Type EE blackleg

[cross_7]

denvermartinfarms

As you feed protein tubs and it is a known fact that "
Cattle that are on a high plane of nutrition," "are most susceptible to the disease " of blackleg and
protein tubs can also cause symptoms that mimic blackleg.
Also it is known that protein tubs can be toxic and can cause all kinds of problems as many toxins are passive,
I would recommend you take a serious look at your cattle's complete diet.
Liz

Sl with all due respect, I aint buying that
Can you provide documented proof of that claim ?

 

[cross_7]

This may be your EE - enterotox- emia,
Easier to read here
http://www.thebeefsite.com/articles/127 ... aby-calves

Clostridium perfringens Infections in Baby CalvesFriday, January 18, 2008 By Russ Daly, DVM, Extension Veterinarian and Lori Rotert, Pre-Veterinary Student. South Dakota Cooperative Extension Service. Illnesses and death losses in baby calves are significant problems for producers raising calves in beef or dairy operations. .Several of these issues, especially sudden deaths and certain enteric (intestinal) conditions, are potential effects of infections due to Clostridium perfringens. Clostridium perfringens are Gram-positive, spore-forming, anaerobic bacteria that are very commonly found in many environments, including soil, water, poorly preserved feeds, contaminated or improperly thawed colostrum or milk, calfhousing environments, and the normal bovine intestinal tract. In small amounts, these bacteria are generally harmless in the intestine, but under the right conditions they may grow and proliferate, resulting in enterotox- emia, a condition in which specific toxins produced by the bacteria in the small intestine result in both local damage and systemic (whole body) effects. Pathogenesis: How C. perfringens causes disease Because of the widespread nature of the organism, calves are readily exposed to C. perfringens in their environment and commonly ingest the bacteria in various quantities, after which it enters the stomach and intestine. Sometimes bacteria are ingested in sufficient quantities to cause disease, but oftentimes small quantities are ingested, followed by rapid proliferation in the intestine. Enterotoxemia due to C. perfringensis more likely to affect baby calves (within the first two months of age) than mature cattle because the calves lack a fully functioning rumen. C. perfringens feeds on starches and sugars in the small intestine. In mature cattle, these starches and sugars are predominantly digested in the rumen, so they are not available to the C. perfringens microbes for use. However, in baby calves, nearly all feed bypasses the rumen and is digested in the abomasum (true stomach) and the small intestine, so the starches are available for the microbes to feed on. This, coupled with a normal intestinal flora that has not yet developed, provides a suitable environment for the C. perfringens to proliferate. Several factors can contribute to this rapid proliferation. Primary among these are abrupt changes in feeding patterns (see "Prevention" below), physical or environmental stress, nutritional deficiencies, and conditions that impair movement of the intestine (such as diarrhea due to other causes). As C. perfringensproliferates in the gut, the bacteria secrete toxins that have profound effects not only on the local intestinal environment (causing damage to the intestinal lining), but throughout the body as well. Death occurs when high levels of these bacterial toxins enter the bloodstream, leading to inflammation, shock, and cardiac arrest. C. perfringens is not spread from calf to calf, but it is not uncommon for several calves in a group to be affected at the same time, due to similar exposure and management practices. Types of C. perfringens There are five types of C. perfringens (see Table 1 below), designated A through E, which are identified based on the toxins they produce. It is the effect of these specific toxins that results in the clinical signs and syndrome attributable to each type. Table 1. C. perfringens types, major toxins, and associated syndromes TOXIN TYPE MAJOR TOXIN SYNDROMES A Alpha 1. Abomastitis (stomach inflammation) in calves 2. Bloating in calves 3. Mild diarrhea in calves 4. May be associated with hemorrhagic bowel syndrome (HBS) in dairy cattle B Beta, Alpha, Epsilon 1. Hemorrhagic enteritis (NOT FOUND IN U.S.) C Beta, Alpha 1. Sudden death in very young calves 2. Hemorrhagic enteritis (bloody scours) D Epsilon, Alpha 1. Enterotoxemia resulting in sudden death, usually in calves on feed (finishing cattle) E Iota, Alpha 1. Fatal enterotoxemia in newborn calves Type C is one of the more commonly encountered types of C. perfringens. It is especially virulent in calves less than 10 days old (and often less than five days old). Enterotoxemia due to C. perfringens Type C may result in severe bloody diarrhea, although oftentimes calves die before diarrhea develops. Clostridium perfringens Type A has been increasingly identified as a cause of abomasal inflammation, which may result in abdominal distension (bloating) or abomasal ulcers in young calves. Varying degrees of diarrhea, and occasionally sudden onset of weakness and coma, have also been associated with Type A, which generally affects a slightly older (2-4 weeks old) calf. It is also occasionally associated with wound contamination and gas gangrene. Diagnosis of Type A enterotoxemia can be difficult due to the fact that it is a very common inhabitant of the normal intestinal tract; therefore, culture results need to be matched to clinical signs and lesions in the tissues (see "Diagnosis" below). Enterotoxemia due to C. perfringens Type D is sometimes associated with sudden death in finishing cattle because it proliferates when there are high amounts of carbohydrates available in the diet, which is often the case in cattle being fed high amounts of grain in finishing diets. Type E enterotoxemia has been diagnosed, although infrequently, in South Dakota calves. It causes a severe local intestinal necrosis and systemic toxemia similar to the syndrome described with Type C. Type B is almost non-existent and has not been found in North America. Diagnosis of C. perfringens Necropsy of the calf, in cases of Types C and E, will sometimes reveal severe necrosis (tissue damage) and hemorrhage in the small intestine. Calves affected with Type A will often show inflammation, ulceration, and hemorrhage of the lining of the rumen and abomasum. Because C. perfringensis often found in the intestine of normal calves, a simple culture of the organism from the calf is not sufficient by itself to confirm a diagnosis of disease due to C. perfringens. Culture results are matched with clinical signs, lesions in the tissues, and, in some cases, toxin identification, to obtain a true diagnosis. Tissue samples from calves suspected of having clostridial enterotoxemia should be collected soon after death and kept well-preserved (after the death of the calf, normal populations of clostridial organisms can overgrow and confuse diagnosis). TREATMENT The treatment of syndromes caused by C. perfringens is frequently unsuccessful. Because clinical signs are usually a result of the toxin, not the bacteria itself, treatment with antibiotics (which act solely on the bacteria and not the toxins) is often less than rewarding. In addition, with many of these syndromes, death or severe illness occurs before treatment can even be attempted; therefore, early detection becomes essential if treatment is to be successful. Typical treatments for calves with milder clinical signs consist largely of antibiotics (especially penicillin) and the use of C. perfringens antitoxin products. Several injectable antitoxin preparations that contain specific antibodies directed against toxins produced by C. perfringens are currently available. While these antitoxin products are developed expressly for use against toxins produced by Types C and D (beta and epsilon toxins), there may be some effect against alpha toxin (Type A) as well. Supportive care with oral or IV fluids and antiinflammatories may also be indicated. Any treatment plan needs to be developed in close consultation with the herd veterinarian. PREVENTION Prevention of enterotoxemia due to C. perfringens infection focuses on three areas: 1) minimizing exposure, 2) enhancing immunity in the young calf, and 3) managing feeding practices to discourage the proliferation of C. perfringensin the gut. Minimizing exposure. Despite the fact that clostridial organisms are ubiquitous in the calf's environment, the more organisms a newborn calf is exposed to the more likely it is to succumb to disease. For that reason, careful attention must be paid to sanitation of the calving area, whether it be a maternity pen in a dairy or a calving pen in a beef operation. Buildup of all enteric pathogens occurs when the same calving area is used throughout the calving season, as these organisms are generally very hardy in the environment. Enhancing immunity. Colostral (passive) immunity is of utmost importance in the resistance of calves to C. perfringens enterotoxemia, since these calves are generally too young (and clinical signs occur too early) to respond to active vaccination. Antibodies against C. perfringensand its toxins are passed from dam to calf through colostrum. Calves should consume an adequate amount (4 quarts) of high-quality colostrum within the first 18-24 hours of life to gain maximum protection . A strategy for maximizing colostral antibody levels is vaccinating the dam before she calves. Vaccines against clostridial diseases are typically "bacterin-toxoids," meaning that the vaccine is meant to stimulate a response against both the bacteria and the toxin produced by the bacteria. Several pre-calving vaccines ("scour shots") contain C. perfringens Type C (and occasionally D) bacterin-toxoids. A separate vaccine against Type A antigens has been conditionally licensed and is available. Since vaccines for Type C (against the beta toxin) do not cross-protect against other types (other toxins), and while not expressly labeled for this use, this vaccine has been used in cows pre-calving to try to maximize colostral protection against Type A enterotoxemia (alpha toxin). Along with colostral antibodies, antitoxin preparations, as mentioned above, are available. In certain situations of excessive exposure, these products may be administered to calves at birth in an attempt to prevent clinical disease. Active vaccination of young calves with C. perfringens vaccines (such as 7-ways or 2-ways containing Types C and D, or the Type A vaccine) is frequently attempted, but little is known about how these vaccines perform in very young (<1 month) calves. Again, these vaccines do not offer protection against the other types (other toxins) not included in the vaccine. Managing feeding practices. While cow-calf producers have very little control over their calves' feeding practices, those raising calves (e.g., dairy calves in hutches) have complete control over their calves' dietary intake. In those operations, it is extremely important to follow strict calf-feeding guidelines. C. perfringens overgrowth in the intestine is aided by any of the following: Milk replacer is improperly mixed (too much or too little water added). Milk replacer is incompletely mixed (clumps of powder still present at feeding). Additives such as electrolytes are added to the milk replacer, creating excessive osmolarity or sodium concentrations. The temperature of milk replacer is too high or low when the calf is fed. Milk replacer temperature should be close to the calf's body temperature (~101° F). Feeding schedules are erratic. Regular, consistent schedules and delivery methods (bucket vs. bottle) are important in avoiding clostridial overgrowth. Changes in diets are made suddenly. Calves drink too quickly (e.g., nipple opening is too large). Equipment (buckets, bottles, nipples, etc.) becomes contaminated due to lack of hygiene. Clostridial infections have been and will continue to be significant challenges to beef and dairy producers. Attention must be paid to all aspects of the disease, including the newborn calf's environment, immunity, and feeding practices. With these aspects in mind, and with close consultation with a veterinarian, it is possible to manage and minimize the effect of these syndromes in our operations today. - See more at: http://www.thebeefsite.com/articles/127 ... 1lXqa.dpuf

 

[cross_7]

I think after reading that Kenny and HD were both on the right track

A strategy for maximizing colostral antibody levels is vaccinating the dam before she calves. Vaccines against clostridial diseases are typically "bacterin-toxoids," meaning that the vaccine is meant to stimulate a response against both the bacteria and the toxin produced by the bacteria. Several pre-calving vaccines ("scour shots") contain C. perfringens Type C (and occasionally D) bacterin-toxoids. A separate vaccine against Type A antigens has been conditionally licensed and is available. Since vaccines for Type C (against the beta toxin) do not cross-protect against other types (other toxins), and while not expressly labeled for this use, this vaccine has been used in cows pre-calving to try to maximize colostral protection against Type A enterotoxemia (alpha toxin). - See more at: http://www.thebeefsite.com/articles/127 ... e0wIi.dpuf

 

[denvermartinfarms]

denvermartinfarms

As you feed protein tubs and it is a known fact that "
Cattle that are on a high plane of nutrition," "are most susceptible to the disease " of blackleg and
protein tubs can also cause symptoms that mimic blackleg.
Also it is known that protein tubs can be toxic and can cause all kinds of problems as many toxins are passive,
I would recommend you take a serious look at your cattle's complete diet.
Liz

Sl with all due respect, I aint buying that
Can you provide documented proof of that claim ?

Don't think so, my 7 day old calves that died hadn't had anything but momma, and this one at 60 days hadn't been in the tub much. If you have blackleg on your place it's just there and vaccinating isn't even 100% effective when you have it.

 

[NC Liz 2]

cross_7

Can you provide documented proof of that claim ?

Exactly what statement are you having a problem with?
Liz

 

[cross_7]

cross_7

Can you provide documented proof of that claim ?

Exactly what statement are you having a problem with?
Liz

Don't play your BS games with me
I'm trying to be polite but I'm short on patience

protein tubs can also cause symptoms that mimic blackleg.
Also it is known that protein tubs can be toxic and can cause all kinds of problems as many toxins are passive,

 

[NC Liz 2]

Denvermartinfarms

Don't think so, my 7 day old calves that died hadn't had anything but momma, and this one at 60 days hadn't been in the tub much.

Exactly, and that is why I suggest you take a close look at momma's diet as toxins are passive.
Meaning, toxins can be passed from the momma to the calf in both her blood and milk.
And it would be very uncommon for calves that age to contract blackleg.
Liz

 

[NC Liz 2]

denvermartinfarms

I would suggest you talk to the previous property owner and ask who his vet was.
Then ask if he had any problems with blackleg or a high mortality rate and discuss your problem with him.
Also check with your neighbors to see if they are having the same problem on adjoining lands.
Then talk to his vet.
That should tell you if you are barking up the right tree or not.
Liz

 

[cross_7]

denvermartinfarms

I would suggest you talk to the previous property owner and ask who his vet was.
Then ask if he had any problems with blackleg or a high mortality rate and discuss your problem with him.
Then talk to his vet.
That should tell you if you are barking up the right tree or not.
Liz

Again with all due respect quit screwing up the thread with this nonsense
You throw off the wall unfounded statements around and seem to just make things up as you go

 

[NC Liz 2]

Cross_7

protein tubs can also cause symptoms that mimic blackleg.

OK. From denvermartinfarms

All the ones that have died were sudden

That is not a symptom of blackleg but is a symptom of toxicity and we all know high levels of sulfur can be toxic.
From denvermartinfarms

They have all had a frothy and sometimes bloody foam at the anus and mouth they have also had alot of gas under the skin.

Those symptoms can be both blackleg and toxic poisoning.
From denvermartinfarms

This one today had white fibers around the intestine area.

That too is both symptomatic of blackleg and toxic poisoning.

Also it is known that protein tubs can be toxic and can cause all kinds of problems as many toxins are passive,

See: http://www.ethanolproducer.com/articles ... r-build-up
Liz

 

[bigbull338]

denver your going to have to start blackleg vaccing all your cows an calves asap.im surprised that you hadnt already had cows drop dead from blackleg yet.

 

[denvermartinfarms]

denver your going to have to start blackleg vaccing all your cows an calves asap.im surprised that you hadnt already had cows drop dead from blackleg yet.

I started doing all the cows about 8 months ago, and now I am giving it to all the new calves and again at 2 weeks.

 

[cross_7]

So today I pretty much found out that it's very possible I may have to sell my farm and move because I have something that there is nothing you can do about.

I wouldn't sell the farm just yet
I'd try vaccinating the bred cows with 8 way plus scour guard
I might not keep but a few there just in case it didn't work
from the article

Several pre-calving vaccines ("scour shots") contain C. perfringens Type C (and occasionally D) bacterin-toxoids. A separate vaccine against Type A antigens has been conditionally licensed and is available. Since vaccines for Type C (against the beta toxin) do not cross-protect against other types (other toxins), and while not expressly labeled for this use, this vaccine has been used in cows pre-calving to try to maximize colostral protection against Type A enterotoxemia (alpha toxin). - See more at: http://www.thebeefsite.com/articles/127 ... Xdsov.dpuf

 

[denvermartinfarms]

Thanks cross, I'm not jumping on anything to quick. Well see how it goes in the next few months.

 

[highgrit]

I can't believe you haven't been vaccinating for Blackleg DM. I am going to leave it at that, I am shocked.

 

[NC Liz 2]

FYI:
Combating Sulfur Toxicity In Range Cattle
May 3, 2013

Erica Koller, an Edgemont, SD-based DVM, says cattle are typically able to adjust to high sulfur content in their drinking water. What often causes them to exhibit sulfur toxicity is when a protein supplement is fed in conjunction with the water.
"Ethanol-derived dried distillers grains (DDGs) is a huge byproduct used in cakes, mineral tubs and almost any other supplement that someone might use, mainly because it tends to be a cheaper, more readily available protein source. The issue is that some ethanol plants clean with sulfuric acid, and each batch of DDGs could contain anywhere from 0.4% to 1% sulfur," she says.
With maximum diet sulfur levels for cattle suggested at 0.3-0.4%, in the right scenario, adding a supplemental feed could quickly surpass even a well-adjusted cow's ability to avoid toxicity.

http://beefmagazine.com/pasture-range/c ... nge-cattle

 

[cross_7]

I can't believe you haven't been vaccinating for Blackleg DM. I am going to leave it at that, I am shocked.

by denvermartinfarms » Sun Jan 12, 2014 9:21 pm

Before this I had never had any blackleg in my cattle, but I always gave all my calves a 7 way and type A shot when I worked them and when I weaned. When we got here to the new place I started losing healthy calves at 7 to 14 days old, so then I cought most every calf born and at 7 days or less I gave them shots, so far that was working.

 

[denvermartinfarms]

I can't believe you haven't been vaccinating for Blackleg DM. I am going to leave it at that, I am shocked.

I had done everything necessary up until this. We had never had blackleg, I always vaccinated the calves with 2 rounds, but since I had never had any kind of an issue I wasn't blackleging the cows. I made it 10 years with not 1 problem.

 

[tnwalkingred]

Denver,

I hate to hear you're having trouble with blackleg. Losing one calf was bad enough for me earlier this year so I can't imagine losing a bunch. My neighbor lost a few calves to blackleg last year and I've been vaccinating ALL my cattle ever since. I wouldn't move but I would definitely make sure I give all my cattle the recommended shots. We're you not able to send the last calf to the lab? I know here in TN it's a free service the state offers.

Kyle

 

[presmudjo]

I am terrible at remembering names, but was wondering if the poor bugger on here who bought the 45 or so calves in florida and had them all about die, got calves with this type of blackleg. I read that whole article at the beginning and it made me wonder. Certainly sounded like it could have been the way I read the article. I hope you can get ahead of it with your new plan of action of additional vaccine intervals.