Infectious GI disease Flashcards
Etiology of Coccidiosis
Species specific
o Eimeria zurnii and E. bovis
T/F: Any coccidioid organisms present will cause clinical signs
False. Low level of infection may exist in all cattle, usually without clinical signs
What is the preferred environment for Eimerial organisms?
Warm, moist climates favor the growth and life cycle of the organism
Crowded conditions where opportunity to eat off the ground
What is the typical presentation (signalment) for coccidiosis and why?
Mostly a clinical disease of calves less than 6 months of age, but may occur in older animals
- young have less immunity and related to unsanitary environment (ie overcrowding)
- they are exposed to feces of older animals
Crowded conditions where opportunity to eat off the ground
Clinical signs for Coccidiosis
o Diarrhea with variable amounts of fresh red blood - can be confused with Salmonellosis, but
cows with Salmonella are usually feeling worse
o Straining, anemia, weight loss
o Some animals may show nervous signs
Diagnosis for Coccidiosis
o Clinical signs & High Oocysts count in feces
Treatments for Coccidiosis
o Blood transfusion in severe cases
o Epidural anesthesia in severe causes of straining – relaxes muscles to relieve straining
o Amprolium (Corid) for 5 days at 10 mg/kg, sulfonamides - most of the time this suffices
- Can give oral - treat every calf orally, or add to feed or water and make this the
only available water source for a few days
o Sulfonamides
Preventative drug dosing for Coccidiosis
o Amprolium (Corid) 5 mg/kg for 21-28 days
- Mix with feed or water
- Make sure there is only one water source or cows
will avoid drinking treated water
o Decoquinate 22.7 mg/100lbs for 28 days
o Rumensin 100-360 mg/head/day
What is Johne’s disease and what causes it?
Johne’s (pronounced “Yoh-nees”) disease and paratuberculosis are two names for the same animal disease. Named after a German veterinarian*, this fatal gastrointestinal disease was first clearly described in a dairy cow in 1895. A bacterium named Mycobacterium avium ss. paratuberculosis (let’s abbreviate that long name to “MAP”) causes Johne’s disease. MorphologyThe infection happens in the first few months of an animal’s life but the animal may stay healthy for a long time. Symptoms of disease may not show up for many months to years later. This infection is contagious, which means it can spread from one animal to another. MAP is hardy - while it cannot replicate outside of an infected animal, it is resistant to heat, cold and drying.
What kinds of animals can get Johne’s disease?
Johne’s disease is primarily a health problem for ruminant species (ruminants are hoofed mammals that chew their cud and have a 3-4 chambered stomach) and occurs most frequently in domestic agriculture herds. Some of the more common ruminants are cattle, sheep, goats, deer, antelope, and bison. It is particularly common in dairy cattle, not because they are more susceptible to infection but because they are more frequently exposed to the organism that causes Johne’s disease (MAP). Infected ruminants have been reported from all parts of the world. Non-ruminants such as omnivores or carnivores (birds, raccoons, fox, mice, etc.) may become infected, but rarely do they become sick because of the infection.
What are the symptoms of Johne’s disease?
There really are only two clinical signs of Johne’s disease: rapid weight loss and diarrhea. In some animal species, like sheep and goats, diarrhea is less common. While virtually all animals are infected in the first months of life, signs of disease usually do not appear until the animals are adults. Despite continuing to eat well, they become emaciated and weak.Since the signs of Johne’s disease are similar to those for several other diseases, laboratory tests are needed to confirm a diagnosis. If a case of Johne’s disease occurs, it is very likely that other infected animals (who may still appear healthy) are in the herd.
What Causes the symptoms of Johne’s disease?
No one yet understands what causes a clinically normal animal that has been infected by MAP for months or years to suddenly become sick from the infection. We do know that at some point the MAP that have been lying quiet within cells of the last section of the small intestine Gut(called the ileum) start to replicate and take over more and more of the tissue. The animal’s immune system responds to all these organisms with what is called granulomatous inflammation. This inflammation thickens the intestinal wall, preventing it from functioning normally.This, among other factors, means the animal cannot absorb the nutrition it needs and thus begins to lose body condition, milk production drops off, and diarrhea may occur. In effect, an animal with Johne’s disease is starving in spite of having a good appetite and eating well.
How common is Johne’s disease?
Every country that has tested their domestic agriculture species for Johne’s disease has found cases of infection. In the U.S. it is estimated that 8% of the beef herds and 68% of the dairy herds contain at least one animal infected with MAP. Infection rates in cattle in other countries are generally similar, although with significant effort some countries, notably Australia, have reduced the prevalence. In general however, the number of cases keeps going up. Commonly reported in sheep and goats as well as cattle, cases have also been seen in captive elk, deer, bison, and llamas. The infection is much more prevalent in captive ruminants than in free-ranging ruminants such as deer or elk.
How do animals get infected?
Johne’s disease typically enters a herd or flock of animals when an infected, but healthy-looking, animal is purchased. This infected animal then sheds the organism onto the premises – perhaps onto pasture or into water shared by its new herdmates. Young animals are far more susceptible to infection than are adults: these kids, lambs, or calves swallow the organism along with grass or water. Perhaps they are bottle-fed with MAP-contaminated milk collected from the infected but healthy-appearing new animal. (The milk may become contaminated from the environment (manure-stained teats) or, in the advanced stages of the infection, the bacterium is shed directly into the milk.) Animals may even have been infected before they are born (in utero transmission). Thus the infection spreads, often without the owner’s being aware of it.
How can you prevent your animals from getting Johne’s disease?
Do not introduce it! Try to purchase animals from a source herd free of Johne’s disease. Second best is to work with producer who knows the level of Johne’s disease in his or her herd, follows good infection control practices, and then purchase test-negative animals from test-negative dams. Remember that Johne’s disease is a herd problem, and that knowing the test-status of numerous adults in the source herd will give you a much better sense of the risk of purchasing an infected animal than the one test result you might get on the one animal you wish to buy. Evaluating a source herd is not always easy but keeping the infection out of your herd is much less cost and trouble than controlling it once it gets in. Laboratory tests are available for any species – you can even test the environment nowadays.
How do you test animals for Johne’s disease?
New approaches are now available for testing that are cheaper and more reliable than ever before. The three common ways to test a herd for Johne’s disease are: culture of fecal samples (individual or pooled; collected directly from the animal or the barn or pasture) to isolate MAP, direct PCR with the same type of samples to detect MAP DNA, and blood, or tests on blood or milk samples for antibodies by the animal in response to MAP infection.
How do you control Johne’s disease?
Specific methods for MAP infection control depend on the animal species, the resources available, the goals of the animal enterprise, and the methods of animal husbandry. All control approaches however rely on two core strategies that must be employed at the same time:
1 Newborn animals must be protected from infection by being born and raised in a clean environment and fed milk and water free of MAP contamination. The primary source of MAP contamination is manure from an infected adult animal.
2 Adult animals infected with MAP must be identified and managed to ensure no young animals are exposed to their milk or manure.
Can Johne’s disease be cured with antibiotics?
No. In the few studies that attempted to treat Johne’s disease with antibiotics, symptoms appeared to subside but animals relapsed after therapy was halted. As with other mycobacterial infections (for instance, human tuberculosis) multiple antibiotics must be injected or given orally daily for months. For most animals, this is cost-prohibitive as well as infeasible.
Can humans get Johne’s disease?
The term “Johne’s disease” is used only to describe the clinical illness in ruminants that occurs after MAP infection.
There is a human ailment however called “Crohn’s disease” that in several ways resembles Johne’s disease. Crohn’s disease is a chronic inflammatory bowel disease (IBD) that has no known cause and no known cure. In some studies MAP has been found in tissues of Crohn’s disease patients more often than controls. Some researchers believe MAP is the cause of Crohn’s disease for at least a subset of patients. The majority of gastroenterologists, however, do not; they believe that MAP, if found in this subset of patients, is simply a by-stander amongst the many other organisms that are found in a malfunctioning gastrointestinal tract. No connection has been shown between contact with animals with Johne’s disease, dairy product consumption and Crohn’s disease. This aspect of MAP is a complex and controversial area of scientific investigation.
Route of transmission of Salmonella
Fecal - oral route. Can be in feed or water
The main points of the case at “Hudson Farm”
Calves are purchased at a sale, brought to the farm, die, owner then moves the dead animals with the front end loader, which he later uses to feed all the other animals. Eventually other animals get sick, then people who drank raw milk get sick and it is traced back to Hudson Farm. Front end loader was responsible for spreading the salmonellosis.
o When rumen is not functioning normally then salmonella outbreak occurs
2 factors that contribute to a salmonellosis case( outbreak)
Stress factors
Contaminated feed or water
Clinical signs of peracute salmonellosis
Peracute
- Most common form seen in newborn, colostrum deprived calves
- Fever, depression, dehydration
- Diarrhea, abdominal pain, feces yellow in color and blood flecked
- High mortality
- Endotoxic shock develops rapidly
Clinical signs of acute salmonellosis
Acute
- Fever, bloody diarrhea
- Mortality usually less than 50%
- May recover and become a chronic carrier
Clinical signs associated with chronic salmonellosis
Chronic
- May cause abortion or mastitis
- Fever, watery diarrhea, blood and mucus may not be present
- Low mortality, slow recovery
Detection of a subclinical or carrier case of salmonellosis
Subclinical or carrier
- Continual shedding of organism to calves and mature cattle
- May require repeated cultures at 7-10 intervals to detect
Diagnosis of salmonellosis
o Clinical signs
o Isolation of the organism – definitive diagnosis
o Can be in raw milk
Treatment for Salmonellosis
o Fluids, electrolytes – more important - trying to re-inoculate intestinal tract with healthy organisms to crowd out salmonella
- This is why giving tetracycline to horses can cause
salmonellosis - the abx changes GI flora and
causes Salmonella to overgrow
o ABX??? May be more useful in calves with septicemia than in adults or carriers - most salmonella in food animals is resistant to all ABX
o probiotics
o Plasma product
Control and prevention of salmonella
o Sanitation is most important
o Chlorinate water supplies
o Vaccination – need autogenous vaccine using culture from animals on same farm
o If you have a barn where numerous animals are housed from different owners you HAVE TO get
them all on the same vaccination schedule.
Regarding the salmonellosis outbreak on Hudson farm that was discussed in an assigned reference, how was the infection introduced on the farm?
New calves –> front loader that was mixing feces and feed.
6 diseases that have an “iceberg” effect
- Anaplasmosis
- Johne’s Dz
- Bovine leukosis
- Salmonella
- BVD
- Mastitis (?)
Transmission of Salmonella
Fecal-oral transmission
a. Aerosol is uncommon
b. Look in feed and water supply – always check
4 factors that can contribute to salmonella disease
Contributors to disease
a. Host resistance
b. # organisms/dose of salmonella
c. Virulence/pathogenicity of strain
d. Periparturient cows
Which livestock animals are susceptible to Salmonella?
Affects anything in livestock department with intestinal tract
Majority of Salmonella cases in cattle are clinical or subclinical?
Majority of cases are subclinical in cattle
By which routes do septicemic animals shed salmonella?
Septicemic animals shed in oral secretions, urine, feces and aerosol
How is salmonella killed naturally in cattle?
Salmonella killed by exposure of VFAs from normal functioning rumens
a. VERY IMPORTANT to feed cows properly
b. Maximize rumen function by dry matter intake, esp. in periparturient and fresh cows
How hardy is salmonella in the environment?
Survives long periods in the environment - it needs minimal amounts of moisture; may be killed by
direct sunlight
Replicates in moist environments, even with scarce nutrients
T/F: Salmonella is not zoonotic
False: It causes significant zoonotic disease, esp. in children (S. typhimurium)
Corona virus is the causative agent for which disease?
Winter Dysentery
Clinical signs for Winter Dysentery
o Usually a herd problem of dairy cattle during winter stabling
o Occurs very suddenly with a high morbidity (many animals at the same time); 20% overnight
o Watery, brown, fetid diarrhea with flecks of blood
o Usually low or no fever, appetite remains good
- Different from: BVD and Salmonella – high fevers
and not eating or drinking
o Milk production severely depressed - lose a lot of fluid with diarrhea, so milk production decreases
o Within a few days, the entire herd may show signs
How long will a course of winter dysentery run for?
o Individual course may run 2-3 days, but recovery in milk production may take much longer
Diagnosis of Winter dysentery is made by:
o Clinical signs
o Need to differentiate from other causes of acute
diarrhea, including feed changes
Treatment for winter dysentery and how long until animal is back to normal?
Treatment – intestinal astringents such as oral tannic acid or copper sulfate
o Takes awhile for animal to recovery and return to normal milk production
Name the two notable intestinal parasites in cattle
Ostertagia and trichostrongylus (also lung worms)
T/F: There is a vaccine against lung worms
True
Ostertagia is a big parasite in cattle, what is it’s cousin in sheep?
Haemonchus
What organ are ostertagia found in?
The abomasum
T/F: Dairy cattle in confinement aren’t exposed to oocysts and don’t need to be dewormed
True!!
Heifers out grazing more susceptible to nematodes
What cattle are dewormed for ostertagia?
Deworm only grazing/pasture cattle
How does ostertagia affect young vs. older cattle?
- Develop some degree of resistance with age
- Young –> impaired digestion d/t losing parietal cells
- Loss of hydrochloric acid producing parietal cells
results in failure of conversion of pepsinogen to
pepsin leading to impaired digestion of feed stuff
in cattle
• Elevated serum plasma pepsinogen values may be indicative of Ostertagia infection
Why might elevated serum plasma pepsinogen be indictive of an ostertagia infection?
Loss of hydrochloric acid producing parietal cells results in failure of conversion of pepsinogen to
pepsin leading to impaired digestion of feed stuff in cattle
What factors are involved in parasitism?
o Climactic conditions – more problem in spring and summer
o Age of the animal – resistance develops with age -young more likely to be affected
o Season of the year - more in spring and fall
o Nutritional level
o Sanitary conditions
o Genetic resistance - see that with sheep and Haemonchus (Red Masai) and BBB
Clinical signs of parasitism
o Ill thrift, poor hair coat
o Diarrhea
o Weight loss, poor BCS
o Evidence of hypoproteinemia – bottle jaw – check plasma pepsinogen
