4.3 Bovine Common Diseases & Management
Key Takeaways
- Milk fever progresses through hyperexcitable stage 1, sternal recumbent stage 2 (S-shaped neck), and lateral recumbent stage 3; treat slowly with IV calcium gluconate.
- Mannheimia haemolytica is the principal shipping fever pathogen, causing severe fibrinous pleuropneumonia via neutrophil-lysing leukotoxins.
- BVDV persistently infected (PI) calves result from in utero non-cytopathic viral exposure between 40-120 days of gestation; diagnose via ear notch ELISA.
- Frothy bloat requires anti-foaming agents like poloxalene, whereas free gas bloat is relieved via orogastric tubing or emergency trocarization.
4.3 Bovine Common Diseases & Management
Managing individual and herd-level diseases is a cornerstone of bovine veterinary practice. Practitioners must recognize pathognomonic clinical signs, understand underlying pathophysiologies, and implement effective treatment and prevention protocols.
Metabolic Diseases
Metabolic diseases typically occur during the transition period, when dairy cows transition from gestation to lactation.
Ketosis
Ketosis is characterized by elevated ketone bodies (BHBA, acetoacetate, acetone) in blood, milk, and urine.
- Pathophysiology: Caused by negative energy balance (NEB). Inadequate dry matter intake relative to milk demand forces mobilization of adipose tissue. Excessive NEFAs are transported to the liver, leading to hepatic lipidosis and incomplete oxidation of fats into ketone bodies.
- Type I Ketosis (Peak Ketosis): Occurs 3–6 weeks post-partum, coinciding with peak milk yield. It is primarily a nutritional shortage of glucose.
- Type II Ketosis (Fatty Liver/Ketosis): Occurs 1–2 weeks post-partum. It begins pre-partum with insulin resistance and excessive fat accumulation in the liver.
- Treatment:
- Oral Propylene Glycol: 300–400 grams once daily for 3–5 days (serves as a glucose precursor).
- Intravenous 50% Dextrose: 500 mL IV (provides immediate glucose, though short-lived).
- Corticosteroids: Dexamethasone (stimulates gluconeogenesis and reduces milk yield temporarily).
Milk Fever (Parturient Paresis)
Milk fever is an acute hypocalcemia occurring at or near calving.
- Pathophysiology: The onset of lactation creates a massive drain on blood calcium. If bone resorption and intestinal absorption cannot adapt quickly enough, blood calcium drops.
- Stages:
- Stage 1: Standing but hyperexcitable, mild muscle tremors, ear twitching.
- Stage 2: Sternal recumbency, head tucked into the flank (forming a characteristic "S-shaped" curve), cold extremities, dry muzzle, weak heart sounds, and tachycardia.
- Stage 3: Lateral recumbency, flaccid paralysis, severe bloat, coma, and death.
- Treatment: Slow IV administration of 500 mL of 23% calcium gluconate. The heart must be auscultated during administration. Calcium is cardiotoxic and can cause bradycardia, arrhythmias, or cardiac arrest.
- Prevention: Feed a Dietary Cation-Anion Difference (DCAD) diet pre-partum. Anionic salts (chloride, sulfate) create a mild metabolic acidosis, which increases the tissue sensitivity to parathyroid hormone (PTH), enhancing osteoclastic calcium resorption and renal vitamin D synthesis.
Infectious Diseases
Bovine Mastitis
Mastitis is the inflammation of the mammary gland, categorised by pathogen origin.
Contagious Pathogens
Contagious mastitis pathogens spread from cow to cow, primarily during the milking process via milkers' hands, towels, or milking machines.
- Staphylococcus aureus: Causes chronic, subclinical mastitis with high SCC, microabscesses in the parenchyma, and low cure rates due to deep tissue encapsulation. Can cause gangrenous mastitis ("blue bag") in fresh cows, leading to tissue necrosis, sloughing, and systemic toxemia.
- Streptococcus agalactiae: An obligate intramammary pathogen. It lacks cell wall modifications that resist penicillin, making it highly sensitive to beta-lactam antibiotics and thus possible to eradicate from a herd.
- Mycoplasma bovis: Causes severe mastitis affecting multiple quarters, rapid milk drop, and joint/respiratory signs. It is highly contagious and does not respond to antibiotic therapy, requiring the culling of positive cows.
- Control: Implementation of the standard 'Five-Point Plan' including post-milking teat dipping, dry cow antibiotic therapy (intramammary cephalosporins/cloxacillin), internal teat sealants (bismuth subnitrate), segregation or culling of positive cows, and proper milking machine maintenance.
Environmental Pathogens
Environmental pathogens are found in the cow's surroundings (manure, bedding, mud).
- Escherichia coli & Klebsiella spp. (Coliforms): Cause acute, systemic mastitis due to endotoxin (LPS) release when bacteria die. Signs include recumbency, watery/yellow milk with serum-like flakes, high fever, cold extremities, and severe endotoxic shock.
- Streptococcus uberis & Streptococcus dysgalactiae: Environmental streptococci, commonly found in organic bedding material like straw or sawdust.
- Control: Keeping stalls clean and dry (sand bedding is ideal because it does not support bacterial growth), pre-milking teat dipping, and keeping cows standing for 30 minutes post-milking until the teat sphincter closes.
Bovine Respiratory Disease (BRD) Complex
BRD (shipping fever) is a multifactorial disease involving viral pathogens, bacterial pathogens, and environmental stressors (weaning, transport, commingling). Stress impairs the mucociliary elevator, allowing normal upper respiratory tract commensals to colonize the lower respiratory tract.
- Viral Triggers: Bovine Viral Diarrhea Virus (BVDV) (causes immunosuppression), Infectious Bovine Rhinotracheitis (IBR) (caused by BoHV-1; causes necrotic tracheitis and red nose), and Bovine Respiratory Syncytial Virus (BRSV) (causes severe interstitial pneumonia and emphysema).
- Bacterial Pathogens:
- Mannheimia haemolytica: The primary cause of severe fibrinous pleuropneumonia. Its main virulence factor is a leukotoxin that lyses bovine leukocytes, causing massive tissue necrosis.
- Pasteurella multocida: Causes purulent bronchopneumonia.
- Histophilus somni: Causes fibrinous pleuritis and can lead to thrombotic meningoencephalitis (TME).
- Treatment and Control: Treatment involves antimicrobials with good lung penetration (e.g., tulathromycin, florfenicol, ceftiofur) and NSAIDs. Control centers on minimizing stress and administering pre-conditioning vaccines.
Bovine Viral Diarrhea Virus (BVDV) PI Calves
- Persistent Infection (PI) Pathogenesis: A PI calf is created when a pregnant cow is exposed to a non-cytopathic strain of BVDV between 40 and 120 days of gestation. The fetal immune system is developing and recognizes the virus as "self," resulting in immunotolerance. The calf sheds billions of viral particles daily for life.
- Diagnosis: Ear notch ELISA or immunohistochemistry (IHC) on skin biopsies. PI calves must be culled.
Digestive and Traumatic Conditions
Bloat (Ruminal Tympany)
- Frothy Bloat (Primary): Ingestion of soluble proteins from legumes (clover, alfalfa) or high-grain diets forms a stable foam that traps fermentation gases. Treatment: Poloxalene or mineral oil to break the foam.
- Free Gas Bloat (Secondary): Physical or functional eructation failure (e.g., esophageal choke, vagal indigestion, or recumbency). Treatment: Stomach tube passage or emergency rumen trocarization.
Hardware Disease (Traumatic Reticuloperitonitis)
- Pathogenesis: Ingested metal objects (wire, nails) settle in the reticulum. Reticular contractions push the object through the cranial wall. This causes localized peritonitis, and if it crosses the diaphragm, reticulopericarditis.
- Clinical Signs: Arched back, abducted elbows, painful grunt on wither pinch test. Pericarditis causes a "washing machine" murmur, brisket edema, and jugular pulses.
- Prevention: Oral administration of a rumen magnet at 6–12 months of age.
An ear notch ELISA is positive for Bovine Viral Diarrhea Virus (BVDV) in a 2-month-old calf. What is the biological mechanism that led to this calf becoming persistently infected (PI)?
A dairy veterinarian is treating a post-partum cow with Stage 2 milk fever. Which of the following sets of clinical signs is most characteristic of this stage, and what is the primary cardiotoxic risk associated with its treatment?
A feedlot steer is presented with severe dyspnea, an orthopneic stance (elbows abducted, head and neck extended), and a high fever. Necropsy of a similar steer reveals severe fibrinous pleuropneumonia. Which of the following bacterial pathogens is the primary causative agent of this condition, and what is its main virulence factor?