NAVLE Reproductive

Bovine Mastitis Study Guide

📅 March 28, 2026 ⏱ 25 min read

Overview and Clinical Importance

Bovine mastitis is defined as inflammation of the mammary gland (udder) in cattle. It represents the most economically significant disease affecting the dairy industry worldwide, with annual losses estimated at $147 per cow. Mastitis occurs when microorganisms enter the teat canal and establish infection within the mammary gland parenchyma, triggering an inflammatory response characterized by elevated somatic cell counts (SCC), altered milk composition, and in severe cases, systemic illness.

Understanding mastitis pathophysiology, particularly endotoxemia associated with coliform infections, is critical for NAVLE success. Coliform mastitis, though representing only 2-4% of cases, causes the highest fatality rates (30-50%) due to systemic effects of lipopolysaccharide (LPS) endotoxin release.

High-YieldFor NAVLE, remember that subclinical mastitis causes 60-70% of total mastitis-related economic losses despite showing no visible signs. Every doubling of SCC greater than 50,000 cells/mL results in approximately 0.5 kg/milk/day loss.

Category	Pathogens	Key Characteristics
Contagious	Staphylococcus aureus Streptococcus agalactiae Mycoplasma bovis	Reservoir: Infected udders Spread during milking Chronic, subclinical infections
Environmental	Escherichia coli Klebsiella spp. Streptococcus uberis Enterobacter spp.	Reservoir: Bedding, manure, soil Between-milking exposure Acute clinical mastitis common
Opportunistic	Coagulase-negative staphylococci Trueperella pyogenes Pseudomonas aeruginosa	Variable reservoir Often mild infections (CNS) T. pyogenes: summer mastitis

Etiology and Classification of Mastitis Pathogens

Mastitis pathogens are classified based on their primary reservoir and mode of transmission. This distinction is critical for implementing appropriate control measures.

Mastitis Pathogen Classification

NAVLE TipS. aureus forms biofilms and abscesses within mammary tissue, making it extremely difficult to treat. Cure rates are only 20-30% with lactational therapy. When you see chronic, recurring mastitis with low cure rates, think S. aureus first.

Form	Clinical Signs	Common Pathogens
Subclinical	No visible abnormalities Elevated SCC (greater than 200,000/mL) Decreased milk production	S. aureus, S. agalactiae, CNS
Mild Clinical	Abnormal milk: flakes, clots, watery Mild udder firmness No systemic signs	Environmental streptococci, CNS, mild E. coli
Moderate Clinical	Swollen, hot, painful quarter Abnormal milk appearance Mild fever, decreased appetite	S. uberis, E. coli, S. aureus
Severe/Peracute	High fever (105-107 F) Severe depression, anorexia Dehydration, weakness Watery or serosanguineous milk	E. coli, Klebsiella, peracute S. aureus
Gangrenous	Blue/black discoloration of teat/quarter Cold to touch (ischemia) Severe systemic illness High mortality without treatment	S. aureus (alpha-toxin), E. coli, Clostridium perfringens

Clinical Classification of Mastitis

System	Clinical Findings
Cardiovascular	Tachycardia, weak pulse, poor peripheral perfusion, cold extremities
Gastrointestinal	Rumen atony, decreased or absent gut sounds, anorexia, diarrhea
Neurologic	Depression, weakness, recumbency (dysstasia), dull mentation
Metabolic	Hypoglycemia, metabolic acidosis, elevated NEFA, hypocalcemia
Hematologic	Neutropenia with left shift, thrombocytopenia, decreased antithrombin, hemoconcentration
Local (Udder)	Marked edema, hemorrhage, watery/serosanguineous secretion, necrosis in severe cases

Pathophysiology of Coliform Mastitis and Endotoxemia

Coliform mastitis, particularly caused by Escherichia coli and Klebsiella spp., can range from mild, self-limiting infections to severe, life-threatening endotoxemia. The key virulence factor is lipopolysaccharide (LPS), the endotoxin component of the gram-negative bacterial cell wall.

Mechanism of Endotoxemia

Step 1 - Bacterial Entry: Coliform bacteria enter through the teat canal during the inter-milking period. Environmental sources include bedding, manure, and contaminated water.

Step 2 - Bacterial Proliferation: Bacteria multiply rapidly within the milk, reaching high concentrations. The mammary gland environment (nutrients, body temperature) supports rapid growth.

Step 3 - Immune Response and LPS Release: Polymorphonuclear cells (neutrophils) migrate to the udder and phagocytize bacteria. During bacterial death and cell lysis, LPS is released from the bacterial cell wall.

Step 4 - TLR4 Activation: LPS binds to Toll-like receptor 4 (TLR4) on host immune cells, triggering massive release of pro-inflammatory cytokines including IL-1 beta, IL-6, and TNF-alpha.

Step 5 - Systemic Effects: Cytokine storm leads to systemic inflammatory response syndrome (SIRS), distributive shock, disseminated intravascular coagulation (DIC), and multi-organ dysfunction.

Clinical Signs of Endotoxemia in Coliform Mastitis

High-YieldOn NAVLE, dysstasia (inability to rise) is a major prognostic indicator for poor outcome in acute E. coli mastitis. Other negative prognostic indicators include thrombocytopenia, decreased antithrombin activity, elevated hematocrit, and elevated NEFA concentrations.

Score	Reaction Description	Estimated SCC (cells/mL)
Negative (N)	No thickening, mixture remains liquid	Less than 200,000
Trace (T)	Slight thickening, disappears with rotation	200,000 - 400,000
1+	Distinct thickening, no gel formation	400,000 - 1,200,000
2+	Immediate thickening with slight gel	1,200,000 - 5,000,000
3+	Distinct gel formation, sticks to paddle	Greater than 5,000,000

Diagnosis of Bovine Mastitis

California Mastitis Test (CMT)

The California Mastitis Test (CMT) is the most widely used cow-side screening test for mastitis. It provides a semi-quantitative estimate of somatic cell count by measuring the DNA content of milk through a gel reaction.

CMT Procedure

Collect foremilk from each quarter into the four-well paddle
Add equal volume of CMT reagent (anionic surfactant)
Gently rotate the paddle in a horizontal motion
Interpret results within 15 seconds based on gel formation

CMT Score Interpretation

NAVLE TipDo NOT perform CMT before day 3 post-calving or just before dry-off, as SCC is physiologically elevated during these periods. The threshold for subclinical mastitis diagnosis is SCC greater than 200,000 cells/mL.

Laboratory Diagnostic Methods

Bacterial Culture: Gold standard for pathogen identification. Milk samples streaked on blood agar and MacConkey agar. Note: 30-40% of clinical mastitis samples may be culture-negative.

Somatic Cell Count (SCC): Quantitative measurement using electronic cell counters (Fossomatic). SCC greater than 200,000 cells/mL indicates subclinical mastitis.

PCR Testing: Rapid pathogen identification with high sensitivity and specificity. Can detect growth-inhibited samples that are culture-negative.

Condition	Treatment Approach	Key Drugs
Mild-Moderate E. coli	Non-antimicrobial approach first Frequent stripping, NSAIDs High spontaneous cure rate	Flunixin meglumine (NSAID) Oxytocin for milk letdown
Severe Coliform/Endotoxemia	Aggressive IV fluid therapy Systemic antibiotics Anti-inflammatory therapy Frequent stripping	Ceftiofur or fluoroquinolones (parenteral) Flunixin meglumine 20+ liters isotonic fluids IV
S. aureus (Lactation)	Extended therapy (7-10 days) Combined IMM + systemic Low cure rate (20-30%)	Pirlimycin (IMM) Penicillin (if sensitive) Consider culling chronic cases
Strep. agalactiae	Highly responsive to therapy Cure rate 90-95%	Penicillin or cephalosporins (IMM) Standard treatment duration
Gangrenous Mastitis	Emergency treatment Systemic antibiotics + fluids May require teat amputation	Ceftiofur or tetracycline (systemic) Flunixin meglumine Surgical drainage if needed

Treatment of Bovine Mastitis

Treatment Based on Severity and Pathogen

High-YieldFor NAVLE: Intramammary antibiotics have little to no effect on coliform mastitis outcomes due to high spontaneous cure rates. The priority in severe coliform mastitis is supportive care (fluids, NSAIDs, frequent milking). Parenteral antibiotics are indicated only in severe cases with bacteremia risk.

MASTITIS = M.A.S.T.I.T.I.S. M - Milk out frequently (strip affected quarter) A - Anti-inflammatory drugs (Flunixin meglumine) S - Supportive care (IV fluids in severe cases) T - Target pathogen with appropriate antibiotic I - Identify the causative organism (culture) T - Treat based on severity and pathogen I - Isolate affected cows (milk last) S - Salvage or cull chronic non-responders

Dry Cow Therapy

Dry cow therapy (DCT) is one of the most effective tools for mastitis control. It serves two purposes: eliminating existing subclinical infections and preventing new infections during the dry period.

Advantages of Dry Cow Therapy

Higher antibiotic concentrations achievable (no milk dilution)
Longer drug retention in udder
No milk residue concerns during treatment
Damaged mammary tissue can regenerate before calving
Higher cure rates than lactational therapy

Blanket vs. Selective Dry Cow Therapy

Blanket DCT (BDCT): All quarters of all cows treated at dry-off. Traditional approach that has significantly reduced S. aureus and S. agalactiae prevalence.

Selective DCT (SDCT): Only cows meeting criteria receive antibiotic treatment. Requires: herd SCC below 250,000, low S. aureus prevalence, good records, and use of internal teat sealant in all quarters.

NAVLE TipInternal teat sealants (bismuth subnitrate) create a physical barrier in the teat canal and are critical for SDCT programs. They prevent new infections during the dry period, especially in quarters not receiving antibiotic therapy.

Prevention and Control of Mastitis

Five-Point Mastitis Control Plan

1. Post-milking teat disinfection: Apply germicidal teat dip (iodine, chlorhexidine) immediately after milking to all teats. Prevents contagious pathogen transmission.

2. Dry cow therapy: Treat all quarters at dry-off with long-acting intramammary antibiotics. Consider internal teat sealants.

3. Prompt treatment of clinical cases: Identify and treat clinical mastitis early to minimize spread and tissue damage.

4. Culling chronically infected cows: Remove cows with persistent S. aureus or other chronic infections that serve as reservoirs.

5. Regular milking machine maintenance: Annual evaluation of vacuum levels, pulsation, and liner condition to prevent teat-end damage.

Environmental Mastitis Prevention

Clean, dry bedding - change frequently to reduce bacterial load
Pre-milking teat preparation with germicidal predip
Dry teats thoroughly before unit attachment
J5 bacterin vaccination for coliform mastitis prevention

High-YieldJ5 core antigen vaccine (E. coli mutant) provides cross-protection against multiple gram-negative bacteria by stimulating antibodies against conserved LPS core antigens. It reduces severity of coliform mastitis but does not prevent infection. Administer 30 days pre-partum and again at calving.

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