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Losses of calves in beef herds to Clostridial diseases continues to be a problem. In a large 1991 Colorado study1 of 47 herds with 11,767 cows reported that two of the most common causes of calf mortality were enteric and sudden death diseases. Both of these entities are consistent with Clostridial disease. Unfortunately, less than 1% of the calves that died were ever presented to a diagnostic lab for confirmation of death and 99% was based on producer perception. A smaller study2 conducted in 1992-93 of 15 beef herds in Colorado, Wyoming and Nebraska with 3,273 calves born attempted to at least get a better handle on the extent of Clostridial related disease. In this study, a total of 153 died (4.7%) with 93 calves dying between 48 hours and branding at about 2 months of age. All 93 calves were submitted for field necropsy and sample submission for confirmatory laboratory diagnosis. This was a cooperative effort involving 8 local veterinary practitioners who received uniform training and 2 state diagnostic laboratories. Causes of death were categorized into 1) abomasitis, 2) abomasal ulcer, 3) clostridial enteritis, 4) general enteritis, 5) respiratory/pneumonia, and 5) other causes of death. Samples were submitted to diagnostic labs in Colorado and Nebraska and the information assimilated into the same six categories reported by the practioners. Table 1 reports the association between field necropsy and diagnostic lab results.
Multiple theories have been presented in an effort to explain the development of Clostridial diseases. Commonly, these theories suggested feed changes, environmental or physical stress, and nutritional deficiencies in addition to the bacteriology as some of the disease factors. Many organisms have been isolated from affected abomasal tissues in affected neonatal calves. Still it remains an enigma for both veterinarians and producers. It is probable that multiple factors and multiple disease-producing agents may be involved. The objective of today s presentation is to update producers, in as much as possible, with the current understanding of this problem.
Is copper deficiency involved and if so what is its role?
The idea that ulcer formation may be related to a copper deficiency was first proposed by Lilly, et al. in 19853. The association of copper deficiency with abomasal ulcers is summed up in a quote from that publication, "Our statistical data have shown a highly significant correlation between abomasal ulcers and copper deficiency. The exact role that copper efficiency plays in abomasal ulcers, however, is purely speculative". 1985:86). This statement pretty well sums up where we are with copper and its association with abomasal ulcers today. That copper deficiency is associated with increased disease incidence is not questioned but its association with specific diseases remains speculative. Although a small study2, the herd with the lowest mean cow copper levels had the lowest IgG levels in calves, highest calf morbidity to disease (47%), and close to the highest calf mortality (7.7%) of all the herds. Possible impacts of copper deficiencies include (1) decreased immune function (decrease macrophage and cytochrome oxidase activities) and (2) compromised microvasculature of the abomasum leading to decreased motility and an impaired ability of the mucosa to protect itself from acid/pepsin digestion3. Results from other studies4,5 indicate copper concentrations (serum and tissue) are not related to the occurrence of abomasal ulcers. However, no numeric values were reported for either liver or serum copper concentrations in the first study4 and the second study5 only reported serum concentrations. One other consideration with regard to copper concentration is defining at what point do animals become deficient. Lilly, et al.3 reported hepatic copper values of between 45-48 ppm (dry weight) in their diseased animals, considering these to be significantly lower than their control group. Jelinski6 suggested, based on two separate sources (Personal communication with Dr. M. Smart, University of Saskatchewan; Puls, 1988:76), that a more reasonable cutoff point for defining hepatic copper deficiencies would be 35 ppm (dry weight) and 10 ppm (wet weight).
Bacteriology
The idea that Clostridium perfringens infections are associated with abomasal ulcers was started with two studies published by Kansas workers4,5. The first study involved isolating C. perfringens from eight neonatal calves with suspected abomasal displacement or intestinal obstruction. Toxin neutralization tests in mice concluded seven of the 8 cases were C. perfringens type A. The second study involved inoculating eight calves intrarumenally with toxigenic C. perfringens type A and then evaluating the calves for 10 days. All calves in the second study manifested signs of abdominal tympany or abomasitis to some degree, with two deaths being presumably due to inoculation with C. perfringens type A. However, a more recent study6 has reported finding "no compelling evidence that Clostridium perfringens type A ... [is] involved in ulcer formation". This study evaluated histological sections and bacterial cultures for 30 unweaned calves (all <3 months of age) that were necropsied for fatal ulcers (14 cases) or unrelated deaths (16 controls). Clostridium perfringens as a group of organisms is divided into 5 types by its ability to produce one or more toxins. A number of diseases have been associated with these toxins (See Table 2)
Because Type A organisms are a part of the normal flora of the intestinal tract of virtually all warm-blooded animals, the veterinary community has been reluctant to accept a Type A etiology for enteritis and entertoxemia7. Type A Clostridium perfringens has been associated with gastrointestinal lesions8 and is the predominate isolate found in cattle with enterotoxemia in different studies9,10. Further, unlike Types B, C, D, and E which are defined by what toxins they do produce (beta, epsilon, and iota), Type A is a loosely defined group of organisms that do not produce these toxins7. Thus, Type A is still a pool of organisms that do not fit the other types and therefore as yet undetermined groups within Type A may be associated with specific disease syndromes.
Vaccines
Protection against the diseases produced by the toxins is afforded by an immune response to the toxoid agent. Lack of association seen in some studies is most likely associated with failure to recognize the many facets of Clostridial diseases, misdiagnosis, and possibly improper vaccination protocols. Type C and D toxoids do not afford protection against Type A diseases. Autogenous vaccines have provided assistance in this area. Work is being done at a number of institutions in the development of a more complete vaccine.
Summary
Diagnostic techniques are currently available or becoming more available for typing out specific Clostridium perfringens isolates and toxins produced by those isolates. With this new technology, several studies are being conducted to better define the pathogenicity of the various syndromes associated with Clostridium perfringens Type A.
References
1Salman, MD et al. Annual disease incidence in Colorado Cow-Calf Herds Participating in Rounds 2 and 3 of National Animal Health Monitoring Sytem from 1986 to 1988. J Am Vet Med Assoc 198(6): 962-967, 1991.
2Tombs RE, et al. Postnatal Calf Losses in Beef Herds: Causes and Epidemiological Characteristics. Large Animal Practice Jul/Aug 1998: 19(4), 16-24.
3Lilley CW, et al. Linking Copper and bacteria with abomasal ulcers in beef calves. Veterinary Medicine, Oct 1985: 85-88.
4Roeder BL, et al. Isolation of Clostridium perfringens from neonatal calves with ruminal and abomasal typany, abomasitis, and abomasal ulceration. JAVMA 1987:1550.
5Roeder BL, et al. Experimental induction of abdominal typany, abomasitis, and abomasal ulceration by intraruminal inoculation of Clostridium perfringens type A in neonatal calves. Am J Vet Res 1988:201
6Jelinski MD, et al. 1995. The relationship between the presence of Helicobacter pylori, Clostridium perfringens type A, Campylobacter spp, or fungi and fatal abomasal ulcers in unweaned beef calves. Can Vet J 36:379-382.
7Songer JG. Clostridium perfringens Type A infection in Cattle. 1999 AABP Proceedings.
8Al-Mashat RR, Taylor DJ. 1983. Bacteria in enteric lesions in cattle. Vet Rec 112: 5-10.
9Daube G et al. 1989. Diarrhea associated with Clostridium perfringens type A enterotoxin in neonatal pigs. J Vet Diagn Invest 1:351-353.
10Yoo HS et al. 1997. Molecular typing and epidemiological survey of prevalence of Clostridium perfringens types by multiplex PCR. J Clin Microbiol 35: 228-232.
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