Caprine Mastitis: Etiology, Epidemiology, Pathophysiology, Diagnostics, Therapeutics, and Immunoprophylactic Strategies

Dr. Kirti Dadaram Fanase1, Dr. Pranav Sunil Jadhav2 Dr. Rajwardhan Chandrakant Nimbalkar3*1MVSc Veterinary Pathology, College of Veterinary Science & Animal Husbandry, Sardarkrushinagar.2MVSc Animal Nutrition, Indian Veterinary Research Instituten Bareilly3MVSc, Poultry Science, ICAR- Central Avian Research Institute, Izatnagar, Bareilly, Corresponding Author: Dr. Rajwardhan Chandrakant Nimbalkare-mail: rajnimbalkar700@gmail.com doi.org/10.5281/IndianVetMagazine.23477282

AbstractCaprine mastitis represents one of the most economically detrimental diseases impacting goat milk production, animal welfare, and farm viability globally. Caused primarily by bacterial pathogens—notably coagulase-negative Staphylococci (CNS), Staphylococcus aureus, Streptococcus spp., Mycoplasma agalactiae, Escherichia coli, and Pseudomonas aeruginosa— the disease occurs in acute gangrenous, chronic clinical, and insidious subclinical forms. Transmission occurs via galactogenic pathways, faulty milking machinery, milker hands, kid suckling, and environmental bedding contamination. Host factors including parity, late lactation stage, high milk yield, udder conformation (pendulous udders, supernumerary teats), and specific dairy breeds (Saanen, Alpine) exhibit increased susceptibility, while environmental drivers like high humidity, poor shed sanitation, and trauma exacerbate infection rates. Pathophysiologically, intramammary infection causes severe inflammatory destruction of parenchyma, causing dramatic drops in milk volume, altered milk composition (elevated electrical conductivity, reduced lactose and fat, elevated somatic cell counts), and systemic illness in acute gangrenous cases. Laboratory alterations include leukocytosis with neutrophilia and toxic left shift in acute cases, marked elevations in acute-phase proteins (Serum Amyloid A, haptoglobin), elevated liver diagnostic enzymes (AST, ALT, lactate dehydrogenase), hyperbilirubinemia, and hypocalcemia. Diagnostic modalities range from field-level California Mastitis Test (CMT), modified somatic cell counting (SCC), and electrical conductivity to definitive bacterial culture, MALDI-TOF MS, real-time PCR, and B-mode udder ultrasonography. Therapeutic management involves targeted intramammary and parenteral antimicrobials (penicillins, ceftiofur, florfenicol, fluoroquinolones), non-steroidal antiinflammatory drugs (meloxicam, flunixin meglumine), fluid therapy, and surgical teat amputation in irreversible gangrenous cases. Immunoprophylaxis utilizing commercial and autogenous polyvalent Staphylococcal and Mycoplasma agalactiae bacterins shows variable efficacy, emphasizing the absolute necessity of integrated milking hygiene and dry-period therapy. This comprehensive review synthesizes peer-reviewed evidence from high-impact veterinary journals (NAAS rating > 6.0) to serve as an authoritative, publication-ready guide.