From Teat Canal to Mammary Tissue: How Subclinical Mastitis Develops

Subclinical mastitis does not begin with an obviously swollen udder or visibly abnormal milk. The process can start much earlier, when microorganisms gain access through the teat canal and establish themselves within the mammary gland. 

Understanding this progression helps explain why an apparently healthy buffalo can still have ongoing mammary inflammation. 

The Teat Canal: The First Barrier 

The teat canal is the primary route through which mastitis-causing microorganisms enter the mammary gland^[1]. 

Normally, the teat sphincter and keratin lining provide important physical and biological protection against microbial entry. However, this barrier is not continuously closed. The teat canal can remain open for up to approximately two hours after milking, creating a period when microorganisms have greater opportunity to enter^[2],[3]. 

Around parturition, pressure and changes affecting the teat canal can further influence this protective barrier^[4],[5]. 

Once Microorganisms Enter 

After entering through the teat canal, microorganisms can reach the teat cistern and multiply within the mammary gland^[6]. 

The mammary gland responds by recruiting neutrophils and other leukocytes to attack invading microorganisms. This immune response is an important defence mechanism, but it can also contribute to tissue injury as the inflammatory process develops^[6]. 

At this stage, the buffalo may still show no obvious clinical signs. That is one reason subclinical mastitis can remain undetected during routine examinations. 

Inflammation Changes the Milk^[6] 

The inflammatory response does not remain confined to the tissue. 

As epithelial cells are damaged and inflammatory cells accumulate, cellular components enter the milk. This contributes to an increase in somatic cell count (SCC). 

Mammary tissue damage can also lead to the release of enzymes such as N-acetyl-β-D-glucosaminidase (NAGase) and lactate dehydrogenase (LDH). 

These changes provide a measurable indication that inflammatory activity is occurring even when the udder appears normal. 

From Cellular Damage to Milk Changes^[6] 

As the inflammatory process becomes more pronounced, damage to the mammary epithelium can interfere with normal milk production and quality. 

In more advanced tissue damage, changes within the mammary gland can also affect milk composition, including an increase in milk pH. 

This creates an important clinical contrast: The udder may look normal while measurable changes are already occurring at the cellular and milk level. 

Why This Matters in Subclinical Mastitis 

The progression from microbial entry to inflammation and epithelial damage explains why waiting for visible mastitis can miss an important part of the disease process. 

The teat canal is the entry point. Microbial multiplication triggers the immune response. Inflammation then produces cellular and biochemical changes that can affect milk and mammary tissue before obvious clinical signs appear. 

Clinical Takeaway 

Subclinical mastitis can begin at the teat canal and progress within the mammary gland without immediately producing visible abnormalities. Recognising this sequence helps veterinarians understand why changes in SCC and other milk parameters can provide important clues to mammary inflammation before clinical mastitis becomes apparent.

References:

1. Petersson-Wolfe CS, Leslie KE, Swartz TH. An update on the effect of clinical mastitis on the welfare of dairy cows and potential therapies. Veterinary Clinics: Food Animal Practice. 2018 Nov 1;34(3):525-35. https://www.academia.edu/download/114366087/j.cvfa.2018.07.00620240510-1-aca955.pdf
2. Zalewska M, Kawecka-Grochocka E, Słoniewska D, Kościuczuk E, Marczak S, Jarmuż W, Zwierzchowski L, Bagnicka E. Acute phase protein expressions in secretory and cistern lining epithelium tissues of the dairy cattle mammary gland during chronic mastitis caused by staphylococci. BMC Veterinary Research. 2020 Aug 31;16(1):320. https://link.springer.com/content/pdf/10.1186/s12917-020-02544-8.pdf
3. Zigo F, Farkašová Z, Výrostková J, Regecová I, Ondrašovičová S, Vargová M, Sasáková N, Pecka-Kielb E, Bursová Š, Kiss DS. Dairy cows’ udder pathogens and occurrence of virulence factors in Staphylococci. Animals. 2022 Feb 14;12(4):470. https://www.mdpi.com/2076-2615/12/4/470
4. Fagiolo A, Lai O. Mastitis in buffalo. Italian Journal of Animal Science. 2007 Jan 1;6(sup2):200-6. https://www.tandfonline.com/doi/pdf/10.4081/ijas.2007.s2.200
5. Zigo F, Vasil' M, Ondrašovičová S, Výrostková J, Bujok J, Pecka-Kielb E. Maintaining optimal mammary gland health and prevention of mastitis. Frontiers in veterinary science. 2021 Feb 17;8:607311. https://www.frontiersin.org/journals/veterinary-science/articles/10.3389/fvets.2021.607311/pdf
6. Chowdhury MS, Rahman MM, Hossain H, Ghosh PK, Islam MR, Lamichhane B, Gomaa FA, Selim HM, Hossain MM, Helmy YA, El Zowalaty ME. Subclinical mastitis of buffaloes in Asia: prevalence, pathogenesis, risk factors, antimicrobial resistance, and current treatment strategies. Journal of Animal Science and Technology. 2026 Jan 31;68(1):18. https://pmc.ncbi.nlm.nih.gov/articles/PMC12923260/