VIN Class 2 - Bovine Info Flashcards
VIN + VetPrep Power Pages
Topic: Mastitis
1. Define mastitis
2. What is the difference between subclinical and clinical mastitis? Which is more common?
3. How can you detect subclinical mastitis?
4 How can you detect clinical mastitis?
5. Once the infection is eliminated, how long until the SCC count returns to normal?
1.Mastitis is inflammation of the mammary gland most frequently caused by bacteria or mycoplasma.
2. Subclinical mastitis is more common than clinical mastitis and results in a drop in milk production and alteration in milk composition but there are no signs of systemic illness. Clinical mastitis results in visible milk changes, the milk gland itself is inflamed, there is a drop in milk production, and the cow may exhibit signs of systemic illness
3. Somatic cell count, California Milk Test, and Electricl conductivity are the three ways you can detect subclinical mastitis.
- An SCC > 100,000 cells/ml is consistent with inflammation while an SCC > 200,000 cells/ ml is consistent with infection.
- For the CMT: 2-3 ml of milk is stripped from each quarter, the reagent is added the lyse the cells and the mixture is gelled. The degree of gelling is graded from 0-3 and corresponds to the number of cells present. A grade of 0 means there are fewer than 200,000 cells/ml.
- Electrical conductivity: With mastitis, there is an increase in sodium and chloride and a decrease in
potassium concentration in the milk, resulting in an increase in electrical conductivity. This can be
measured automatically while the cow is being milked, which results in early detection and
treatment.
4. Mild clinical mastitis: milk has abnormal viscosity, color or consistency. (flakes, clots). Moderate clinical mastitis: Milk is abnormal + gland is swollen, firm, red, and painful + milk production is decreased. Severe clinical mastitis: Milk is abnormal + cow is systemically ill.
5. SCC count returns to normal within 2 weeks.
Topic: Contagious Mastitis
1. Name the MAJOR pathogens associated with contagious mastitis.
2. Name the MINOR pathogens.
3. What pathogen is normally seen in other body sites but can contribute to contagious mastitis?
- Streptococcus agalactiae and Staphylococcus aureus are the major pathogens.
- Corynebacterium bovis is a minor pathogen.
- Mycoplasma spp. are carried in sites other than the mammary gland but once they gain access to the gland they become highly contagious.
Topic: Contagious Mastitis
1. How do you detect/diagnose contagious mastitis?
2. List the ways in which you can PREVENT NEW contagious mastitis infections.
3. List the ways in which you can CONTROL EXISTING contagious mastitis infections. What pathogens does this method of control apply to?
4. What contagious mastitis pathogens are more difficult to treat? Explain what ends up happening to these poor creatures affected :(
5. List other general control methods used to prevent contagious mastitis infection.
- Culture milk samples.
- Post-milking teat dipping with a germicidal solution, usually iodine-based, helps prevent new infections.
- Treating all dry cows with an intramammary antimicrobial product effectively controls existing
infections with S. agalactiae and C. bovis. - Staphylococcus aureus and Mycoplasma are more difficult to eradicate, and animals infected with
these pathogens are often culled. In some cases, cows with Staphylococcus aureus infection are
treated and recultured, and cases still positive are culled. - Additional steps to help control contagious pathogens include:
a. Milkers wearing rubber gloves.
b. A backflush system on the milking cluster.
c. Heifers can be milked before cows to prevent heifers from becoming infected.
d. Sometimes, S. aureus-positive cows can be segregated into a separate string and milked last
Topic: Environmental Mastitis
1. List the sources of infection of environmental mastitis?
2. Name the pathogens that can cause environmental mastitis. Which of these is more severe and can result in death?
3. List the methods of control for environmental mastitis.
4. Which cows are often affected? What steps must you take to protect them as well.
- Bedding, fecal material, soil, contaminated water.
- Coliforms and environmental streptococcus including S. uberis, dysgalactiae, etc. Coliforms are more severe and may result in death.
- Frequent manure removal.
● Using appropriate free stalls and managing the bedding.
● Providing pastured cows with clean locations to lie down.
a. Sand is a preferred bedding material.
b. Wood products are to be avoided as they predispose to Klebsiella mastitis.
● Pre-dipping teats and having clean dry udders at milking are important - Dry cows are often infected, so maintaining clean bedding areas for the herd must include the dry cows.
Dry cow treatment with intramammary antimicrobials and a teat sealant are also useful.
Topic: Mastitis
Which pathogens can be either contagious or environmental?
Coagulase negative Staph - Staph hyicus, epidermidis, etc.
They are the most heavily isolated from the milk of cows and heifers.
Topic: Mastitis
Name less common pathogens that can cause mastitis
Arcanobacterium pyogenes, Prototheca, yeasts, Pseudomonas, Serratia, Nocardia, Mycobacterium, and Pasteurella.
Topic: Calf Diarrhea
List the age of onset for the following etiologic agents:
1. E.coli aka K 99
2. Rotavirus
3. Coronavirus
4. Cryptosporidia
5. Salmonella
6. Coccidia (Eimeria bovis and zuernii)
- E.coli aka K 99 = 0-3 days
- Rotavirus = 5-15 days
- Coronavirus = 5-15 days
- Cryptosporidia = second week of life
- Salmonella = > 14 days
- Coccidia (Eimeria bovis and zuernii) = > 30 days
What is the most common VIRAL cause of calf diarrhea?
Rotavirus
A 50-kg calf is presented 10% dehydrated. What volume of fluids is needed to rehydrate the animal?
(50-kg calf) x (0.10 dehydration) = 5.0 liters total volume.
A 45-kg calf is presented with a base deficit of -15 mEq/l. Assuming that the extracellular fluid volume is 60%, what volume of 150 mEq/liter HCO3 fluids is needed to correct this base deficit in the animal?
(0.6% body weight ECF) x (45-kg calf) x (15 mEq base deficit) = 405 mEq HCO3 needed.
(405 mEq HCO3)/(150 mEq/liter isotonic HCO3) = 2.7 liters of isotonic bicarb.
Topic Bovine Abortion
List the causes of Bovine abortion in the early, mid and late trimesters. List the causes of abortion during ANY point of gestation.
- Early-term/1st half of gestation = Tritrichomonas foetus AKA Trichomoniasis
- Mid-term (4-6 mo): Neospora Caninum AKA Neosporosis
- Late-term: Essentially everything else (Lepto - last trimester)
◦ THERE ARE SEVERAL WITH VARIABLE TIMELINES:
- IBR (4-9 mo)
- BVD (up to 4 mo)
- Campylobacter (5-8 mo)
- Mycotic abortion (4 mo - term)
- Trueperella pyogenes
- Listeria (any stage)
- Brucella abortus (Second half of gestation, ~ 7 mo)
Topic: Abortion - Neospora caninum
1. Is there a likelihood of recurrence in cases of Neosporosis in cattle?
2. Describe how calves are affected.
3. If a calf is born alive, what risks are there?
4. Is there a treatment for Neosporosis?
5. What is seen on necropsy?
6. Methods of prevention?
7. Major clinical sign of Neosporosis in puppies?
- Susceptibility decreases with the # of births
- Calves can either be aborted, born stillborn, born paralyzed, or born alive with infection.
- Calves that are born alive can pass Neospora to their own offspring.
- No treatment
- Lesions, in brain, heart, muscle
- Prevent contamination of feed by dog feces but vertical transmission most importan.
- Causes ascending paralysis in puppies.
What is the most common VIRAL cause of abortion in cattle?
IBR
Topic: Abortion - IBR
1. How long after initial infection do abortions occur?
2. How is IBR diagnosis made? **
3. How is IBR controlled within a herd? What is a risk factor associated with this control method?
- Abortion can occur several weeks after disease has gone through the herd. Vaccination in the face of an outbreak will not decrease abortions.
- Diagnose via immunological staining of fetal kidney, adrenals, or viral isolation from placenta, serology of dam.
- Vaccinate herd. NOTE: Modified live vaccine can cause abortions!!
Topic: Abortion - Brucella abortus
1. What is important to remember about this disease?
2. What preventative method is used?
3. Infected animals shed the virus via?
4. What is the incubation time?
5. How is Brucella abortus diagnosed?
6. What screening methods are used?
7. Treatment?
8. Is Brucellosis in the U.S.?
9. How are horses infected with Brucella abortus affected?
- Zoonotic, reportable
- Vaccinate with RB51 strain
- Infected animals shed virus in milk for life, spread by ingestion of contaminated fetal and placental tissues/fluids
- Incubation time is 2-4 weeks
- serum agglutination test
- Brucella milk ring test
- no treatment
- As of July 2009 U.S. cattle were declared Brucellosis-free by the USDA, but brucellosis in wild bison and elk herds in Montana, Wyoming threaten the brucellosis-free status of cattle in the surrounding states.
- B. abortus causes fistulous withers in horses
Topic: Abortion - BVD
1. Transmitted via?
2. Carrier animals are ?
3. Infection at < 125 days affects the fetus by?
4. Infection at > 125 days affects the fetus by?
5. How is BVD spread prevented?
- aerosol or contact
- Persistently infected from birth
- Infection of fetus < 125 days can cause absorption, fetal death, mummification, fetal abnormalities, or persistent infection of calf.
- infection at gestational age > 125 days can result in abortion or clearing of virus from fetus
- remove PI animals and vaccinate herd
Topic: Abortion - Leptospira interrogans
1. Is there a risk of recurrence in cows infected with Leptospira interrogans?
2. What is important to remember about Lepto?
3. Lepto affect cattle that appear?
4. How is lepto prevented? **
5. Can be spread via?
6. Diagnostics? **
- Affected cows remain vulnerable to all other strains EXCEPT for the one that causes abortion.
- It is zoonotic!
- Healthy
- twice yearly booster vaccination in high-risk herd
- Vertical or horizontal transmission
- check dam’s urine for leptospires, FA test placenta, fetus
Topic: Abortion - Campylobacter fetus
1. What strain of C. fetus is a major cause of abortion in sheep?
2. C. fetus fetus and C. jejuni are spread by?
3. What is the major abnormality found in fetuses?
4. Diagnostics?
- Campylobacter fetus fetus is a major cause of abortion in sheep
- ingestion
- Bronchopneumonia
- darkfield exam and culture of abomasal contents, culture
Topic: Abortion - Listeria monocytogenes
1. What is important to remember about this disease?
2. Outbreaks often associated with?
3. Diagnostics
- Zoonotic
- Outbreaks often associated with spoiled silage
- Culture from fetus, placenta
Topic: Abortion - Mycotic Abortion
1. List the causes of mycotic abortion in cattle.
2. Most common during what season?
3. What is seen grossly?
4. Diagnostics?
5. What should be avoided?
- Ponderosa Pine Needles, Locoweed, Moldy sweet clover, And others
- Most common in winter
- Severe placentitis
- Dx: culture fungi from stomach contents; Presence of fungal hyphae in placenta
- Avoid moldy feed
Topic: Abortion - Tritrichomonas foetus aka trichomoniasis
1. Trichomoniasis is a __________ disease, ______ organism
2. Infection causes what two major consequences?
3. Abortion occurs during what part of gestation?
4. How are infected bulls affected? Cows?
5. Preventative methods? **
6. Clinical signs are similar to what other etiologic agent?
7. Diagnose via? **
- Venereal disease; Protozoal organism
- protozoan causes infertility and extended calving interval.
- Abortion in first half of gestation, 4. bulls infected indefinitely.
- Cows clear infection but can be re-infected
- Avoid reinfection by using artificial insemination with semen from bulls negative for T. foetus. Test and cull positive bulls, breed only uninfected bulls to uninfected cows/virgin heifers.
- Clinical signs same as Campylobacteriosis.
- Dx by preputial epithelial scrapings from bulls, vaginal discharge/douche; dark field microscopy/culture for organism
Topic: Abortion - Campylobacter fetus venerealis and Campylobacter fetus fetus
1. Campylobacteriosis is a __________ disease, ______ organism
2. Transmitted via?
3. A.I., bulls > 4 years become ?
4. Cows (but not bulls) experience?
5. What is NOT diagnostic?
6. What is diagnostic? **
7. Treatment **
- Venereal disease, gram-negative flagellated bacteria
- Breeding, contaminated instruments, bedding
- chronic carriers
- immune, ow pregnancy rates, extended calving interval.
- Antibody responses are not diagnostic because often due to nonpathogenic Campylobacter spp
- vaginal mucus agglutination test or ELISA of vaginal mucus, fluorescent antibody test of preputial washing or scraping (sample bulls 2x)
- vaccinate for treatment (though cows may remain carriers!) and prophylaxis as vaccination hastens clearing of infection; bulls can be treated with subcutaneous streptomycin and streptomycin applied topically to penis.
Topic: IBR
1. IBR is what type of disease?
2. List the clinical manifestations of IBR
3. List the etiologic agent of IBR
4. When was IBR originally recognized?
5. How is it transmitted? **
6. Latent infection is maintained in the?
7. What may trigger recurrence of infection?
- viral disease of cattle
- several clinical manifestations including abortion, ocular disease, respiratory
disease (red nose) , Infectious pustular vulvovaginitis, Generalized neonatal infection, Encephalitis - Bovine Herpesvirus-1 with 3 subtypes called BHV-1.1 (respiratory), BHV-1.2 (respiratory and genital), and BHV type 5 (neurologic).
- 1950s
- Airborne or contact transmission. Can also have spread via: Breeding, In utero, During birth if passing through an infected vagina.
- ganglia
- Stress may result in recurrence of infection in those previously recovered.
Topic: IBR cont.
1. List the clinical signs of each form of IBR **
1a. Respiratory
Important feedlot disease with role in bovine respiratory disease complex
● Fever 104-107°F
● Immunosuppression
● Red Nose (inflammation of muzzle and nostrils) and nasal discharge. Often see small white plaques in nares.
● Decreased appetite, depression, and rapid breathing
● Usually the entire herd is affected
● Tracheitis, may have nonproductive cough
● Death uncommon unless secondary bacterial pneumonia occurs
1b. Ocular
● May occur alone or in conjunction with respiratory form.
● Severe conjunctivitis.
● Excessive clear ocular discharge with corneal opacity in some cases.
a. May make the surrounding haired areas look crusty
b. Differentiate from Moraxella bovis
1c. Infectious Pustular Vulvovaginitis
● Vulvar discharge.
● Dairy cows show drop in milk production.
● Red spots and pustules lining the vulva and vagina.
● Excessive tail twitching.
● Frequent urination.
● Persists for approximately 2-3 weeks.
● Males will also get pustular lesions on the penis with exudate and inflammation (balanoposthitis).
1d. Abortion
● Most IBR abortions occur at about 5-6 months of gestation.
● Animals can usually breed back.
● Abortion is a result of fetal death and the fetus is typically partially decomposed.
● Can induce abortion by giving modified live virus to pregnant animals or those in contact with pregnant animals.
1e. Neonatal Generalized Infection **
● Respiratory tract, GI tract, liver, kidneys, and adrenals involved
● Usually fatal
● Can be caused by wild virus or live vaccines
Topic: IBR Cont. 3
1. Describe the tx and control for IBR **
No effective treatment.
a. Supportive care and antimicrobials to prevent secondary bacterial infections in
respiratory form.
b. Flunixin or other NSAID, shade, water and good feed.
● Isolate new additions for 30 days prior to introduction to the herd.
● Isolate infected animals immediately to prevent rapid spread.
● Vaccinate before outbreak.
a. Be careful which type of vaccine you use (killed vs. live) to avoid abortion.
b. Use either intranasal or IM live vaccines in feedlot aged and adult cattle.
c. Do not use live vaccines in neonatal calves.
Topic: Polioencephalomalacia
1. What type of disorder is Polioencephalomalacia?
2. What is believed to be the main cause? What are other proposed causes?
3. Name the predisposing factors of this disease. **
4. What are the clinical signs? **
- Polioencephalomalacia is a neurologic disorder seen in ruminants.
- A deficiency of thiamine is believed to be the main cause of the disease although others have been suggested, including excess intake of sulfur, lead, or sodium.
- ● High concentrate diets (pastured animals can also develop disease)
● Feed with corn or sugar cane byproducts
● High grain intake may promote proliferation of thiaminase producing bacteria
● Rations with added sulfate to limit intake
● Ingestion of plant thiaminases or thiamine analogs - Depending on the nature of the underlying cause, this can appear as an isolated
disease or a herd problem. - Acute Form
● Blindness
● Seizures
● Recumbency
Subacute Form
● Initial signs
a. Decreased appetite
b. Twitching (ears and face)
c. Separation from the herd
d. Hold head up in an elevated position
e. Staggering, hypermetric gait
Later signs
a. Cortical blindness
i. Absent menace, intact palpebral reflex and pupillary light response
b. Dorsomedial strabismus
c. Head pressing
d. Teeth grinding
e. Opisthotonus
Topic: Polioencephalomalacia Cont.
1. Diagnostics
2. Pre-mortem findings
3. Post-mortem findings **
4. Treatment
1.Diagnosis can be challenging. Consider differentials such as listeriosis, nervous coccidiosis, salt toxicity, meningoencephalitis, rabies, vitamin A deficiency, pregnancy toxemia (sheep).
a. Clinical presentation is useful to help differentiate polioencephalomalacia
from many of these conditions.
- Pre-mortem diagnostic testing can be unreliable and not available in many laboratories.
a. i.e. Blood thiamine levels, transketolase activity to assess thiamine. - Post-mortem findings.
a. Gyral flattening, brain swelling.
b. Brain tissue may fluoresce under UV light.
c. Cerebrocortical neuronal necrosis.
d. Cortical spongiosis.
e. Cavitation of cortical tissue.
f. Multifocal vascular necrosis, hemorrhage, and necrosis in deep gray matter. - Early treatment is critical.
● Treat with thiamine, regardless of cause.
a. 10-20mg/kg IM or SC TID.
b. Expect to see improvement within 1-3 days.
● If cerebral edema is suspected, can administer 1-2 mg/kg of dexamethasone.
● Supportive care.
● Consider thiamine supplementation in feed for prevention of disease in other animals, supply
roughage, and investigate environment for sources of thiaminases or excessive sulfur levels.
● Animals with advanced disease may continue to show significant neurologic impairment
after treatment.
Topic: Bovine Spongiform Encephalopathy (BSE)
- Etiology & Transmission
1b. What is so special about this etiologic agent?
1c. Who is most susceptible? - Clinical Signs
- Diagnosis? What is characteristically seen in this disease?
- Treatment
- This disease is similar to _____ found in humans?
1 + 1b. The causative agent of this diseases is still a topic of debate but a prion (abnormal protein) is theorized. The agent is extremely resistant to heat and normal sterilization procedures. BSE is not contagious through casual contact between cattle. The primary source is contaminated commercial feed from incorporating ingredients (i.e. Bone meal) from rendered infected cattle.
1c. Young animals are most susceptible.
2. Onset over several months
a. Nervousness or aggression progressing to hyperesthesia (exaggerated reflexes)
b. Incoordination, abnormal posture, difficulty rising, progressive ataxia, fine tremor
c. Weight loss, decreased milk production
d. Persistent licking of the muzzle **
3. BSE - requires histology of the brain for characteristic changes of bilaterally symmetric intracytoplasmic
vacuolation of neurons. Can confirm with immunohistochemistry for prion protein fibrils.
- There is no effective treatment. Report cases of BSE and cull animals.
- Creutzfeldt-Jakob Disease -
A chronic and fatal neurodegenerative disease of humans. In 1996, a new variant (vCJD) was discovered in
the UK, and experimental and epidemiologic studies have linked these cases to consumption of food
containing ingredients of BSE infected cattle. This led to a ban on the use of non-ambulatory cattle in the human food chain and additional controls to inspect slaughtered cattle and forbid the use of mechanically separated meat in human food.
Topic: Bovine Respiratory Disease Complex
- BRDC is also known as?
- Why is this disease so important?
- List the predisposing factors of BRDC.
- BRDC is most commonly associated with?
- Name the viral causes of BRD. **
- Name the bacterial causes of BRD.
- Treatment **
- Prevention and control?
- Shipping fever pneumonia
- This disease is the most common and costly disease affecting the North American beef cattle industry.
- Environmental factors (eg, weaning, transport, commingling, crowding, inclement weather, dust, and inadequate ventilation) serve as stressors that adversely affect specific and nonspecific host defense mechanisms of the host animal. In addition, certain environmental factors (eg, crowding and inadequate ventilation) can enhance the transmission of infectious agents among animals.
- BRD is most commonly associated with the transport and assembly of large groups of recently weaned calves into feedlots, hence its alternate name, shipping fever pneumonia.
- Viruses associated with BRD include the following:
- bovine herpesvirus 1 (BHV-1)
- bovine respiratory syncytial virus (BRSV)
- parainfluenza-3 virus (PI-3)
- bovine viral diarrhea virus (BVDV)
- bovine adenovirus
- bovine coronavirus - Bacteria associated with BRD include the following:
- Mannheimia haemolytica
- Pasteurella multocida
- Histophilus somni
- Mycoplasma bovis
- Bibersteinia trehalosi - The use of broad-spectrum antimicrobials labeled for BRD is the primary treatment, with macrolides and phenicols most commonly used as first-line treatment.
- Prevention and control are achieved via vaccination programs, preconditioning, identification and treatment of subclinically affected animals, and biosecurity.
Topic: Blackleg
1. Etiologic agent
2. Signalment
3. Transmission and Epi
4. C/S
5. Diagnostics and Lesions
6. Treatment and Prevention
- Clostridium chauvoei
- Cattle between 6 months and 2 years of age, commonly after transport, handling, injection, or other rough activity. In sheep, it is almost always
due to a wound or at parturition. - Endospores ingested –> G.I. –> bloodstream –> deposited throughout body OR enter view wound –> bacteria multiply in anaerobic environment esp bruised or damaged muscle tissue.
- Lameness, fever, depression, anorexia; Swelling with possible palpable crepitus from gas bubbles; Animals die rapidly without signs of illness (within 12-48 hours)
- Presumptive diagnosis can be based on gaseous swelling in a young animal.
● On postmortem, the infected area is black and necrotic with gas bubbles.
a. A foul, sweet odor, often described as resembling “rancid butter”, is present. - The disease is often fatal unless identified early and treated with penicillin.
a. Survivors may have permanent deformity.
● Carcass should be immediately disposed of without contaminating environment.
● Prevented by vaccination with 7-way bacterin vaccine: two doses at one-month intervals.
a. Often given as a “7-way” vaccine against Clostridium chauvoei, septicum, novyi types A and B,
sordellii and perfringens types C & D.
Topic: Malignant Edema
1. Etiologic agent
2. Signalment
3. Transmission and Epi
4. C/S
5. Diagnostics and Lesions
6. Treatment and Prevention
- Clostridium chauvoei, septicum, novyi types A and B, sordellii and perfringens types C & D.
- Affects cattle, sheep, goats, and horses of any age
- Disease develops when an open wound is infected with bacteria.
a. May be introduced from injury, castration, difficult parturition, fighting, etc. - Localized swelling and edema that may gravitate to dependent portion of the wound
● Depression, anorexia, high fever
● Death often occurs within 24-48 hours - On postmortem, the infected area is darkened with a foul odor. There is swelling without gas accumulation.
- Often fatal unless identified early and treated with penicillin
● Prevented by vaccination with two doses of 7-way bacterin vaccine, clean surgery, and clean environment following a surgical procedure.
Bighead in sheep is a form of Malignant edema caused mainly by ?
C. novyi type A
Topic: Redwater
1. Etiologic agent
2. Signalment **
3. Transmission and Epi
4. C/S
5. Diagnostics and Lesions
6. Treatment and Prevention **
- (Clostridium haemolyticum)- Bacillary Hemoglobinuria
- Affects cattle and sheep
- Endospores are ingested and the bacteria lodge in the liver.
● When damage occurs in the liver (often due to the liver fluke, Fasciola hepatica),
the bacteria replicates.
● The toxin released results in red blood cell lysis. - Reddish discoloration of urine due to hemoglobinuria secondary to red blood cell lysis
● Labored breathing
● Anemia, icterus
● Dehydration, fever - Extremely pale animal with red urine in the bladder and thin, watery blood.
● Often a large necrotic area in the liver - Early treatment with antibiotics (penicillin or tetracycline) and antitoxin serum.
● Prevented by vaccination with two doses of bacterin with booster given every 6 months, and by controlling liver flukes.
Topic: Black Disease **
1. Etiologic agent
2. Signalment
3. Transmission and Epi
4. C/S
5. Diagnostics and Lesions
6. Treatment and Prevention
- (Clostridium novyi Type B) - Infectious Necrotic Hepatitis
- Primarily affects sheep, but occasionally cattle on a high grain ration.
- Endospores are ingested, and the bacteria lodge in the liver (similar to C. haemolyticum).
a. In sheep, the liver fluke, Fasciola hepatica, plays an important role in the disease in creating a desirable environment for the bacteria to grow.
● Toxins released cause severe liver damage and result in red blood cell destruction. - Sheep are often found dead, with no evidence of clinical signs.
● The disease is less common in cattle and clinical signs may be reluctance to move, lost appetite, and a dull and listless appearance. - Large areas of damaged tissue in liver appear gray to black with a foul smell.
- Usually no effective treatment, as disease often progresses rapidly.
- Prevented by two doses of 7-way bacterin vaccine.
Topic: Tetanus
1. Etiologic agent
2. Signalment **
3. Transmission and Epi
4. C/S
5. Diagnostics and Lesions
6. Treatment and Prevention **
- (Clostridium tetani)
- Found worldwide and can affect most animals, although horses and pigs are most susceptible.
- Organism is found widespread in soil and is introduced through injuries such as puncture wounds,
castration sites, banding, and dehorning.
a. Organism does not actively invade or create a larger wound.
● Incubation period of 10-21 days followed by production of a potent nervous system toxin. - Extended “sawhorse” stance
● Difficulty chewing food (“lock jaw”)
● Stiff tail, prolapsed third eyelid, flared nostrils
● Severe muscle tremors/spasms
● Sensitivity to noise and movement - Diagnosis is based on clinical signs; often no postmortem lesions are present.
- Treated with tranquilization and antibiotics (penicillin), tetanus antitoxin, and supportive care to
prevent dehydration or starvation.
● Prevention with vaccination and by diligent cleaning of surgical instruments, placing animals in clean environment after surgical procedures.
Topic: Botulism
1. Etiologic agent
2. Signalment **
3. Transmission and Epi
4. C/S
5. Diagnostics and Lesions **
6. Treatment and Prevention **
- Clostridium botulinum
- Relatively rare in livestock but outbreaks do occur; horses appear especially susceptible to type B toxin
- Produces type A, B, or C toxins
- Foals susceptible to toxicoinfectious form where the toxin forms in the GI tract. Often called Shaker Foal Syndrome. - Usually introduced through contaminated feed (dead cat or rabbit in silage or hay) where the organism has already produced high levels of toxin into the foodstuff.
- Starts with muscle tremors and fasciculations, then ascending paralysis leading to respiratory paralysis and death. Mydriasis and ptosis, as well as a weak tongue often seen.
- No specific postmortem signs. Detection of toxin in serum, intestine, or feed for confirming the diagnosis and type.
- No effective treatment for most species. In horses, botulism antitoxin has been used with varying success.
● Type B vaccine available; requires 3 doses at 4-week intervals. Booster dose to mare 8 weeks before foaling. Colostrum will protect foal for 8 to 12 weeks. There is a type C vaccine approved for mink that has been used in livestock.
Topic: Enterotoxemia
1. Etiologic agent
2. Signalment
3. Transmission and Epi
4. C/S
5. Diagnostics and Lesions
6. Treatment and Prevention **
- Clostridium perfringens Type B, C and E)
- Usually seen in calves, lambs, kids, piglets, or foals less than 7 days old.
- A normal GI tract inhabitant that only causes disease under certain circumstances.
- Sudden onset, some calves may die without showing any symptoms
● Clinical signs include:
a. Weakness
b. Abdominal distension
c. Bloody diarrhea
d. Convulsions
● Often associated with an increase in dietary intake allowing proper growth environment for bacteria - Extremely reddened sections of fluid-filled small intestines; “purple gut”.
- Usually fatal once signs are present. Can attempt to treat by correcting dehydration and electrolyte imbalances with IV fluids and giving broad spectrum antibiotics and specific antitoxin.
● Prevention by herd vaccination. Can administer antitoxin (antiserum) at birth or can vaccinate dam twice with bacterin/toxoid.
Topic: Overeating Disease
1. Etiologic agent
2. Signalment
3. Transmission and Epi
4. C/S
5. Treatment and Prevention
- Clostridium perfringens Type D; Also known as “pulpy kidney disease” in sheep (name comes from rapid carcass decomposition, which leads
to pulpy kidneys on postmortem, though this is not always found) . - More common in sheep and goats than cattle, most commonly less than 2 years of age, typically on a high grain ration or fattening lambs on rich pasture.
- A normal GI tract inhabitant that only causes disease after excessive ingestion of feed or grain.
4.Decrease in appetite
● Weakness, incoordination
● Diarrhea
● Nervous signs, death
● Glucosuria common - Prevented by two doses of 7-way bacterin vaccine
Topic: Clostridium perfringens Type A
1. Signalment
2. Transmission and Epi
3. C/S
4. Diagnostics and Lesions
5. Treatment and Prevention
- Causes jejunal hemorrhage syndrome (JHS also called hemorrhagic bowel syndrome, or hemorrhagic enteritis in adult dairy cattle), as well as yellow lamb disease, intestinal clostridiosis
in horses and others. - Cows affected with JHS may be found dead acutely or have normal to subnormal temperature,
increased HR, enlarged abdomen (ileus), and may have digested or clotted blood in
feces if they live long enough.
● Lambs show icterus, weakness, and death occurs rapidly. - Cows with JHS can be diagnosed using abdominal US and finding increased small intestinal
diameter. Hyperglycemia, hyponatremia, hypochloremia, hypokalemia,
and hypermagnesemia frequently occur.
● Lambs with yellow lamb disease have hemolysis, anemia, hemoglobinuria,
icterus, fever. Death occurs rapidly - It is not known whether repeated vaccination can prevent JHS, but increasing the amount of long
stem fiber in the diet has decreased the number of cases.
● No Cl. perfringens type A vaccines are available in the USA.
Topic: Ketosis
1. The central process in ketosis revolves around?
2. Signalment
3. What is ketosis also known as in ewes and does? Explain why.
4. What other primary diseases may result in secondary ketosis?
5. Ketosis is characterized by an elevation in?
- Negative energy balance and inadequate feed intake.
Fats are consequently mobilized to support energy production but, in some instances, the body is unable to utilize all these fats (and/or their metabolites) thus resulting in excess production of ketone bodies - Ketosis occurs most commonly in lactating cows because the energy (glucose) necessary to
support heavy milk production exceeds caloric and nutrient intake - Ketosis is also known as pregnancy toxemia in ewes and does; it occurs during the last 2-4 weeks of gestation when there is increased energy demands from rapidly growing fetuses (i.e. twins) combined with insufficient feed intake.
- Displaced abomasum, metritis,
peritonitis and mastitis, among others. - Acetoacetic acid, Acetone, B-hydroxybutyric acid
Topic: Ketosis Cont.
- What are the clinical signs of ketosis?
- How is ketosis diagnosed?
- Treatment?
- Frequent non-specific:
a. Depression.
b. Decreased appetite.
c. Weight loss.
d. Decreased rumen motility.
e. Decreased milk production.
f. The odor of ketones may also be detected on the breath of affected animals.
Pregnancy toxemia is characterized by non-specific signs of anorexia, weakness and depression - Based on history (recent parturition and heavy lactation).
● Elevated ketones in the blood, urine and/or milk.
● Decreased blood glucose.
● Liver enzymes may be elevated due to the central role that the liver plays in energy
metabolism and gluconeogenesis - Correction of any primary disease that may be contributing to anorexia or inappetance should be initiated. Additionally:
- IV glucose
- Oral propylene glycol
- Corticosteroids (Dexamethasone. - used to prolong hyperglycemia because of their gluceoneogenic and appetite
stimulating effects)
- Tube feeding
- +/- insulin
Note: If treating pregnancy toxemia, induced parturition or cesarean section should be instituted along
with IV and oral glucose supplementation.
● Clinical signs may spontaneously resolve without treatment if an equilibrium between milk
production and dietary intake can be reached.
Topic: Ketosis
1. Prevention and control of ketosis
- Prevention and control of ketosis includes feeding and husbandry strategies during late lactation and the
dry period that aid in good body condition at calving.
See transcript from VIN Class 3 for further notes (was speaking too fast)
One problem with urine tests for ketones is that ketones are concentrated as they pass through the distal tubules, so urine tests are oversensitive.
* Milk tests are more specific than urine tests.
* Ketosis in cattle is a common cause of decreased milk production and clinical or subclinical disease.
Signs can be very subtle; but may include:
* Anorexia
* Decreased milk production, and
* In a smaller subset of patients, nervous signs such as apparent blindness, incoordination, pica, and bellowing.
The goal of treatment is reestablishment of normoglycemia.
* Dextrose rapidly replenishes blood glucose but has an incomplete and transitory effect.
* Note that hyperketonemia in cattle is not concurrent with acidemia.
Type 1 Ketosis - cow lactating 4-6 weeks with high production but not enough energy.
* Type 2 Ketosis - cow freshens and is overly conditioned (too fat)
* Measuring of ketone bodies is done using handheld meters
Topic: Infectious Bovine Keratoconjunctivitis
- Etiologic Agent (both major and minor)
- How does this affect the cattle industry as a whole?
- What environmental factors can lead to conjunctivitis?
- Moraxella bovis; Chlamydia, Infectious bovine rhinotracheitis (bovine herpesvirus-1), Mycoplasma, Neisseria catarrhalis
- Hundreds of millions of dollars annually; The financial impact of this disease is enormous and is primarily due to decreased weight gain, milk production, and the cost of treatment.
- Excessive ultraviolet light (sunlight)
a. Lack of pigmentation around eye results in UV damage and subsequent inflammation thus sensitizing eye to infection.
b. Hereford cattle now bred for pigment around eyes because of pinkeye and squamous cell carcinomas. Infectious Bovine Ieratoconjunctivitis (IBK).
● Flies
a. Irritate the eye by feeding off secretions and serve as a vector.
b. Musca domestica (house fly). **
c. Stomoxys calcitrans (stable fly).
d. Musca autumnalis (face fly). **
■ Face fly remains infected for 3 days after feeding on infected secretions.
● Dust and plant material
a. Airborne irritants
b. Mechanical vectors such as plant awns
c. Overhead feeders more likely to irritate eyes
Topic: IBK
- How is IBK transmitted?
- List the c/s
- Diagnostics **
- Direct contact.
● Flies **
● Inanimate objects.
● Infected and asymptomatic carriers harbor infection in nasal secretions.
● See higher incidence in summer and fall due to increased flies, UV light, and pollen production ** - Younger cattle more commonly affected. **
● Conjunctivitis. **
● Blepharospasm. **
● Epiphora.
● Blindness due to corneal opacity or
permanently following rupture.
● Decreased appetite and weight loss.
● Decreased milk production.
● Small opaque region in center of cornea progresses to deep central ulceration **
a. Perforation of corneal ulcer is uncommon.
● Submit conjunctival swab and lacrimal secretion for culture.
Topic: IBK
- Treatment
- Prevention
- Antibiotics
a. Oxytetracycline (LA-200) systematically –> Labeled for treatment of IBK **
c. Ceftiofur (Naxcel) SQ
d. Penicillin subconjunctivally
e. Florfenicol IM
f. Tulathromycin SQ
● Surgical intervention
a. Can perform third eyelid flap or tarsorrhaphy.
● Eliminate environmental factors
a. Protect eyes from UV light by using glue on eye patch
b. Control fly population with face rubbers and ear tags
c. Grass, weed, and brush control to minimize mechanical irritation
d. Eliminate overhead feeding - Prevent other predisposing diseases
a. Vaccinate for BVD and IBR
b. Isolate infected animals
● Vaccination for IBK
a. Mixed results. If both humoral IgG and secretory IgA directed at M. bovis antigens are present, these appear to be protective.
b. Not consistently effective therefore not yet in widespread use.
Topic: White Muscle Disease/Nutritional Myodegeneration
- What type of disease process is this?
- Signalment **
- Pathogenesis
- Clinical signs
- White muscle disease (WMD) is a myodegenerative disease associated with deficiency of vitamin E
and/or selenium - horses, ruminants, pigs and poultry; WMD is more common in young growing animals (foals, calves, kids, lambs).
- Suboptimal concentrations of vitamin E and/or selenium impairs the animals’ ability to control oxidative damage to cells, resulting in muscle damage. Two main clinical manifestations of WMD are the cardiac form and skeletal form
- Cardiac Form – sudden onset; animal may be severely debilitated or found dead. Animals frequently die within 24 hours despite medical therapy. Lesions may be found in the heart, diaphragm and/or intercostal muscles.
a. Depression.
b. Respiratory distress.
c. Nasal discharge (from pulmonary edema).
d. Rapid and possibly irregular heartbeat.
e. Weakness & recumbency.
Skeletal Form – slower onset; more responsive to medical therapy. Common muscle groups affected include the biceps, semitendinosus, semimembranosus, gluteal muscles and musculature of the neck.
a. Muscular weakness and/or stiffness.
b. Recumbency, may be unable to stand.
c. If able to stand, muscle weakness and trembling.
d. Skeletal muscles may be hard and painful.
e. Respiratory difficulty/distress (involvement of the diaphragm).
f. Dysphagia (muscle involvement of the tongue, pharyngeal and masticatory muscles).
g. Lethargy.
Topic: White Muscle Disease
- Clinicopathologic Findings
- Gross Histologic Findings
- Treatment
- Tx
- Acute disease may demonstrate significant elevations in AST and CK along with hyperkalemia, hyponatremia and/or hypochloremia. **
● Myoglobinuria may be detected in some affected animals.
● Decreased serum selenium concentrations; decreased glutathione peroxidase activity is a suitable means to evaluate selenium. **
● Decreased whole blood selenium (can also be measured in liver samples) and/or decreased
glutathione peroxidase activity.
● Decreased serum vitamin E concentrations. - Grossly, affected muscles of the limbs, diaphragm, heart and tongue may appear gray to white (hence the name) **. Microscopically, bilaterally symmetric myodegeneration is consistently observed.
Hyaline degeneration of myofibers may be observed; regeneration of myofibers may be observed in the recovery stages. - Limit physical activity.
● Administer vitamin E and selenium.
● Anti-inflammatory medications and supportive care (nasogastric feeding, antibiotics, fluid therapy).
Topic: BVD
- Virus type? Family?
- Viral classification?
- List the clinical forms of BVD
- Pestivirus in the family Flaviviridae and is thus an RNA virus
- The virus can be classified into type A and type B infections based on genotype
a. Both types can exist as either cytopathic (CP) or non-cytopathic (NCP) biotype.
b. Biotype does not indicate virulence, but only how the isolate behaves in tissue culture. - Subclinical, acute BVD, hemorrhagic syndrome, reproductive loss, mucosal disease or chronic BVD
Topic: BVD
- Describe each clinical form of BVD
Subclinical
● Many animals which have never been observed to be ill have antibody present.
Acute BVD
● Most common in cattle 6 to 24 months of age.
● After 5 to 7 days incubation, causes fever, leukopenia, anorexia, oculonasal discharge,
oral erosions and ulcers, and diarrhea.
● Virus damages the epithelium of the mouth, esophagus, intestine and bronchi.
● Immunosuppression and pneumonia from bacterial pathogens can occur.
Hemorrhagic Syndrome
● BVD virus-induced thrombocytopenia
Reproductive Loss
● Infertility and early embryonic death. Early embryonic death or abortion can occur at any stage of
gestation
● Congenital defects are most common when infection occurs at 100 to 150 days gestation, and
include hydrocephalus, cerebellar hypoplasia, hypomyelinogenesis, ocular defects,
hypotrichosis, and brachygnathia.
● Persistent fetal infection occurs at 40 to 125 days if the fetus is exposed to a NCP biotype.
a. In this form, the fetus is immunotolerant and if it survives, the animal acts as a reservoir and
consistently sheds virus.
b. These carriers are persistently infected and called PI animals. They are the main way that
BVD is maintained in a herd.
Mucosal Disease or Chronic BVD
● Occurs when a persistently infected animal is superinfected with a CP biotype of BVDV or the NCP
biotype switches to the CP biotype
● Mucosal disease is a peracute often fatal attack of BVD
● Chronic BVD is eventually fatal
Topic: BVD
- Diagnosis
- DDx. Explain why
- Based on antigen detection
a. Fluorescent antibody, immunohistochemistry, or antigen capture ELISA can be utilized.
b. Ear notches are often used for immunohistochemistry detection of carriers.
● PCR or serology can also be used. - MCF.
a. Typically has greater lymph node enlargement and bilateral corneal opacity, whereas corneal
opacity probably occurs in only 1 % of BVD cases.
● Rinderpest.
● FMD.
● Vesicular stomatitis, and bovine papular stomatitis.
a. Usually are associated with oral lesions but are not associated with diarrhea.
Topic: BVD: 1
- Treatment
- Prevention and Control
- Treatment of acute BVD cases is generally aimed at preventing serious secondary infections such
as Mannheimia hemolytica pneumonia and at providing fluids and electrolytes. - Biosecurity, vaccination, and detection and elimination of carriers (PI animals) are the principle
means of preventing and controlling BVDV.
● Vaccination aimed at protecting young animals as maternal immunity wanes.
● Vaccination of cows is aimed at preventing PI calves and reproductive losses via fetal infection.
● Killed virus vaccines require two doses, whereas modified live virus vaccines only require one dose.
● Replacement heifers are vaccinated with modified live virus vaccine at 5 to 6 months of age.
● Cows are vaccinated prior to breeding season using modified live virus vaccine containing
both type 1 and type 2 viruses.
● Pregnant cows can be safely vaccinated with killed vaccine; however fetal protection appears to bebetter when modified live virus vaccines are used.
