Large Animal Notes
Equine
Equine Infectious Anemia (EIA)
Definition and Characteristics:
Equine Infectious Anemia (EIA) is an incurable, infectious disease caused by a virus.
It affects horses, donkeys, and other equine species.
The virus primary action is to destroy red blood cells.
Transmission:
Spread through blood-to-blood contact.
It is not spread through close proximity or casual contact.
Primary vectors/methods: Biting flies, unsterilized or contaminated medical instruments, or blood transfusions.
Disease Forms:
Acute: Equines develop fever, go off feed, or die suddenly. These responses usually occur between 7 and 30,days after initial exposure. The animal may test negative for 16 to 42,days because the immune system has not produced detectable antibodies yet.
Chronic: Chronically infected equines test positive and may develop symptoms including weight loss, weakness, anemia, and swelling of the chest, abdomen, and lower legs. Symptoms may subside but frequently reoccur.
In-apparent: These equines show no outward symptoms but test positive for the disease. These pose the greatest danger for spreading the disease because unsuspecting owners are unaware of the risk.
Texas Regulations:
All equine animals (except zebras) 8,months of age or older must have a negative EIA test within the previous 12,months before a change-of-ownership (subject to specific exemptions).
Zebras: TAHC regulations require zebras entering Texas to have a negative EIA test within the previous 12,months and a Certificate of Veterinary Inspection (CVI/health certificate) issued within the past 45,days, unless moving between approved zoos.
All zebras (including those from Texas) must have a negative EIA test within the past 12,months when entering fairs, exhibitions, shows, or other assemblies.
Diagnosis and Management:
Diagnosis: Performed via ‐‐‐‐Coggin’s‐‐‐‐ Testing.
Treatment: None.
Prevention/Management: Euthanasia, permanent isolation (200,yards from any other equine), annual testing, fly spray, and general isolation.
Tetanus (Clostridium tetanii)
Etiology:
Caused by the bacterium Clostridium tetanii.
Found in soil and droppings nearly everywhere; it survives in the environment for long periods.
Infection Pathophysiology:
Enters the body through wounds, specifically dirty puncture wounds.
Acquisition can occur via the intestines through eating contaminated soil/droppings or via gastric/intestinal ulcers.
In foals, infection can occur through the umbilicus (navel).
Anaerobic Nature: The bacteria are anaerobic and multiply rapidly in damaged tissues at the injury site.
Neurotoxin: They produce a potent neurotoxin (tetanus toxin) which causes the classic clinical signs.
Clinical Symptoms:
The toxin attacks nerves controlling muscles.
Progressively worsening muscular stiffness and spasms.
Difficulty moving and eating.
Third Eyelid: Starts to protrude across the eye, especially if the horse is startled.
Straight tail carriage and an "anxious expression" due to facial muscle spasms. Stimuli sensitivity: Loud sounds, bright light, or touch can exacerbate signs.
Sweating.
Advanced cases: Collapse, convulsions, and death due to respiratory failure.
Treatment and Prognosis:
Goals: Destroy the bacteria to stop toxin production and reduce the effects of existing toxins.
Large doses of antibiotics (Penicillin) used with Tetanus Antitoxin.
Severe cases may require slinging, intravenous fluids, and bladder catheterization.
Overall prognosis is poor.
Prevention:
Vaccination with "tetanus toxoid."
Foals: Cannot respond to vaccine before 4,months of age. They usually receive tetanus antitoxin soon after birth and get protection via colostrum if the mare is vaccinated.
Good first aid and pasture management.
Colic: Abdominal Pain
Definition: General term for pain in the horse’s abdomen; it is the leading medical cause of death in horses.
Etiology: Majority of episodes are idiopathic (unknown cause).
Types of Colic:
Idiopathic: No root cause determined (accounts for over 80% of all colics).
Enteritis: Inflammation of the intestine caused by infections, viruses, or bacteria.
Gas (Spasmodic): Excess fluid or gas build-up, often from over-fermentation of carbohydrates in the hindgut. Pressure and inflammation cause discomfort.
Intussusception: Most often caused by parasites (tapeworms); the intestine slides like a telescope into another portion, potentially cutting off blood supply and creating a blockage.
Impaction: Accumulation of sand, dirt, feed, or indigestible material in the colon, making waste disposal difficult or impossible.
Gastric Rupture: Relatively rare; occurs when impaction reaches the stomach or gas build-up causes the stomach to dilate and burst.
Strangulation/Torsion: Lethal form involving a twist in the colon or small intestine, leading to cut-off blood supply and necrotic tissue.
Symptoms:
Anxiety or depression.
Pawing at the ground, looking/biting at the flank, and rolling/wanting to lie down. Playing in water buckets without drinking.
Lack of defecation and appetite.
Excessive sweating.
Abnormally high pulse rate (over 50,bpm).
Lack of normal gut noises.
Frequent attempts to urinate (stretching out).
Diagnosis:
Evaluation of clinical signs, TPR (Temperature, Pulse, Respiration).
Elevated Heart Rate (HR) and Respiratory Rate (RR).
Rectal Palpation and Auscultation.
Examination of Mucous Membrane (MM) Color and Capillary Refill Time (CRT). Checking for a "toxic line."
Treatment:
Medical: Water or mineral oil/laxatives via nasogastric (NG) tube, NSAIDs (Banamine), Analgesics (Butorphanol, Detomidine), Reflux management, IV fluids, and antiparasitics.
Surgical: Required to relieve torsion or remove obstructions.
Prevention: Access to fresh water, good roughage, proper dental care.
Equine Influenza (Equine Flu)
Characteristics: Widespread infectious viral disease, mainly affecting young horses (2 to 3,years old).
Pathology: Targets the respiratory system, damaging the lining and mucous membranes of the respiratory tract.
Incubation: Only 1 to 3,days after exposure.
Causes: Several strains exist, but Type A is most common. It is airborne and spreads horse-to-horse. Carriers can be contagious without showing symptoms.
Symptoms:
Fever, anorexia, and depression.
Nasal discharge (usually clear).
Dry, deep cough.
Muscle pain and reluctance to move.
Enlarged lymph nodes.
Complications: Pneumonia (frequent secondary infection), heart and liver complications in severe cases.
Management: No specific treatment; supportive care and antibiotics for secondary infections. Prevention via vaccine and isolation of new animals.
Navel Ill (Septic Arthritis / Joint III)
Definition: Joint infection in foals caused by bacteria or septic arthritis.
Entry: Bacteria enter via the umbilical cord due to unsanitary birthing conditions or dirty bedding. Infection may spread to surrounding bones.
Target Population: Foals less than 1,week old (though up to 4,months possible).
Symptoms: Swollen legs/joints, lameness, diarrhea, swollen/painful navel that does not dry, abscess/discharge, fever, reluctance to feed, uncoordinated movements, and lethargy.
Diagnosis: Blood work (elevated WBC), swollen joints, Joint tap (Synovial fluid evaluation showing elevated WBC), and Radiographs to check for bone involvement.
Treatment: Antibiotics, joint lavage, and restricted exercise/weight-bearing.
Recovery: Full recovery possible with quick aggressive treatment; partial recovery may leave permanent lameness.
Prevention: Clean birthing stalls and iodine dip for the umbilicus.
Choke (Esophageal Obstruction)
Cause: Lodging of material in the esophagus. Primary cause is food.
Risk Factors: Fast eaters, poor dentition.
Common Materials: Pelleted feeds, apples, and corn cobs.
Symptoms: History of fast eating, outstretched neck, cough/gagging, repeated swallowing, drooling, food source seen from nares (nostrils), and palpable protrusion in the esophagus.
Treatment: Sedation and nasogastric tube to clear blockage.
Post-unblockage care: NSAIDs, antibiotics, and "soupy" feed. Choking horses are at risk for aspiration pneumonia.
Equine Protozoal Myeloencephalitis (EPM)
Characteristics: Common neurological disease in the Americas caused by the protozoan Sarcocystis neurona.
Transmission: Ingestion of sporocysts in contaminated feed or water.
Hosts:
Definitive Host: Opossum (USA).
Intermediate Hosts: Nine-Banded Armadillo, Striped Skunk, Raccoon (Sarcocyst in skeletal muscle).
Dead-End Host: Horse (Ingests sporocysts, lesions develop in spinal cord and brain).
Symptoms: Asymmetric or symmetric weakness, ataxia, muscle atrophy, spontaneous sweating, loss of reflexes, head tilt, facial paralysis, seizures, and recumbency.
Diagnosis: Serology for antibody, CNS lesions (postmortem), and ruling out other differentials (Trauma, Rabies, West Nile, etc.).
Treatment: Antiprotozoal therapy (30 to 90,days) using Ponazuril, Diclazuril, or a combination of sulfadiazine and pyrimethamine.
Prevention: No proven vaccine. Keep opossums away from feed, seal feed in galvanized metal containers, and do not leave pet food out.
Equine Herpesvirus (EHV-1 and EHV-4)
Taxonomy: Family Alphaherpesviridae. There are 5 alpha herpesviruses for horses; EHV-1 and EHV-4 are the most serious.
Types:
EHV-1: Formerly "equine abortion virus," causes respiratory and neurological disease worldwide.
EHV-4: "Equine Rhinopneumonitis virus"; most common in foals and yearlings. Also causes abortion and neuro disease.
Transmission: Direct contact (nose-to-nose) or indirect (buckets, clothing, blankets) via nasal discharge. Can travel short distances via aerosol or contact with aborted fetuses/placental fluids. Virus can be latent and reactivated by stress.
Symptoms (Incubation 2 to 10,days):
Respiratory: Fever (102 to 107^{circ}F) for 1 to 7,days, coughing, and nasal discharge.
Abortion: Usually occurs between months 7 and 11 of gestation.
Neurologic: Hindlimb paralysis, recumbency, loss of bladder/tail function, and loss of skin sensation in hindquarters.
Diagnosis: Nasopharyngeal culture, tissue culture from aborted fetus, and antibody titers.
Management: Supportive care, NSAIDs. Vaccinations reduce severity but do not totally prevent the disease.
Special Musculoskeletal and Eye Conditions
Hyperkalemic Periodic Paralysis (HYPP):
Genetics: Muscular genetic disease involving a leaky potassium channel.
Signs: Tremors, fasciculations, respiratory difficulty, paralysis, and death. No cure.
Management: Genetic testing and strict diet management.
Laminitis: Inflammation of the laminae, often due to interrupted blood flow secondary to other diseases. Managed with shoeing, NSAIDs, and diet.
Melanoma: Common in gray horses; usually benign. Prevention is unavailable; recommendation is often to leave them alone if possible.
Equine Recurrent Uveitis (Moon Blindness):
Most common eye disease and leading cause of blindness.
Immune-mediated (body attacks its own eye tissue) with waxing/waning periods.
Symptoms: Squinting, tearing, cloudy eye, swelling, and sunlight sensitivity.
Treatment: Steroidal/non-steroidal anti-inflammatories, Atropine (dilating agent), flymasks, or surgical eye removal.
Risk: Appaloosas are at higher risk.
Guttural Pouch Mycosis: Caused by Aspergillus spp. (fungus) through spore inhalation. Can lead to severe hemorrhage ("bleed out").
Strangles (Streptococcus equi)
Characteristics: Infectious, highly contagious disease characterized by abscessation of upper respiratory lymphoid tissue. Also known as "Equine Distemper."
Etiology: Streptococcus equi is host-adapted only to horses, donkeys, and mules.
Transmission: High morbidity, low mortality. Transmitted via fomites or direct contact with exudates. Survives in environment within mucoid secretions; killed by heat and sunlight.
Clinical Findings:
Incubation: 3 to 14,days.
Sign 1: Fever (103 to 106^{circ}F).
Follow-up: Mucopurulent nasal discharge, depression, and submandibular lymphadenopathy.
Bastard Strangles (Metastatic): Abscesses in abdominal or thoracic lymph nodes or brain.
Diagnosis: Bacterial culture (abscess/nasal swab), CBC (neutrophilic leukocytosis), and endoscopy/ultrasound/skull radiographs.
Treatment: Warm, dry environment, warm compresses, flushing ruptured abscesses with 5% povidone-iodine. NSAIDs for pain. Tracheotomy may be needed for pharyngeal compression. Penicillin used for severe cases.
Prevention: Modified live intranasal vaccines are more effective than killed injectables. Quarantine new additions for 14 to 21,days. Horses may shed for 1,month post-recovery; require 3 negative swabs at 4 to 7,day intervals for release.
Encephalitis Diseases (Sleeping Sickness)
Types and Geography:
Eastern (EEE): Eastern US and Canada.
Western (WEE): Argentina to Western Canada.
Venezuelan (VEE): Central/South America, Mexico, and US.
Commonalities: Mosquito-vectored, zoonotic (EEE and VEE). High mortality rates.
West Nile Virus: Inflammation of brain/spinal cord. Mosquitos are vectors; birds are reservoir hosts. Humans and horses are incidental hosts.
Symptoms: Nervous system signs including fever, hind limb weakness/paralysis, ataxia, head pressing, aimless wandering, convulsions, circling, and coma.
Management: No cure. Treatment is symptomatic (nutrition, anti-inflammatories). Survivors often have permanent neurologic deficits.
Prevention: Vaccines (VEWT - Venezuelan, Eastern, Western, and Tetanus). West Nile vaccines. Mosquito population control and repellent use.
Cattle
Anthrax and Blackleg: Bacterial Spore-Forming Diseases
Anthrax (Splenic Fever)
Causative Agent: Bacillus anthracis.
Biological Characteristic: When the bacteria are exposed to O_2 (oxygen), they produce spores.
Forms of Infection: The disease manifests in three forms:
Cutaneous.
Gastrointestinal.
Respiratory.
Regulatory and Health Status:
Identified as a Reportable disease.
It is Zoonotic, meaning it can be transmitted from animals to humans.
It can affect all warm-blooded animals.
Transmission and Environment: Contamination of pasture or feed items typically occurs after flooding in endemic areas.
Prevention and Management:
Vaccination is necessary in endemic areas.
Utilize proper carcass removal protocols.
Clinical Signs and Diagnosis:
Sudden death.
Bleeding from orifices.
Absence of rigor mortis.
Diagnostic methods include blood samples and observation of clinical signs.
Critical Warning: DO NOT NECROPSYan animal suspected of having Anthrax, as this exposes the bacteria to oxygen, facilitating spore formation.
Blackleg (Clostridial Myositis)
Causative Agent: Clostridium chauvoei.
Pathogenesis: The bacteria travel to the muscles and multiply, releasing toxins that destroy muscle tissue and produce gas.
Habitat: The bacteria live in the soil.
Transmission: Ingestion through contaminated feed or pasture.
Progression:Rapid death within 24-48,{hours}.
Treatment: Medical intervention is usually unsuccessful.
Prevention: Vaccination; considered a core vaccine for cattle.
Bovine Respiratory and Viral Disease Complexes
Bovine Respiratory Disease (BRD)
Common Name: Shipping Fever.
Nature of Condition: It is a disease complex rather than a single ailment.
Primary Components: Involves Bovine Viral Diarrhea (BVD), Infectious Bovine Rhinotracheitis (IBR), Parainfluenza, and Bovine Respiratory Syncytial Virus (BRSV).
Complications: Often accompanied by secondary bacterial infections.
Prevention: Primarily achieved through good health management practices.
Bovine Viral Diarrhea (BVD)
Causative Agent: Pestivirus.
Associated Problems: Causes both respiratory and reproductive (repro) problems.
Transmission and Carriers: Infection occurring in uteroresults in the calf becoming a lifetime carrier.
Clinical Signs: Abortion, diarrhea, fever, and other symptoms.
Progression: Can lead to the broader Bovine Respiratory Disease (BRD) complex.
Management:
Cull infected cattle.
Provide supportive care.
Prevention through vaccination.
Infectious Bovine Rhinotracheitis (IBR)
Causative Agent: Bovine herpesvirus-1.
Common Name:Red Nose.
Transmission:
Direct contact with nasal secretions.
Breeding (the virus is present in the genitals).
Impact: Can cause abortion in addition to respiratory issues.
Prevention: Vaccination and maintaining high standards of biosecurity.
Major Reproductive and Regulatory Diseases
Brucellosis
Causative Agent: Brucella abortus.
Common Name: Bang’s disease.
Classification:Reproductive disease.
Transmission: Direct contact with infectious sources.
Regulatory Status:Reportable disease.
Prevention and Management:
Vaccination: Performed on heifers between 4-12,{mo} of age.
Requirement: Vaccination MUST be performed by an Accredited Veterinarian only.
Requires permanent identification.
Treatment: No treatment available.
Control: Cull infected animals.
Vibriosis
Causative Agent: Campylobacter fetus.
Transmission Path: Genital tract; transmitted from bulls to cows during breeding, and then potentially to calves in utero.
Clinical Signs: Poor conception rates and abortion.
Management: Vaccination.
Test bulls before breeding; bulls typically remain asymptomatic.
Bovine Trichomoniasis
Causative Agent: Tritrichomonas foetus.
System Affected: Reproductive system.
Major Sign: Infertility.
Transmission: Breeding.
Carrier Status: Bulls are infected for life.
Testing: Testing is performed prior to breeding; testing can only be done on bulls.
Infectious Hoof and Oral Conditions
Foot Rot
Causative Agents: Fusobacterium necrophorum and Porphyromonas levii.
Environmental Triggers: Wet environments and/or wounds to the interdigital space.
Significance: This is the most common cause of lameness in cattle.
Characteristics: Highly infectious; primarily affects the interdigital space in the hoof.
Complications: Can progress to affect tissues, joints, and bones if left untreated.
Management:
Maintain a dry environment.
Administer antibiotics.
Isolation of infected cattle.
Calf Diphtheria (Necrobacillosis)
Causative Agent: Fusobacterium necrophorum.
Nature: Part of the normal flora but acts as an opportunistic pathogen.
Forms of Infection:
Oral: Characterized by ulcers and swollen cheeks; can progress to laryngeal signs.
Laryngeal: Characterized by coughing, dyspnea (difficulty breathing), fever, and difficulty eating or swallowing.
Risk Factors: Unsanitary conditions (notably, the same agent also causes Foot Rot).
Management:
Treatment: Antibiotics.
Prevention: Biosecurity, good health management, and sanitary conditions.
Foot and Mouth Disease
Target Species: All cloven-hooved animals.
Regulatory Status: Reportable disease.
Characteristics: Highly contagious.
Transmission: Saliva, mucus, feces, and milk.
Differential Diagnosis: Looks similar to other diseases, complicating identification.
Immediate Protocol:Suspected cases require testing and isolation of the entire farm.
Treatment: No treatment exists; animals are euthanized and burned.
Historical Note: Nt i 1929.
Wooden Tongue (Actinobacillus)
Causative Agent: Actinobacillus lignieresii.
Etiology: Enters through wounds or abrasions in the mouth, often caused by rough forage.
Signs: Formation of fibrous tissue in the mouth and soft tissues.
Management:
No vaccine available.
Can spread through shared feeding areas.
Requires prompt treatment and isolation.
Chronic, Zoonotic, and Neoplastic Conditions
Johne’s Disease
Causative Agent: Mycobacterium paratuberculosis.
Disease Progression: Progresses slowly. The incubation period can last for 10,{years}, with clinical signs appearing around 18,{mo}.
Trigger: Often manifests during high-stress periods.
Transmission Paths: Fecal-oral route, transplacental, and through milk.
Clinical Signs: Severe diarrhea and weight loss.
Management:Testing is available; there is no treatment, so infected animals must be culled.
Tuberculosis
Causative Agent: Mycobacterium bovis.
Environmental Persistence: Lives in warm, wet soil and cow feces; however, it is killed by UV (ultraviolet) light.
Transmission: Body fluids, breath, and discharge from lesions.
Regulatory Status: Reportable and Zoonotic.
Diagnosis: Testing must be performed by a Licensed Accredited Veterinarian using an intradermal test.
Status in the US: Has been eradicated in the US, but sporadic cases can still occur.
Management: No vaccine available; results in cull and euthanasia of infected animals.
Bovine Lymphosarcoma (Bovine Leukosis)
Classification: Most common neoplastic (cancerous) disease in cattle.
Causative Agent: Bovine Leukemia virus (BLV).
Signs: Rapid onset of tumors across various body systems.
Contagion: Direct contact with blood or other bodily fluids.
Diagnosis: ELISA or serologic testing.
Management: No vaccine available; infected animals should be euthanized or culled.
Leptospirosis
Causative Agent: Many different strains of the bacteria.
Transmission: Contaminated water or direct contact with bodily secretions like milk, urine, and afterbirth.
Health Impact: Zoonotic; causes abortion.
Prevention: Vaccination and environmental management, specifically targeting standing water.
Listeriosis (Circling Disease/Silage Sickness)
Causative Agent: Listeria monocytogenes or Listeria ivanovii.
Transmission: Contaminated soil or food (silage).
Demographics: Typical age of onset is 1-3,{years}.
Manifestations (4 Forms): 1. Septicemic/visceral form. 2. Abortion. 3. Ophthalmic. 4. Encephalitis/mastitis.
Health Status: Zoonotic.
Prevention: No vaccine; prevent cattle from eating off the ground and ensure proper silage care.
Ocular, Udder, and Skin Health
Infectious Keratoconjunctivitis (Pinkeye)
Causative Agent: Moraxella bovis.
Transmission: Direct contact, fomites (inanimate objects), and flies.
High-Risk Factors: Previous irritation to the eye or exposure to excessive UV light.
Management:
No vaccine.
Fly control (topical treatments, ear tags).
Isolation of infected cattle.
Treatment with antibiotics.
Mastitis
Con: Seen more frequently in dairy cattle.
Etiology: Teat invasion, wounds, and unsanitary conditions.
Pathological Indicator: Increase in somatic cells.
Testing: California Mastitis Test (CMT) and somatic cell count.
Prevention: Clean environment, cleaning teats prior to milking, regular examination, and the use of teat dips.
Pseudocowpox (Milker’s Nodule)
Causative Agent: Parapoxvirus.
Health Status: Zoonotic.
Transmission: Infected milking equipment or human contact during the milking process.
Human Impact:Causes painful ulcers on the hands.
Management: No vaccine; rely on biosecurity and proper sanitation.
Metabolic Diseases and Nutritional Disorders
Acetonemia (Ketosis)
Nature: Metabolic disease caused by increased energy needs coupled with insufficient intake.
Physiology: The body utilizes fat for energy through a process called gluconeogenesis.
Treatment:Glucose administration and corticosteroids.
Prevention: Maintain good body condition, use feed additives to increase feed efficiency, and increase feed intake gradually prior to calving.
Bloat (Ruminal Tympany)
Mechanism: Accumulation of gas, which is a by-product of fermentation.
Normal Function: Gas is usually expelled through eructation (burping).
Types: There are 2 types of bloat.
Prevention: Avoid lush pasture or alfalfa; prevent ingestion of foreign objects.
Grass Tetany (Hypomagnesemia)
Nature: Metabolic disease caused by insufficient Magnesium (Mg) stores and intake.
Risk Group: Grazing, lactating cattle.
Signs: Muscle spasms, dyspnea, convulsions, and hyperexcitability.
Milk Fever (Post-parturient hypocalcemia/Parturient Paresis)
Nature: Metabolic disease characterized by Hypocalcemia (low calcium).
Risk Group: Dairy cattle within 48,{hours} after calving.
Stages of Milk Fever:
1. Stage 1: Ataxia, animal remains upright and ambulatory.
2. Stage 2: Animal is unable to stand, stays in sternal recumbency, exhibits tachycardia and is hypothermic.
3. Stage 3: Flaccid muscles, animal becomes comatose.
Treatment: Calcium (Ca) administration.
Prevention: Improve Body Condition Score (BCS) and provide quality food material.
Rumen Acidosis (Grain Overload/Lactic Acidosis)
Nature: Metabolic disease typically caused by high grain diets.
pH Parameters:
Normal pH: 6.5-7.0.
Acidosis occurs when pH falls below 5.5.
Effect: Results in an atonic rumen.
Treatment: Removal of rumen contents and transfaunation (transfer of rumen microflora).
Gastrointestinal, Neurological, and Calf-Specific Disorders
Bovine Spongiform Encephalopathy (Mad Cow Disease)
Causative Agent: Prion.
Incubation Period:2-8,{years}.
Disease Type: Neurologic disease.
Transmission Source: Animal byproducts.
Zoonotic Link: Related to Creutzfeldt-Jakob Disease in humans.
Management: No treatment; results in euthanasia.
Displaced Abomasum
Physiological Con: The normal location of the abomasum is on the floor of the abdomen.
Variations: Left (LDA) or Right (RDA) displacement.
Comparison: LDA is more common and easier to treat; RDA is life-threatening.
Etiology: Nonfunctioning abomasum (due to gas) or recent calving.
Prevention: Ensure adequate roughage intake after calving, proper eating habits, and good quality food.
Traumatic Gastritis (Traumatic Reticulitis/Hardware Disease)
Etiology: Ingestion of foreign metallic objects that penetrate the reticulum.
Complications: Pleuritis and pericarditis.
Diagnosis: Performed via the "withers pinch test."
Treatment: Rumenotomy or the use of a magnet.
Calf Scours (Diarrhea)
Pathology: The animal is not absorbing nutrients.
Causes: Viral, bacterial, or parasitic agents.
Management: Supportive care.
Prevention: Proper sanitation, biosecurity, and ensuring timely intake of colostrum.
Sheep & Goats
Anthrax and Blackleg: Bacterial Spore-Forming Diseases
Anthrax (Splenic Fever)
Causative Agent: Bacillus anthracis.
Biological Characteristic: When the bacteria are exposed to O_2 (oxygen), they produce spores.
Forms of Infection: The disease manifests in three forms:
Cutaneous.
Gastrointestinal.
Respiratory.
Regulatory and Health Status:
Identified as a Reportable disease.
It is Zoonotic, meaning it can be transmitted from animals to humans.
It can affect all warm-blooded animals.
Transmission and Environment: Contamination of pasture or feed items typically occurs after flooding in endemic areas.
Prevention and Management:
Vaccination is necessary in endemic areas.
Utilize proper carcass removal protocols.
Clinical Signs and Diagnosis:
Sudden death.
Bleeding from orifices.
Absence of rigor mortis.
Diagnostic methods include blood samples and observation of clinical signs.
Critical Warning: DO NOT NECROPSYan animal suspected of having Anthrax, as this exposes the bacteria to oxygen, facilitating spore formation.
Blackleg (Clostridial Myositis)
Causative Agent: Clostridium chauvoei.
Pathogenesis: The bacteria travel to the muscles and multiply, releasing toxins that destroy muscle tissue and produce gas.
Habitat: The bacteria live in the soil.
Transmission: Ingestion through contaminated feed or pasture.
Progression:Rapid death within 24-48,{hours}.
Treatment: Medical intervention is usually unsuccessful.
Prevention: Vaccination; considered a core vaccine for cattle.
Bovine Respiratory and Viral Disease Complexes
Bovine Respiratory Disease (BRD)
Common Name: Shipping Fever.
Nature of Condition: It is a disease complex rather than a single ailment.
Primary Components: Involves Bovine Viral Diarrhea (BVD), Infectious Bovine Rhinotracheitis (IBR), Parainfluenza, and Bovine Respiratory Syncytial Virus (BRSV).
Complications: Often accompanied by secondary bacterial infections.
Prevention: Primarily achieved through good health management practices.
Bovine Viral Diarrhea (BVD)
Causative Agent: Pestivirus.
Associated Problems: Causes both respiratory and reproductive (repro) problems.
Transmission and Carriers: Infection occurring in utero results in the calf becoming a lifetime carrier.
Clinical Signs: Abortion, diarrhea, fever, and other symptoms.
Progression: Can lead to the broader Bovine Respiratory Disease (BRD) complex.
Management:
Cull infected cattle.
Provide supportive care.
Prevention through vaccination.
Infectious Bovine Rhinotracheitis (IBR)
Causative Agent: Bovine herpesvirus-1.
Common Name:Red Nose.
Transmission:
Direct contact with nasal secretions.
Breeding (the virus is present in the genitals).
Impact: Can cause abortion in addition to respiratory issues.
Prevention: Vaccination and maintaining high standards of biosecurity.
Major Reproductive and Regulatory Diseases
Brucellosis
Causative Agent: Brucella abortus.
Common Name: Bang’s disease.
Classification:Reproductive disease.
Transmission: Direct contact with infectious sources.
Regulatory Status:Reportable disease.
Prevention and Management:
Vaccination: Performed on heifers between 4-12,{mo} of age.
Requirement: Vaccination MUST be performed by an Accredited Veterinarian only.
Requires permanent identification.
Treatment: No treatment available.
Control: Cull infected animals.
Vibriosis
Causative Agent: Campylobacter fetus.
Transmission Path: Genital tract; transmitted from bulls to cows during breeding, and then potentially to calves in utero.
Clinical Signs: Poor conception rates and abortion.
Management:
Vaccination.
Test bulls before breeding; bulls typically remain asymptomatic.
Bovine Trichomoniasis
Causative Agent: Tritrichomonas foetus.
System Affected: Reproductive system.
Major Sign: Infertility.
Transmission: Breeding.
Carrier Status: Bulls are infected for life.
Testing: Testing is performed prior to breeding; testing can only be done on bulls.
Infectious Hoof and Oral Conditions
Foot Rot
Causative Agents: Fusobacterium necrophorum and Porphyromonas levii.
Environmental Triggers: Wet environments and/or wounds to the interdigital space.
Significance: This is the most common cause of lameness in cattle.
Characteristics: Highly infectious; primarily affects the interdigital space in the hoof.
Complications: Can progress to affect tissues, joints, and bones if left untreated.
Management:
Maintain a dry environment.
Administer antibiotics.
Isolation of infected cattle.
Calf Diphtheria (Necrobacillosis)
Causative Agent: Fusobacterium necrophorum.
Nature: Part of the normal flora but acts as an opportunistic pathogen.
Forms of Infection:
Oral: Characterized by ulcers and swollen cheeks; can progress to laryngeal signs.
Laryngeal: Characterized by coughing, dyspnea (difficulty breathing), fever, and difficulty eating or swallowing.
Risk Factors: Unsanitary conditions (notably, the same agent also causes Foot Rot).
Management:
Treatment: Antibiotics.
Prevention: Biosecurity, good health management, and sanitary conditions.
Foot and Mouth Disease
Target Species: All cloven-hooved animals.
Regulatory Status: Reportable disease.
Characteristics: Highly contagious.
Transmission: Saliva, mucus, feces, and milk.
Differential Diagnosis: Looks similar to other diseases, complicating identification.
Immediate Protocol:Suspected cases require testing and isolation of the entire farm.
Treatment: No treatment exists; animals are euthanized and burned.
Historical Note: Nt i 1929.
Wooden Tongue (Actinobacillus)
Causative Agent: Actinobacillus lignieresii.
Etiology: Enters through wounds or abrasions in the mouth, often caused by rough forage.
Signs: Formation of fibrous tissue in the mouth and soft tissues.
Management:
No vaccine available.
Can spread through shared feeding areas.
Requires prompt treatment and isolation.
Chronic, Zoonotic, and Neoplastic Conditions
Johne’s Disease
Causative Agent: Mycobacterium paratuberculosis.
Disease Progression: Progresses slowly. The incubation period can last for 10,{years}, with clinical signs appearing around 18,{mo}.
Trigger: Often manifests during high-stress periods.
Transmission Paths: Fecal-oral route, transplacental, and through milk.
Clinical Signs: Severe diarrhea and weight loss.
Management:Testing is available; there is no treatment, so infected animals must be culled.
Tuberculosis
Causative Agent: Mycobacterium bovis.
Environmental Persistence: Lives in warm, wet soil and cow feces; however, it is killed by UV (ultraviolet) light.
Transmission: Body fluids, breath, and discharge from lesions.
Regulatory Status: Reportable and Zoonotic.
Diagnosis: Testing must be performed by a Licensed Accredited Veterinarian using an intradermal test.
Status in the US: Has been eradicated in the US, but sporadic cases can still occur.
Management: No vaccine available; results in cull and euthanasia of infected animals.
Bovine Lymphosarcoma (Bovine Leukosis)
Classification: Most common neoplastic (cancerous) disease in cattle.
Causative Agent: Bovine Leukemia virus (BLV).
Signs: Rapid onset of tumors across various body systems.
Contagion: Direct contact with blood or other bodily fluids.
Diagnosis: ELISA or serologic testing.
Management: No vaccine available; infected animals should be euthanized or culled.
Leptospirosis
Causative Agent: Many different strains of the bacteria.
Transmission: Contaminated water or direct contact with bodily secretions like milk, urine, and afterbirth.
Health Impact: Zoonotic; causes abortion.
Prevention: Vaccination and environmental management, specifically targeting standing water.
Listeriosis (Circling Disease/Silage Sickness)
Causative Agent: Listeria monocytogenes or Listeria ivanovii.
Transmission: Contaminated soil or food (silage).
Demographics: Typical age of onset is 1-3,{years}.
Manifestations (4 Forms):
1. Septicemic/visceral form.
2. Abortion.
3. Ophthalmic.
4. Encephalitis/mastitis.
Health Status: Zoonotic.
Prevention: No vaccine; prevent cattle from eating off the ground and ensure proper silage care.
Ocular, Udder, and Skin Health
Infectious Keratoconjunctivitis (Pinkeye)
Causative Agent: Moraxella bovis.
Transmission: Direct contact, fomites (inanimate objects), and flies.
High-Risk Factors: Previous irritation to the eye or exposure to excessive UV light.
Management:
No vaccine.
Fly control (topical treatments, ear tags).
Isolation of infected cattle.
Treatment with antibiotics.
Mastitis
Con: Seen more frequently in dairy cattle.
Etiology: Teat invasion, wounds, and unsanitary conditions.
Pathological Indicator: Increase in somatic cells.
Testing: California Mastitis Test (CMT) and somatic cell count.
Prevention: Clean environment, cleaning teats prior to milking, regular examination, and the use of teat dips.
Pseudocowpox (Milker’s Nodule)
Causative Agent: Parapoxvirus.
Health Status: Zoonotic.
Transmission: Infected milking equipment or human contact during the milking process.
Human Impact:Causes painful ulcers on the hands.
Management: No vaccine; rely on biosecurity and proper sanitation.
Metabolic Diseases and Nutritional Disorders
Acetonemia (Ketosis)
Nature: Metabolic disease caused by increased energy needs coupled with insufficient intake.
Physiology: The body utilizes fat for energy through a process called gluconeogenesis.
Treatment:Glucose administration and corticosteroids.
Prevention: Maintain good body condition, use feed additives to increase feed efficiency, and increase feed intake gradually prior to calving.
Bloat (Ruminal Tympany)
Mechanism: Accumulation of gas, which is a by-product of fermentation.
Normal Function: Gas is usually expelled through eructation (burping).
Types: There are 2 types of bloat.
Prevention: Avoid lush pasture or alfalfa; prevent ingestion of foreign objects.
Grass Tetany (Hypomagnesemia)
Nature: Metabolic disease caused by insufficient Magnesium (Mg) stores and intake.
Risk Group: Grazing, lactating cattle.
Signs: Muscle spasms, dyspnea, convulsions, and hyperexcitability.
Milk Fever (Post-parturient hypocalcemia/Parturient Paresis)
Nature: Metabolic disease characterized by Hypocalcemia (low calcium).
Risk Group: Dairy cattle within 48,{hours} after calving.
Stages of Milk Fever:
1. Stage 1: Ataxia, animal remains upright and ambulatory.
2. Stage 2: Animal is unable to stand, stays in sternal recumbency, exhibits tachycardia and is hypothermic.
3. Stage 3: Flaccid muscles, animal becomes comatose.
Treatment: Calcium (Ca) administration.
Prevention: Improve Body Condition Score (BCS) and provide quality food material.
Rumen Acidosis (Grain Overload/Lactic Acidosis)
Nature: Metabolic disease typically caused by high grain diets.
pH Parameters:
Normal pH: 6.5-7.0.
Acidosis occurs when pH falls below 5.5.
Effect: Results in an atonic rumen.
Treatment: Removal of rumen contents and transfaunation (transfer of rumen microflora).
Gastrointestinal, Neurological, and Calf-Specific Disorders
Bovine Spongiform Encephalopathy (Mad Cow Disease)
Causative Agent: Prion.
Incubation Period:2-8,{years}.
Disease Type: Neurologic disease.
Transmission Source: Animal byproducts.
Zoonotic Link: Related to Creutzfeldt-Jakob Disease in humans.
Management: No treatment; results in euthanasia.
Displaced Abomasum
Physiological Con: The normal location of the abomasum is on the floor of the abdomen.
Variations: Left (LDA) or Right (RDA) displacement.
Comparison: LDA is more common and easier to treat; RDA is life-threatening.
Etiology: Nonfunctioning abomasum (due to gas) or recent calving.
Prevention: Ensure adequate roughage intake after calving, proper eating habits, and good quality food.
Traumatic Gastritis (Traumatic Reticulitis/Hardware Disease)
Etiology: Ingestion of foreign metallic objects that penetrate the reticulum.
Complications: Pleuritis and pericarditis.
Diagnosis: Performed via the "withers pinch test."
Treatment: Rumenotomy or the use of a magnet.
Calf Scours (Diarrhea)
Pathology: The animal is not absorbing nutrients.
Causes: Viral, bacterial, or parasitic agents.
Management: Supportive care.
Prevention: Proper sanitation, biosecurity, and ensuring timely intake of colostrum.
Swine
Atrophic Rhinitis
Definition and Symptoms: Atrophic rhinitis is a disease of swine characterized by sneezing, followed by the destruction and atrophy of the turbinate bones. This condition may be accompanied by a distortion of the nasal septum and the shortening or twisting of the upper jaw.
Ethiology:
- Bordetella bronchiseptica (Bb): This agent has long been implicated as a major cause of the disease.
- Pasteurella multocida (Pm): Toxigenic strains (Type D), often acting in conjunction with B. bronchiseptica, cause permanent turbinate atrophy and nasal distortion.
Disease Forms:
- Non-progressive Atrophic Rhinitis: Due to B. bronchiseptica only; this form is considered mild.
- Progressive Atrophic Rhinitis: Due to toxigenic P. multocida; this form is severe and results in permanent changes.
Treatment (TX) and Prevention:
- Primary Strategies: Includes chemoprophylaxis, vaccination, and the temporary closure of the herd to the introduction of new pigs.
- Management Improvements: Enhancing ventilation and hygiene, and providing less dusty feed.
- Chemoprophylaxis Protocols: Usually involves the administration of antibacterial drugs to all sows, particularly before the farrowing stage.
- Nutritional Interventions: Medicated rations for weaners and growers, and occasionally sow rations, are often helpful.
Erysipelas (Diamond Skin Disease)
Pathogen: Caused by Erysipelothrix rhusiopathiae.
Transmission and Shedding: The pathogen is shed in manure, urine, and saliva. It can be transmitted via the oral route or through skin abrasions.
Zoonotic Potential: The disease is zoonotic, meaning it can be transmitted from animals to humans.
Primary Forms:
- Acute Form: Presents as septicemia.
- Subacute Form: Characterized by skin lesions (diamond skin lesions).
- Chronic Form: Results in arthritis and endocarditis.
Control Measures: Implementation of vaccination, sanitation, and isolation protocols.
Leptospirosis
Reproductive Indicators: Identified by {SMEDI} (stillbirth, mummification, embryonic death, and infertility).
Transmission: Mainly through urine.
Regulatory and Health Status: This is a Zoonotic and Reportable disease.
Treatment: Treated with antibiotics.
MMA (Mastitis, Metritis, Agalactia)
Timeline: Occurs after farrowing.
Predisposing Factor: Overweight sows are at higher risk.
Nature: Usually bacterial.
Care Guidelines: Management requires monitoring piglets closely and maintaining good sanitation.
Pasteurellosis
Disease Type: Pneumonia.
Pathogen: Caused by Pasteurella multocida.
Classification: Typically a secondary disease.
Symptoms: Characterized by "Thumps."
Transmission: Ingestion, aerosol (air), contact, and poor husbandry practices.
Prevention: Vaccination and maintaining a clean environment.
Porcine Endemic Diarrhea Virus (PEDV)
Pathogen: Corona virus.
Clinical Signs: Diarrhea and vomiting.
Transmission: Fecal-oral route.
Prevention: Strict good biosecurity measures.
Porcine Parvovirus (PPV)
Pathogen: Virus.
Primary Impact: Causes reproductive problems.
Transmission: Oronasal route via feces or secretions.
Clinical Presentation in Sows: No clinical signs are seen in the sow or gilt; signs are seen only in fetuses.
Signs in Offspring: Mostly mummified or stillborn piglets.
Management: There is no treatment; prevention is via vaccination.
Immunity: Recovery grants lifelong immunity.
Porcine Reproductive and Respiratory Syndrome (PRRS)
Synonym: Blue ear disease.
Pathogen type: Virus.
Status: Reportable.
Transmission and Vectors: Spread via feces, body fluids, aerosols, and fomites.
Carrier Status: Carrier pigs are a known factor in spread.
Reproductive Signs: Causes {SMEDI} (stillbirth, mummification, embryonic death, and infertility).
Target Demographics: - Sows: Experience reproductive failure. - Piglets: Primarily exhibit respiratory signs.
Control: Vaccinate; the disease is not treatable.
Malignant Hyperthermia (MH) and Porcine Stress Syndrome (PSS)
Genetic Foundation: Genetic disorder linked to the Hal gene (Dominant gene). It involves a mutation in skeletal muscle that alters the function of calcium (Ca) release.
Pathophysiology: A massive release of Ca causes severe muscle contraction, rapidly leading to a potentially fatal hypermetabolic state.
Meat Quality: Leads to {PSE} (Pale, soft, exudative) meat.
Drug-Induced MH Triggers: Triggered by drugs like Halothane gas and other halogenated inhalation anesthetics (isoflurane, sevoflurane, and desflurane), as well as depolarizing neuromuscular blocking drugs (e.g., succinylcholine).
Timing: Can occur at any time during anesthesia.
Clinical Progression: Characterized by sudden and dramatic rise in body temperature and end-tidal CO_2 (ETCO_2), followed by muscle fasciculation, muscle rigidity, tachypnea, tachycardia, arrhythmias, myoglobinuria, metabolic acidosis, renal failure, and often death.
Porcine Stress Syndrome (PSS): More common in the summer; triggered by environment and genetics (excitement, transport, handling, exercise).
Prognosis: Poor once internal clinical signs appear.
Testing: Testing for the genetic predisposition is available.
Treatment and Prevention: - Use of IV anesthesia or local anesthesia to avoid triggers. - Reduction of stress prior to anesthesia. - Early intervention is critical.
Clostridial Enteritis
Pathogen: Clostridium perfringens Type C.
Targets: Mostly affects newborn piglets.
Clinical Signs: Hemorrhagic diarrhea.
Transmission: Ingestion or wounds.
Management: Treatment is usually not successful; prevention relies on vaccinating the sow prior to farrowing.
Enteric Colibacillosis
Pathogen: E. coli.
Clinical Sign: Diarrhea.
Treatment: Treatment with antibiotics is usually effective.
Prevention: Vaccinate the sow and maintain a proper farrowing facility.
Mycoplasmal Pneumonia
Pathogen: Mycoplasma hypopneumoniae.
Presentation: Usually a mild upper respiratory disease; most herds are affected.
Transmission: Aerosol or direct contact.
Control: Isolation, depopulation, and replacement with a specific-pathogen-free ({SPF}) herd.
Pleuropneumonia (APP)
Pathogen: Actinobacillus pleuropneumoniae.
Age Predisposition: Usually affects swine less than 6 months old.
Clinical Sign: "Thumps" (abdominal breathing).
Complications: Concurrent infections are common; chronic carriers exist.
Management: Antibiotics may be helpful.
Transmissible Gastroenteritis (TGE)
Pathogen: Corona virus.
Status: Reportable.
Transmission: Shed in feces.
Demographics: Affects very young piglets most severely, though all ages can be affected.
Clinical Signs: Watery diarrhea, vomiting, dehydration, and potential abortion. Signs may develop soon after weaning.
Management: Limited treatment options; vaccination is available.
Exudative Dermatitis (Greasy Pig Disease)
Pathogen: Staphylococcus hyicus.
Characteristics: Contagious; primarily affects young pigs.
Clinical Signs: Moist, crusty skin lesions.
Management: Antibiotics are usually effective if the disease is caught early.
Pseudorabies
Synonyms: Aujeszky’s Disease or Mad Itch.
Pathogen: Virus.
Hosts: Swine are the natural host; other mammals can be affected (but not humans).
Transmission: Direct contact, fomites, aerosol, ingestion, reproductive routes, and through nasal and oral secretions.
Clinical Signs: Neurologic signs, intense itching, abortion, stillbirths, and death.
Regulatory Status: REPORTABLE!
Management: Vaccination.
Hog Cholera
Synonym: Classic Swine Fever.
Significance: most economically important swine disease worldwide.
Nature: Highly contagious; related to Bovine Viral Diarrhea ({BVD}).
Clinical Presentation: Mostly neurologic and reproductive disease; fever, lack of appetite, diarrhea, incoordination, coma, and death.
Regulatory Status: Reportable.
U.S. Status: Eradicated; no cases have been reported in the US since 1976.
Swine Influenza
Regulatory Status: Reportable.
Public Health: Transmissible to people (Zoonotic).
Signs: Fever, lack of appetite, coughing, muscular weakness, depression, and death.
Epidemiology: Spreads fast; recovered pigs can continue to harbor the virus.
Prevention: implementation of good management practices.