ISRAEL JOURNAL OF
VETERINARY MEDICINE
VOLUME
54 (3) 1999
FECAL BLOOD LEVELS AND SERUM PROENZYME
PERSINOGEN ACTIVITY OF DAIRY COWS WITH ABOMASAL
DISPLACEMENT
T. Zadnik and M. Mesaric
University of Ljubljana, Veterinary Faculty, Clinic for Ruminants, Cesta v Mestni log 47, 1000
Ljubljana, Slovenia
Summary
Occult blood in the feces and proenzyme pepsinogen (PG) activity were
measured in 26 dairy cows with abomasal displacement using the Weber and
Benzidine tests. Occult blood in the feces occured most frequently in cows
with torsion and left abomasal displacement. PG activity in blood was
significantly higher (P<0,05) in cows with abomasal displacement than in the
control group of 15 cows. Hyperpepsinogenemia and a positive fecal blood
test indicated secondary mucosal damage (erosion, ulcers) to the abomasum.
Laboratory evaluation of fecal blood and measurement of PG activity in blood
offer better information on the mucosal status of the abomasum, and the
course, treatment and prognosis of displacement.
Introduction
Displaced abomasum represents a group of pathological events due to smooth
muscle atony, gas and fluid accumulation following displacement of the abomasum
from its normal ventral position on the abdominal floor (19,20,34,35,36). Recently it
was suggested that the decreased contractility of the mantel muscle of the
abomasum is caused by a loss of cholinergic excitatory and an increase in
nitrooxergic inhibitory tone (12). The disease usually occurs in the first month
after parturition, and is accompanied by a marked negative energy balance,
ketonemia, hepatic lipidosis with hyperbilirubinemia and increased activity of
hepatic enzymes (5,23,35,36). Frequently severe dehydration, hypocalcemia,
hypokloremia, hypokalemia and hyponatremia supervene (36).
Diagnosis of the disease is based on invasive and non-invasive techniques: the
invasive ones are laparotomy and laparoscopy, while non invasive ones are
simultaneous auscultation and percussion, non-ballottement, RTG, sonography, and
rectal exploration (19,20). Diagnosis is also supported by the analysis of blood,
milk, urine, feces, etc. However, it should be emphasized that none of these
methods is a reliable indication of mucosal change which significantly affects
the course and prognosis of the disease.
Any injury to the gastric mucosa allows diffusion of hydrogen ions from the lumen
into the mucosal tissues and also allows diffusion of pepsin into the rest of the mucosa
causing further damage (30).
The clinical status of animals and fecal occult blood detection may help in
assessing the pathological changes in the abomasal mucosa (28,38). Massive loss of
blood resulting in most cases from bleeding abomasal ulcers can be clinically assessed
easily because typical signs of severe pallor of the mucosa, tachycardia, increase in
the rate and depth of respiration and melena are manifested (30).
Occult bleeding which frequently accompany abomasal diseases can be
established by fecal blood detection (10,13,17,28,38). With fecal occult blood
tests it is impossible however, to exactly locate the bleedings and other
pathological changes in the digestive mucosa (1,13,28,29).
In human medicine extensive research is carried out on blood PG in patients with
abdominal diseases (2,8,21). PG is a proenzyme, generated by the parietal cells of
gastric mucosa. Increased PG levels in human blood were established in gastric
tumors, duodenal and gastric ulcers, kidney diseases and hyperthyroidism (6,33). PG
activity was statistically significantly increased in several gastric diseases (2).
ln ruminant blood a certain physiological level of PG exists (3,24,31,32,33). In
ruminants successful measurement of blood PG activity is widely used for the
assessing gastrointestinal parasitization (4,6,7,9,11,14,15,16,18,25,33, 37). Paynter
(27), Hilderson et al (15) and Harvey-White et al (14) found that serum PG values of
zero to 5,0 U/L are normal for young and mature cattle and are not associated with
any clinically relevant damage to the abomasal mucosa.
In the literature there is little information on measurement of PG activity in blood
and pathological changes in abomasal mucosa in cows with abomasal displacement.
V‫צ‬r‫צ‬s et al (34) investigated PG activity in blood, urine and abomasal fluid and
reached the conclusion that increased blood levels are found especially in cows with
left displacement.
Because the incidence of abomasal displacement has been on the increase in
Slovenia (36), we have also included in our laboratory diagnosis the measurement of
PG activity in blood and detection of the presence of occult blood in the feces to
achieve a better prognosis and for monitoring the course of the disease.
Materials and Methods
Twenty six Holstein-Friesian cows with abomasal displacement were used. All
animals were clinically examined including simultaneous auscultation and percussion
(ping effect) and the kind of displacement was estabIished. All types of abomasal
displacements were operated on the standing animal in the right paralumbal fossa via
our own modified method (22). Before surgical interference the feces and blood were
collected. Blood samples were taken by venipuncture of the v. caudalis mediana with
the vacuum technique in Sherwood-Monoject tubes. With regard to the diagnosis the
animals fell into 3 groups:
1. Left-sided displacement of the abomasum (LDA);
2. Right-sided displacement of the abomasum (RDA); and
3. Abomasal torsion - volvolus (TA).
Fpr detection of the presence of occult blood the Weber (Quaiac test) and benzidine
tests were used (17,28,29). PG activity in blood serum was evaluated by Paynter's
method (27).
We carried out hematological analysis (E, Hb, Ht, MCV, L, Diff.L count) with
Coulter Counter type ZF6 and biochemical analysis (Ca, RP, Mg, Na, K, C1, AST,
LDH, GLDH, GGH, Bili, Chol, Urea) with Cobas Mira La Roche analyzer.
The parasitological examination of the feces was also carried out. The results of the
laboratory blood and the feces examinations of test cows were compared with 15
healthy control cows.
All data were statistically processed with SPSS statistical program using analysis of
variance with one entry (26).
Results
Parasitological examination of the feces revealed occasional eggs of
Trichostrongylus ssp.
In 3 cows which died with TA, massive hemorrhages were observed at necropsy as
well as ulcers on the lower part of the abomasal mucosa (Fig. 1).
Fig. 1: Ulcers on the mucosal aspect of the fundic abomasal region.
In all cows with TA, fecal occult blood tests were positive. In cows with RDA, no
occult blood was detected, whereas in 3 cases only in cows with LDA (Table 2).
In cows with abomasal displacement statistically significant higher mean values of
PG activity were established than in the control group of normal cows (P<0,05, Table
3 ).
Analysis of blood samples revealed hypocalcemia, hypokaIemia, hypochloremia,
hyperbilirubinemia and increased AST activity (Table 4).
Discussion
The success rate of treating cows with abomasal displacement was 73%. In 3 cows
which died one day after surgery, and in 4 cows that were slaughtered, higher blood
PG activity was detected than in the cows that recovered (Table 1). The difference in
PG levels between dead and recovered cows was not statistically significant (P
=0,239).
In cows with abomasal displacement fecal occuIt blood was established by the
Weber test in 6 cases (23%), and only in 3 cases (12%) by the benzidine test (Table
2). The greater sensitivity of the Weber test (Guaiac solution) was also confirmed by
Payton et al (28). From 6 cows in which fecal occult blood was detected by the Weber
test, 3 of them died after surgery and the others were slaughtered after a few days of
intensive care. Clinical examination of the feces failed to reveal typical signs of
melena. It is interesting that in all 3 cases with TA, fecal occult blood was detected by
laboratory examination. In contrast no fecal occult blood was detected in cows with
RDA.It has been shown that especially in TA, massive inflammatory changes occured
in the mucosa due to disturbed blood circulation and obstruction of the passage of
abomasal contents rich in hydrochIoric acid, sodium chloride and potassium. In all
abomasal torsions marked hypokalemia, hypochloremia and hypocalcemia werq,
established (Table 4). Mean hematocrit values were at the upper normal levels. The
findings have shown that in abomasal displacement a combination of different disease
events occured and the key role may be attributed to the hypomotility of the
forestomachs and intestines, hypocalcemia, abomasal reflux, metabolic alkalosis and
impairment of bile and pancreatic flow with some hepatic cell degeneration (hepatic
lipidosis).
ln abomasal displacement a statistically significantly increased mean PG value was
established with regard to the control group (P<0,05).
Mean PG values in LDA and RDA+Ta were at the upper physiological level (>5,0)
and almost twice greater than mean values in control cows (Table 3). Paynter (27)
reported that a PG value of above 5,0 U/L indicated more severe damage of the
abomasal mucosa. Our findings showed that there were considerable variations in PG
activity in cows with RDA, and least in control cows. Between the groups of cows
with LDA, and RDA there were no statistically significant differences (P=0,691).
Mean PG activity in the RDA group was slightly higher in the LDA group (Table 3).
V‫צ‬r‫צ‬s et al (34) did not establish any statistically significant differences, though PG
values in LDA were somewhat higher than in the RDA. This latter finding was
contrary to ours. The information on blood PG values regarding the kind of the
abomasal displacement is still inadequate and requires further measurements in a
greater number of cows.
According to the established positive fecal occult blood tests and
hyperpepsinogenemia of cows with displaced abomasum our observation indicated
that mucosal damage was present, yet without massive bleeding from abomasal
ulcers. Our findings also showed that PG levels in cows with displaced abomasum
were largely dependent on the state of the mucosa and the adjacent vascular supply.
Literature
1. Adlercreutz, H., Liewendahl, K., Virkola, P. 1978. Evaluation of Fecatest, a New
Guaiac Test for Occult Blood in Feces. Clin. Chem. 24: 756-61.
2.-Alquezar, A.S., Marchese, M.A., Bezzerra Silvia, T.V. et al. 1978. Serum
pepsinogen: Correlation of techniques and analysis of levels found in different
diseases of the stomach and duodenum. Clinica Chimica Acta 90: 163-9.
3. Andren, A. 1992. Production of prochymosin, pepsinogen and progastricsin, and
their cellular and intracellular localization in bovine abomasal mucosa. Scand J Clin
Lab Invest. 52: 59-64.
4. Armour, J., Bairden, K., Duncan, J.L., Jennings, F.W., Parkins, J.J. 1979.
Observations on ostertagiasis in young cattle over two grazing seasons with special
reference to plasma pepsinogen levels. Vet. Record 105; 500-3.
5. Breukink, H.J., Wensing, Th. 1997. Pathophysiology of the liver in high yealding
dairy cows and its consequences for health and production. Israel Journal of
Veterinary Medicine 52:66-71.
6. Berghen, P., Hilderson, H., Vercruypse, J., Dorny, P. 1993. Evaluation of
pepsinogen, gastrin and antibody response in diagnosing ostertagiasis. Veterinary
Parasitology 46: 175-95.
7. Chalmers, K. 1983. Serum pepsinogen levels and Ostertagia ostertagi populations
in clinically normal adult beef cattle. N. Z. vet. J. 31: 189-91.
8. Chuong, J.J.H., Fisher Rosemarie, L., Choung Roberta L.B., Spiro, H.M. 1986.
Duodenal Ulcer. Incidence, Risk Factors, and Predictive Value of Plasma
Pepsinogen. Digestive Diseases and Sciences 31: 1178-84.
9. Chiejina, S.N. 1978. Field observations on the blood pepsinogen levels in
clinically normal cows and calves and in diarrhoeic adult cattle. Veterinary Record
103: 278-81.
10. Cook, A.K., Gilson, S.D., Fischer, W.D., Kass, P.H. 1992. Effect of diet on
results obtained by use of two commercial test kits for detection of occult blood in
feces of dogs. Am J Vet Res. 53:1749-51.
11. Eckersall, P.D., Macaskill, J., McKellar, Q.A., Bryce, K.L. 1987. Multiple forms
of bovine pepsinogen: isolation and identification in serum from calves with
ostertagiasis. Research in Veterinary Science 43: 279-83.
12. Geishauser T. 1995. Untersuchungen zur Labmagenmotorik von Kuhen mit
Labmagenverlagerung. Habilitationsschrift. Giessen.
13. Gilson, S.D., Parker, B.B., Twed, D.C. 1990. Evaluation of two commercial test
kits for detection of occult blood in feces of dogs. Am J Vet Res 51: 1385-7.
14. Harvey-White, J.D., Smith, J.P., Parbuoni, E., Allen, E.H. 1983. Reference serum
pepsinogen concentrations in dairy cattle. Am J Vet Res 44: 115-7.
15. Hilderson, H., Berghen, P., Vercruysse, J., Dorny, P., Braen, L. 1989. Diagnostic
value of pepsinogen for clinical ostertagiosis. Vet. Rec. 125: 376-7.
16. Kolb, E., Rehbein, S.T., Ribbeck, R., Alawad, A., Leo, M., Siebert, P. 1993. Das
Verhalten hmatologischer Parameter (Hmoglobin, Hmatokrit, Leukozytenzahl) und
klinisch-chemischer Kennwerte im Plasma (Glucose, Gesamtprotein, alpha-AminoN, Harnstoff, Pepsinogen, Ascorbinsaure, Fe, Cu, Zn) sowie der Gehalt an
Ascorbinsaure in Leber, Milz und Nebennieren bei gesunden und bei mit
Haemonchus contortus und Trichostrongylus colubriformis infizierten Lmmern. Berl.
Mnch. Tierrtzl. Wschr. 106: 411-8.
17. Kutter, D. 1976. Schnelltest in der klinischen Diagnostik. Urban k
Schwarzenberg, Mnchen: 166-71.
18. McKellar, Q.A., Mostofa, M., Eckersall, P.D. 1990. Stimulated pepsinogen
secretion from dispersed abomasal glands exposed to Ostertagia species secretion.
Res Vet Sci. 48: 6-11.
19. Mesaric, M., Zadnik, T., Modic, T. 1997. ”Ping effect” – a differential diagnosis
of abdominal diseases in dairy cattle. Proceedings 2nd Slovenian veterinary Congress
Slovenian Veterinary Association: 139-42.
20. Mesaric, M., Zadnik, T., Modic, T. 1997. Clinical diagnosis of abomasal
displacement in dairy cow. Atti del Congresso della federatione Mediterranea sanita e
produzione ruminanti. Editografica Bologna: 203-8.
21. Mirsky, A., Futterman, P., Kaplan, S., Broh-Kahn, R.H. 1952. Blood Plasma
Pepsinogen. Lab. Clin. Med. 40: 17-26.
22. Modic, T., Zadnik, T., Mesaric, M. 1997. Omentopexy of a displaced abomasum
carried out via the Ljubljana method. The 5th Congress of Mediterranean Federation
for Health and Production of Ruminants. Proceeding book. Veterinary Faculty of
Bologna: 197-202.
23. Modic, T., Crne, M., Mesaric, M. Zadnik T. 1998. Liver biopsy tests in cows with
abomasal displacement. The 6th Congress of Mediterranean Federation for Health
and Production of Ruminants. Slovenian Buiatric Association, May 14 – 16,
Postojna, Slovenia, Abstract book: 62.
24. Mostofa, M., McKellar, Q.A. 1990. Comparison of pepsinogen forms in cattle,
sheep and goats. Res. Vet. Sci. 48: 33-7.
25. Mylrea, P.J., Hotson, I.K. 1969. Serum pepsinogen activity and the diagnosis of
bovine ostertagiasis. British Vet. J. 125: 379-88.
26. Nie, N.H., Hull, C.H. Jenkins, G.J., Steinbrenner, K, Dale, H.B. 1975. Statistical
package for the social sciences. 2 ed. New York: McGrow-Hill.
27. Paynter, D.I. 1994. Pepsinogen Activity; Determination in Serum and Plasma.
Australian Standard Diagnostic tehniques
for Animal Diseases, Australia. 28. Payton, Alice J., Glickman, L.T. 1980. Fecal
Occult Blood Tests in Cattle. Am. J. Vet. Res. 41: 918-21.
29. Paccagnini Susanna, Ceriani Rossana, Galli Luciana et al. 1987. Occult blood and
faecal leucocyte tests in acute infectious diarrhoea in children. The Lancet 1: 442.
30. Radostits, O.M., Blood, D.C., Gay, C.C. 1994. Veterinary Nedicine. Bailliere
Tindall, New York.
31. Rehbein, S.T., Bienioschek, S., Sachse, M. 1995. Der Gehalt an Pepsinogen im
Blutplasma helminthfrei aufgezogener und unter natrlichen Bedingungen in einem
Gehege aufgewachsener Damhirsche (Dama dama L.). Berl. Mnch. Tierrztl. Wschr.
108: 321-5.
32. Selman, I.E., Armour, J., Jennings, F.W., Reid. J.F.S. 1977. Interpretation of the
plasma pepsinogen test. Veterinary Record 100: 249-50.
33. Schillhorn van Veen, T.W. 1988. Evaluation of Abomasal Enzyme and Hormone
Levels in the Diagnosis of Ostertagiasis. Veterinary parasitology 27: 139- 49.
34. Voros, K., Meyer, C., Stber, M. 1984. Pepsinogenaktivitt von Serum und Harn
sowie Pepsinaktivitt des Labmagensaftes labmagengesunder und nicht- parasitr
labmagenkranker Rinder. Zbl. Vet. Med. A. 31: 182-92.
35. Zadnik, T., Jazbec, I., Skusek, F. 1989. Dislokacija sirista kod goveda.
Veterinarski Glasnik 43: 803-11.
36. Zadnik, T. 1998. A review of abomasal displacements in slovenia. XX. Word
Buiatrics Congress, AACV Sydney: 115-9.
37. Wiggin, C.J., Gibbs, H.C. 1987. Pathogenesis of simulated natural infections with
Ostertagia ostertagi in calves. Am. J. Vet. Res. 48: 274-80.
38. Winawer, S.J. 1976. Fecal Occult Blood Testing. Am J Digestive Diseases 21:
885-8.