9. Mastisis

What is mastitis?

**Inflammation of mammary gland** characterized by – changes in milk (physical, chemical, bacteriological), pathological changes in the glandular tissue, economic losses, consumers health, polyetiological. Causes economic losses and has epidemiological importance for consumer health

What types of mastitis are there?

Clinical infectious mastitis – macroscopic changes in secretions and tissue 

Infectious subclinical mastitis – detectable with lab methods 

Nonspecific clinical mastitis – no pathogens, inflammatory changes in secretion and tissue

\
Nonspecific subclinical mastitis – no pathogens, detectable with lab methods

What are the aetiological agents for mastitis?

***Contagious mastitis*** – *Streptococcus agalactiae,* ***Staphylococcus aureus****, Corynebacterium bovis, Mycoplasma bovis*

***Environmental mastitis*** *– Streptococcus dysgalactiae, Streptococcus Uberis, Streptococcus bovis, E.coli, Klebisiella, Citrobacter, Enterobacter, Pseudomonas spp*

Which aetiological agents for mastitis are zoonotic?

brucella, mycobacterium, listeria, coxiella

What is the epizootiology of mastitis?

Stage of lactation (first 2 months) being most susceptible. Age of cow – older are more susceptible. Level of inherited resistance – teat shape, anatomy of teat canal. Lesions on teat skin. Immunological status. 

Contributing factors:

\
* Ability to survive in environment
* Resistance to cleaning, disinfection
* Ability to colonise teat duct and adhere to mammary epithelium
* Resistance to antibiotics

What is the transmission of mastitis?

Environmental: infected troughs, contaminated material, hands and equipment 

* M. bovis – aerosol

Summer: acute infections spread by flies

\
Two sources: environment and infected udders

What is the pathogenesis of mastitis?

Pathogenesis consists of three phases

* **Invasion phase**: organism passes from exterior into the teat canal.
* **Infection phase**: organisms multiply and invade the mammary tissue.
* **Inflammation phase**: clinical mastitis or greatly increased somatic cell count.

Streptococcus agalactiae – **replicate in ductus lactiferous**, enter the lymphatic system – enlarge the lymph nodes, inflammatory reaction – **atrophy**

* Few changes in secretory cells with strep

Staphylococcus 🡪 **greater degenerative changes** 

Mycoplasma bovis – in big herds, reservoirs are clinically healthy animals, young calves, transmit through contaminated material, hands. 

Corynebacterium bovis – **subclinical mastitis,** act as normal microflora

What are the clinical signs of clinical mastitis?

Usually caused by environmental pathogens, in addition to Mycoplasma. 

Local signs include changes in size, secretion (presence of flakes or clots), consistency and/or temperature and colour of mammary gland. 

Systemic signs include fever, tachycardia, depression, loss of appetite and dehydration. 

* Per acute mastitis: show all signs of local inflammation, as well as severe systemic signs.
* Acute mastitis: show all signs of local mastitis, with less severe systemic signs.
* Sub-acute: normal signs are subdued, no systemic effect only persistent abnormality of milk
* Chronic mastitis: minimal changes in the milk, mammary gland is hard at palpation, changes over many months or between lactations, terminal stage is atrophy

General signs: hot, swollen udder, fever, rapid pulse, inappetence, dehydration, depression

**Increased SCC** are seen in almost all forms except latent 

Staphylococcal 🡪 local swelling of quarter, hard and sore, gangrene and abscesses

What are the clinical signs of subclinical mastitis?

No clinical signs are present. Disease is recognized by increased somatic cell count indicating udder inflammation, positive bacteriology, and decreased milk production. 

\
Also have latent and abacterial (mechanical) forms

What is the diagnosis for mastitis?

***Adspection*** – size, symmetry, color, injuries (=close inspection)

***Palpation*** – consistency, temperature, pain 

***Examination of milk*** – proper examination of the milk requires the use of a strip cup, preferably one which has a shiny, black plate permitting the detection of discoloration as well as clots flakes. 

* Color, consistency, and smell. 
* pH – 6,5-6,8 (colostrum \~6.4). In **mastitis the milk is more alkaline**. 

Test for milk chlorides; normal concentration increases through mid-lactation to late 

* normal max. 130mg/100ml

Test for electrical conductivity of milk using conductivity meter: 0.4 -0.56S/m

**California Mastitis Test** – reflects total leukocyte, determine quantity of DNA and app the number of leucocytes. 

SCC – **indicates milk quality, good milk <200,000 (<100,000 for uninfected), significant infection >300,000**

Bacteriological examination – Isolation, identification, typing and sensitivity 

* Streptococcus spp – cultivation, **CAMP test** to differentiate Str. Agalactiae from staph aureus, streptotest, catalase reaction -ve (differentiation staph/strep), bacitracin, latex agglutination, ASLO (antistreptolysin)
* Staphylococcus spp – blood agar, Selective mediums (NaCl), grow under anaerobic conditions - plasmocoagulase test, STAPHYtest, catalase test

What is the treatment for mastitis?

Intramammary or systemic ATB 🡪 do sensitivity testing

What is the prevention against mastitis?

***Contagious mastitis:*** increasing hygiene level and improve milking procedures, teat dipping before and after milking, eliminate by treating all cows with dry cow therapy and culling chronic cows. 

***Environmental mastitis***: improve cleanliness of cow’s surroundings, frequent change of bedding or avoid natural bedding material, avoid practices that may damage the teats 

Prevention of **invasion phase is most effective**