Do any of you use a C&D Overeating Shot? If so, do you just give the C&D toxoid or do you just give a blackleg shot with C&D in it? I'm talking about calves that are a day or two old. I know most black leg shots are not labeled before one month of age, but I've heard of some people giving it this way. Just looking for some input from your operations. Thanks!
C&D Overeating shot
- Thread starter Sally
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Anonymous
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I just give the C&D (7-Way) shot at birth (about 1/2 the price)- then give them the 7 Way with somnus when I brand them later.....
BlackCattleRancher
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I give 5ml of CD&T at birth, when banding and tagging. Never had a problem, and hope I never do, but figure the tetanus can't hurt anything as I don't dip navels and also am banding the bulls, plus I know from my very little bit of sheep experience clostridium can take a severe knockout on a lamb crop, so figure it as a very cheap insurance, less than $.50/hd.
BCR 8)
BCR 8)
Soapweed
Well-known member
We give a 7-way blackleg shot to the cows in the fall at preg-checking time. This gives a few months for them to build up immunity to pass on to their calf.
Triangle Bar
Well-known member
We give a 8-way pre-calving to cows to try and increase anti-bodies in the cow's colostrum. Wasn't able to do this this year, my working corrals were snow & drifted in. Shortly after birth (2-3 days) we give a C&D Toxoid. At 1 month of age we give another C&D Toxoid. At branding, bull calves get 8-way and C&D Tetanus, heifer calves get 8-way.
As you might have guessed I have a lot of trouble with overeating disease. This program has reduced the number of sick calves considerably.
When I do have sick calves I treat them with Penicillin and C&D Antitoxin. The Antitoxin is c&d antibodies derived from equine blood serum. The antitoxin saves me 3 to 4 calves every year!
As you might have guessed I have a lot of trouble with overeating disease. This program has reduced the number of sick calves considerably.
When I do have sick calves I treat them with Penicillin and C&D Antitoxin. The Antitoxin is c&d antibodies derived from equine blood serum. The antitoxin saves me 3 to 4 calves every year!
jodywy
Well-known member
cows get a 8 way in the fall and a scourgarud 4 befor calving. But I give each calf a Vision C&D shot at birth and a 7 way at branding.
but also have C&D Antitoxin, Penicillin, and mineral oil on hand as seem there alway a few big calves that start kicking thier bellies
but also have C&D Antitoxin, Penicillin, and mineral oil on hand as seem there alway a few big calves that start kicking thier bellies
John SD
Well-known member
I have been giving Vision 7 to the calves at birth and Vision 7 Somnus at branding. Then a One Shot Ultra 7 with pastueurella in the fall shots.
This year when I get my vaccine I will ask the vet if there is any benefit to giving the Vision 7 Somnus at birth and the One Shot Ultra 7 at branding time to give the calves a boost before fall shot time. Last year I had a couple calves got sick before giving the fall shots.
This year when I get my vaccine I will ask the vet if there is any benefit to giving the Vision 7 Somnus at birth and the One Shot Ultra 7 at branding time to give the calves a boost before fall shot time. Last year I had a couple calves got sick before giving the fall shots.
Nicky
Well-known member
Seems like most folks here on ranchers use 7 way instead of 8 way. Do most of you not have problems with Redwater? And how many of you have liver fluke problems?
Richard Doolittle
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The way I understand it, the C & D is the only thing the calves benefit from at a very young age, other than maybe tetanus if you band your bull calves.
gcreekrch
Well-known member
We treat these calves with Liquamycin LA, mineral oil, and 60 cc of plain yogurt to get the good bacteria working again. Wifey's been pretty successful with this protocol, We have never tried 7-way on baby calves before, thanks to you folks we will this year.
per
Well-known member
Now you guys have me worried. I always though that good cow nutrition was the key to healthy spring calves. The only time that we used scourgaurd was the only time we had a bad scour problem. As far as 7 or 8 way that comes from the cow as well until branding. Should I be worried?
John SD
Well-known member
Nicky said:
I guess I have to plead ignorance!
I've heard of Redwater but right now I can't think of the symptoms. No one I know uses 8-way around here.On liver flukes, I believe that is covered by ivermectin. My cattle get poured a couple times a year.
Nicky
Well-known member
Redwater or Bacillary hemoglobinuria is an acute, infectious, toxemic disease caused by Clostridium haemolyticum ( C novyi type D). It affects primarily cattle but has also been found in sheep and rarely in dogs. It occurs in the western part of the USA, along the Gulf of Mexico, in Venezuela, Chile, Great Britain, the middle East, and other parts of the world.
Etiology:
C haemolyticum is a soilborne organism that may be found naturally in the GI tract of cattle. It can survive for long periods in contaminated soil or in bones from carcasses of infected animals. After ingestion, latent spores ultimately become lodged in the liver. The incubation period is extremely variable, and the onset depends on the presence of a locus of anaerobiosis in the liver. Such a nidus for germination is most often caused by fluke infection, much less often by high nitrate content of the diet, accidental liver puncture, liver biopsy, or any other cause of localized necrosis. When conditions for anaerobiosis are favorable, the spores germinate, and the resulting vegetative cells multiply and produce β toxin (phospholipase C), which causes intravascular hemolysis and its sequelae, including hemolytic anemia and hemoglobinuria.
Clinical Findings:
Cattle may be found dead without premonitory signs. Usually, there is a sudden onset of severe depression, fever, abdominal pain, dyspnea, dysentery, and hemoglobinuria. Anemia and jaundice are present in varying degrees. Edema of the brisket may occur. Hgb and RBC levels are quite low. The duration of clinical signs varies from ~12 hr in pregnant cows to ~3-4 days in other cattle. The mortality in untreated animals is ~95%. Some cattle suffer from subclinical attacks of the disease and thereafter act as immune carriers.
Lesions: Dehydration, anemia, and sometimes subcutaneous edema are present. There is bloody fluid in the abdominal and thoracic cavities. The lungs are not grossly affected, and the trachea contains bloody froth with hemorrhages in the mucosa. The small intestine and occasionally the large intestine are hemorrhagic; their contents often contain free or clotted blood. An anemic infarct in the liver is virtually pathognomonic; it is slightly elevated, lighter in color than the surrounding tissue, and outlined by a bluish red zone of congestion. The kidneys are dark, friable, and usually studded with petechiae. The bladder contains purplish red urine. After death, rigor mortis sets in more rapidly than usual.
Diagnosis:
The general clinical picture usually permits a diagnosis. The most striking sign is the typical port-wine-colored urine, which foams freely when voided or on agitation. The presence of the typical liver infarct is sufficient for a presumptive diagnosis. The normal size and consistency of the spleen serve to exclude anthrax and anaplasmosis. Bracken fern poisoning and leptospirosis also should be considered. Diagnosis can be confirmed by isolating C haemolyticum from the liver infarct, but the organism is difficult to culture. Rapid and accurate diagnosis can be made by demonstrating the organism in the liver tissue by a fluorescent antibody or immunohistochemical test or by demonstrating the toxin in the fluid in the peritoneal cavity or in a saline extract of the infarct.
Control:
Early treatment with penicillin or broad-spectrum antibiotics is essential. Whole blood transfusions and fluid therapy also are helpful. C haemolyticum bacterin prepared from whole cultures confers immunity for ~6 mo. In areas where the disease is seasonal, one preseasonal dose is usually adequate; where the disease occurs throughout the year, semiannual vaccination is necessary. Cattle that are in contact with animals from areas where this disease is endemic should be vaccinated, as the latter may be carriers.
This is from the Merck manual. We've always vaccinated for it, only ever remember one animal dying from it when I was little. Only Ivomec Plus (injectable), and Valbazen kill liver flukes
Etiology:
C haemolyticum is a soilborne organism that may be found naturally in the GI tract of cattle. It can survive for long periods in contaminated soil or in bones from carcasses of infected animals. After ingestion, latent spores ultimately become lodged in the liver. The incubation period is extremely variable, and the onset depends on the presence of a locus of anaerobiosis in the liver. Such a nidus for germination is most often caused by fluke infection, much less often by high nitrate content of the diet, accidental liver puncture, liver biopsy, or any other cause of localized necrosis. When conditions for anaerobiosis are favorable, the spores germinate, and the resulting vegetative cells multiply and produce β toxin (phospholipase C), which causes intravascular hemolysis and its sequelae, including hemolytic anemia and hemoglobinuria.
Clinical Findings:
Cattle may be found dead without premonitory signs. Usually, there is a sudden onset of severe depression, fever, abdominal pain, dyspnea, dysentery, and hemoglobinuria. Anemia and jaundice are present in varying degrees. Edema of the brisket may occur. Hgb and RBC levels are quite low. The duration of clinical signs varies from ~12 hr in pregnant cows to ~3-4 days in other cattle. The mortality in untreated animals is ~95%. Some cattle suffer from subclinical attacks of the disease and thereafter act as immune carriers.
Lesions: Dehydration, anemia, and sometimes subcutaneous edema are present. There is bloody fluid in the abdominal and thoracic cavities. The lungs are not grossly affected, and the trachea contains bloody froth with hemorrhages in the mucosa. The small intestine and occasionally the large intestine are hemorrhagic; their contents often contain free or clotted blood. An anemic infarct in the liver is virtually pathognomonic; it is slightly elevated, lighter in color than the surrounding tissue, and outlined by a bluish red zone of congestion. The kidneys are dark, friable, and usually studded with petechiae. The bladder contains purplish red urine. After death, rigor mortis sets in more rapidly than usual.
Diagnosis:
The general clinical picture usually permits a diagnosis. The most striking sign is the typical port-wine-colored urine, which foams freely when voided or on agitation. The presence of the typical liver infarct is sufficient for a presumptive diagnosis. The normal size and consistency of the spleen serve to exclude anthrax and anaplasmosis. Bracken fern poisoning and leptospirosis also should be considered. Diagnosis can be confirmed by isolating C haemolyticum from the liver infarct, but the organism is difficult to culture. Rapid and accurate diagnosis can be made by demonstrating the organism in the liver tissue by a fluorescent antibody or immunohistochemical test or by demonstrating the toxin in the fluid in the peritoneal cavity or in a saline extract of the infarct.
Control:
Early treatment with penicillin or broad-spectrum antibiotics is essential. Whole blood transfusions and fluid therapy also are helpful. C haemolyticum bacterin prepared from whole cultures confers immunity for ~6 mo. In areas where the disease is seasonal, one preseasonal dose is usually adequate; where the disease occurs throughout the year, semiannual vaccination is necessary. Cattle that are in contact with animals from areas where this disease is endemic should be vaccinated, as the latter may be carriers.
This is from the Merck manual. We've always vaccinated for it, only ever remember one animal dying from it when I was little. Only Ivomec Plus (injectable), and Valbazen kill liver flukes
gcreekrch
Well-known member
per said:
Talked to our vet this morning after my last post. His opinion is that cows should be vaccinated 2 to 4 weeks previous to calving- the calf should then have immunity from the cow until it is 8 to 10 weeks old if you vaccinate the cow herd every year.
As far as scours go, in this country it's not if you get scours, it's when, and how bad.
We went through a bad bout of them in 1996, before we started vaccinating. Life has been so nice since we started that we're scared to quit! :? 
A friend of mine that is fall calving in NE Alberta thought he could get by without scour shots when pasture calving. He did.... for 3 years- lost enough calves 1 fall to pay for a lifetime of vaccine.jodywy
Well-known member
Don't see much if any scours calving on a snow pack here in the mountains. But soon as the green grass hit we can have endotoxicemia hit. That why we and our Vet (suggested) that we Vaccinate at birth with a C&D shot the best luck has been the Vision. We try and brand and vaccinate with a 7way before we have a problem. One spring after losing a few calves and having rainy weather we sorted calves off and vaccinated them all before we were able to brand.
We see one we sub Q anti toxin and penicillin and also dose oral anti toxin, penicillin and mineral oil.
We see one we sub Q anti toxin and penicillin and also dose oral anti toxin, penicillin and mineral oil.
ranch hand
Well-known member
Cows are done in the fall and calves at branding.