AND A. C. WIESE'-'
University of Idaho a
Mitchell, and Kolb (1938) learned that symptoms
W ofINTROBE,
a vitamin B-complex deficiency in suckling pigs could be
temporarily relieved by the administration of crystalline riboflavin.
Hughes (1938, 1939) made similar observations upon pigs of a more
advanced age. Wintrobe (1939) reported some growth response when
suckling pigs on a vitamin deficient ration were given riboflavin.
Hughes (1940) found the mininmm riboflavin reqtfirementfor pigs to
be 1.0 to 3.0 mg. per 100 pounds of body weight. This determination
was made on pigs weighing approximately 40 pounds at the beginning
of the experimental period.
Wintrobe et al (1944) reported that riboflavin deficiency in young
pigs was associated with growth impairment; rough, dry and thin hair
coats; a mottled erythematous eruption together with scaling a n d
ulceration of the skin; lens opacities; normocytic anemia; and abnormal
gait. Krider, Terrill, and Van Pouche (1949) reported that 1.4 mg. of
riboflavin per pound of ration appears to be the practical minimum for
weanling pigs. Mitchell and associates (1950) report that for the
growing suckling pig the estimated riboflavin requirement is 1.2 to 2.3
nag. per kg. of diet.
The trials reported here were undertaken to observe a riboflavin
deficiency in the young suckling pig and to note the response to riboflavin supplementation.
Experimental
Two separate groups of Duroc pigs, 48 hours old, were used as
experimental animals in both trials I and II. The four pigs in each
1 Published with tile approval of the Director of the Idaho Agricultural Experiment Station as
Research Paper No. 345.
o ])epartments of Animal Husbandry and Agricultural Chemistry.
s We wi.~h to ackr~owledge the ~sistance of W. V. Hartweli and R. V. Dahlstrom who helped care
for animals used in the experinaent. Credit is due l)r. L. H. Scrivner and Dr. W. B. Ardrey for
assistance with post murtem studies.
We are also indebted to Merck and Cmnpany, Rabway, New J e r ~ y , through the courtesy of
Dr. 1). F. Green, for supplies of thiamin, riboflavin, pyridoxiue, nicotinic acid, inositol, choline,
p-Aminobenzoic acid. biotin, calcium pantothenate and tocopherol: tu Lederle Laboratories Inc.,
Pearl River, New York, through the courtesy of Dr. E. R. L. Stockstad, for pteruyl-glutamic acid;
to E. I. du Pont de .N,'elnours and Company, New Brunswick. New Jer.~v. through the courtesy
of Dr. S. Waddell, for crystalline vitamin I)a.
RIBOFLAVIN DEFICIENCY IN BABY PIGS
245
trial were litter mates. T h e y were kept in individual metal cages 2.5 b y
2.5 feet in size, equipped with wire mesh bottoms and underlying
screens to facilitate the separation of urine and feces. The experimental
diet was a "synthetic milk" having the composition given in table 1
and containing no riboflavin. The control animals were fed this ration
plus 0.6S rag. riboflavin per kg. "synthetic milk". For complete details
TABLE 1. COMPOSITION OF RATION I
Component
Casein (Labco)
Cerelose
Lard
Salts 2
Percent
30.0
37.4
26.6
6.0
Vitamins Added a
Thiamin
Calcium Pantothenate
Nicotinic Acid
Inositol
Choline
p-Aminobenzoic Acid
Pteroylglutamic Acid
Biotin
Pyridoxine
Alpha-tocopherol
2-methyl-I, 4-naphthoquinone
Vitamin A
Vitamin D
Mg. per
Kg. Milk
0.65
1.30
2.50
26.00
260.00
2.60
0.052
0.01
0.65
1.00
0.28
2,000 I.U./kg.
200 I.U./kg.
1The lard was homogenized with the solution of casein, cerelose and ~lts to produce an
emulsinncontaining13 percent solids.
2 Modified salt mixture of Phillips and Ilart (1935).
a Control animalsalso received 0.65 rag. riboflavin!:)erkg. liquid diet.
concerning the preparation of this diet see Wiese, et al (1947). The
feeding, care, and diet modifications for baby pigs were the same as
that described by Lehrer et al, (1949).
R e s u l t s and D i s c u s s i o n
Signs of nutritional deficiency became apparent within the first one
to two weeks of these experiments. The animals failed to gain in weight
and lost their appetite and normal appearance. Their hair coats and
s k i n - - a t first clean, smooth, and sleek--became thin, coarse and
u n t h r i f t y in appearance. The skin became dry and scaly and hair fell
out readily. As the trials progressed, diarrhea and scours, prevalent in
all deficient animals, became very severe and in some cases ultimatley
resulted in rectal hemorrhaging and inflammation of the anus. Animals
also exhibited an apparent sensitivity to light. All the above symptoms,
246
W. ]'. LEItRER,
JR.
AND A. C. WIESE
with the exception of rectal hemorrhaging and inflammation of anal
mucosa, were reported by Wintrobe, Buschke, Follis, and Humphreys
(1944). These workers reported lens opacities after pigs had been on
a riboflavin-deficient diet for 96 days. This eye abnormality may have
been similar to the condition noted in animals reported in these trials.
An abnormal gait was noted after animals had been on the experimental diet for four weeks. A longitudinal cracking of feet was observed.
The gaits of the pigs appeared stiff, mincing, and hesistant; at times
CONTROL
5C
4~
4C
3~
37
L
J/
AGE IN WEEKS
z/0NE~
~EEK
Figure 3. Growth rate of pigs on riboflavin deficient diet. The arrows
indicate supplementation of riboflavin, the cross shows when pig 35 died.
they walked on the tips of the hoofs. These findings coincide with the
report of Wintrobe, Buschke, Follis, and Humphreys (1944), who
started pigs on a riboflavin deficient diet at 21 days of age.
The slow rate of growth (figure 3) and low dietary intake are consistent with the findings of Mitchell, Johnson, Hamilton, and Haines
(1950).
Estimation of the urinary excretion of riboflavin with riboflavindeficient animals was impossible because of continual scouring and
subsequent contamination of samples with fecal material.
RIBOFLAVIN DEFICIENCY IN BABY PIGS
247
Figure 1 shows poor growth, unthrifty appearance and rough thin
hair of pig 37 after being on the riboflavin deficient diet for 32 days.
A comparison of pig 38 and its normal control litter mate receiving
adequate amounts of riboflavin (0.65 rag. per kg. liquid diet) is presented in figure 2.
Trial / - - T h e treatment of riboflavin-deficient pig 35 began on the
27th day. At the time of supplemental feeding, this pig was extremely
Figure 1. Pig 37 after being on riboflavin deficient diet for 32 days.
weak and refused to eat, thus force-feeding had to be practiced. This
pig was fed 500 ~g. of riboflavin daily up to the time it died on the
30th day.
The remaining two deficient pigs, 34 and 36, were fed 500 ~g. of
riboflavin beginning on the 31st and 33rd days, respectively. This
supplementation was continued for 6 days. Following supplementation,
appetites of both animals improved; scouring ceased and hair coats
became more lustrous. A few days after discontinuing supplementation
(46th day), however, both pigs exhibited recurrence of deficiency
symptoms, On the 50th day, 500 ~g. of riboflavin was fed; this amount
was daily added to their dietary intake of liquid diet until termination
of the trial on the 56th day. That these symptoms were not completely
248
W.P.
LEttRER, JR. AND A. C. WIESE
corrected was possibly due to low level of riboflavin supplementation
or the supplement was not fed for a sufficient period of time.
Macroscopic examination of these animals at the end of the trial
revealed small size, scaly skins, and rough sparse hair coats. Necropsy
showed necrosis and sloughing of the corium with hemorrhage in the
prCiferative germinal layers of the skin. The liver showed leucocytic
infiltration and many polymorphonuclear leucocytes in the liver and
Figure 2. Companion of control P i g 33 on left, and litter mate riboflavin
deficient P i g 38 on right, at 34 days of age.
blood. The kidneys exhibited a subacute glomerulonephritis and cloudy
swelling with destruction of the tubular epithelium. The lungs showed
pneumonia and microscopically there was leucocytic and erthrocytic
infiltration, with many polymorphonuclear leucocytes present.
Trial / / - - W h e n it became evident that the dosage of riboflavin
described above was inadequate, this trial was undertaken to recheck
the riboflavin deficiency symptoms observed in trial I, and to attempt
to more completely alleviate the symptoms with larger supplementations
of riboflavin.
Deficiency symptoms occurred in the same sequence and severity as
did those in trial I. The supplemental feeding of riboflavin began on
the 31st day when 1 rag. of riboflavin was fed to all deficient animals;
RIBOFLAVIN DEFICIENCY IN BABY PIGS
249
supplementation at this amount was continued for the following eight
days. This amount of riboflavin gave immediate relief to all deficiency
symptoms. However, immediately upon removal of riboflavin from the
diet all animals again began scouring and vomiting. On the 48th day
to alleviate these symptoms, and throughout the duration of this trial,
pigs 37 and 39 were fed 1.5 rag. and pig 38 was fed 1 rag. per day of
riboflavin, respectively.
At the termination of this trial, all pigs appeared to be normal in
every respect except for their small size. Postmortem examination,
however, revealed many abnormalities. The liver and kidneys showed
blotchy and subcapsular microscopic hemorrhages. Microscopically, the
liver showed a granulocytic infiltration of the interlobular spaces with
intercolunmar congestion in the subcapsular region. There were many
polymorphonuclear leucocytes in the blood. The kidneys showed an
interstitial congestion with many polymorphs in the blood. The incomplete cure of the internal symptoms was probably due to the short
duration of riboflavin supplementation.
Hughes (1940) using 80 pound pigs indicated the minimum riboflavin requirement for the growing pig was 1.0 to 3.0 mg. per 100 pounds
body weight. From the studies reported above, the suckling pig apparently has a requirement nearer the maximum amount reported by
Hughes (1940) than the minimum.
r
Summary
Riboflavin deficiency of baby pigs is associated with alopecia,
anorexia, poor growth, rough hair coat, dermatitis, scours, ulcerative
colitis, inflammation of anal mucosa, vomiting, light sensitivity, unsteady
gait, and many abnormal internal complications.
The supplementation of 1 to 1.5 rags. of riboflavin per day for 16
days cured the external symptoms. However, many of the internal tissue
changes were not corrected. ]'his may have been due to insufficient
amounts of r~boflavin being fed, or the supplementation was for too
short a period of time.
L i t e r a t u r e Cited
Hughes, E. H. 1938. The vitamin B-complex as related to growth and metabolism
in the pig. Hilgardia 11:515.
Hughes, E. H. 1939. The role of riboflavin and other factors of the vitamin Bcomplex in the nutrition of the pig. Jour. Nutr. 17:527.
Hughes, E. H. 1940. The minimum requirements of riboflavin for the growing pig.
Jour. Nutr. 20:233.
250
W.P.
LEHRER, JR. AND A. C. WIESE
Lehrer, W. P., Jr., P. R. Moore, A. C. Wiese, and O. F. Pahnish. 1949. A synthetic
milk ration for baby pigs. JOUR.N'ALOI~"ANI~rAL SCIENCE 8:107.
Krider, J. L., S. W. Terrill, and R. F. Van Pouche. 1949. Response of weanling pigs
to various levels of riboflavin. JOUR-N'ALOF ANL~tAI. SCl-~.nCE 8:121.
Mitchell, H. H., B. C. Johnson, T. S. Hamilton, and W. T. Haines. 1950. The riboflavin requirement of the growing pig at two environmental temperatures.
Jour. Nutr. 41:317.
Phillips, P. H., and E. B. Hart. 1935. The effect of Organic dietary constituents
upon chronic fluorine toxicosis in the rat. Jour. Biol. Chem. 109:657.
Wiese, A. C., B. C. Johnson, H. H. Mitchell, and W. B. Nevens. 1947. Synthetic
rations ior the dairy calf. Jour. Dairy Sci. 30:87.
Wintrobe, M. M., E. L. Mitchell, and L. C. Kolb. 1938. S e n t r y neuron degeneration in vitamin deficiency. Jour. Exp. Med. 68:207.
Wintrohe, M. M. 1939. Nutritive requirements of young pigs. Am. Jour. Physiol.
126:375.
Wintrobe, M. M., W. Buschke, R. H. Follis, Jr., and S. Humphreys. 1944. Riboflavin deficiency in swine. Johns Hopkins Hosp. Bul. 75:102. Johns Hopkins
University, Baltimore.