Mastitis, Teat/Udder Problems, Mammary Dz

What is the main economic loss associated with mastitis?

Reduced yield

California mastitis test

o Increased gel and purple color with increased SCC

o Negative test doesn't mean she is free of mastitis

Somatic cell counts

o Normal <100,000 cells/ml

o Mastitis acute >10,000,000 cells/ml

o Mastitis chronic 500,000-2,000,000

Culture

o Environmental vs contagious and ID bug is important to assess exposure and predict response to treatment

o Herd problem: narrows down cows effected!

Milk conductivity

Inflammation = increase Na and Cl that causes increased conductivity

Bulk tank testing

o Grade A <750,000

o Goal is <200,000, premiums!

o Helps you see how the herd is doing as a whole

Standard plate count

Indicated general cleanliness

Lab pasteurized count

Indication of system cleaning and sanitation

Coliform count

Indication of environmental contamination

single most effective practice to reduce incidence of contagious mastitis

Post-milk teat dipping

Strep agalactiae

o "Classic" contagious mastitis, cow is the only reservoir and it is primarily subclinical

o Suspect in open herds, SCC climbing rapidly after herd additions

o Gram +

o Biosecurity is going to be really important for control and that post-milking teat dip

Mycoplasma bovis

o Respiratory pathogen, head tilts, sepitcemia in calves with location in joints

o Highly contagious and very easy to spread via hands or equipment

M bovis presentation

o Present as classic swollen, warm udder but typically not febrile or no systemic signs. What points you to this is the poor response to treatment. Can also present subclinical (decent production with moderate to low SCC)

o Milk has sandy, tan like look to it usually

M bovis diagnostics

Hard to culture cause needs CO2, so make sure the lab can type for it

M bovis control

segregate and cull, no treatment

S aureus

o Most prevalent contagious infection!!!

o High probably she will always have this. Can be a gangrenous form

When to be suspicious of S aureus

heifer at first calving because of way it is transmitted by fomites

Why can S aureus be chronic?

Likes to form mini and deep abscesses that antibiotics cannot reach. Once they open up, that is the shedding you are seeing chronically

S aureus control

segregate and cull, might do extended dosing, teat sealant, not great with vaccines

Coag negative staph

o Normal flora of skin and teat orifice means it is an opportunistic pathogen

o Suspect in freshening heifers, elevated SCC or positive CMT

o Most important is aseptic technique

o Can infuse in the teat for this!

Corynebacterium bovis

o Gram +, club shaped

o Spreads in the parlor at milking

Environmental mastitis control important notes

integrity of teat ends immune defenses, pre-milking teat dip, clean housing, hygienic milking practices

Strep isolates

o Uberis, enterococci, dysgalactiae, bovis

o Bedding is primary source, especially straw. Sand is great!

o Half are clinical and half are subclinical

o Some do need extended therapy, check the label

o Control: intramammary treatment, HYGEINE!

Coliform mastitis

E coli and klebsiella. Anywhere that is wet and holds water can hold coliform mastitis

Coliform mastitis pathogenesis

Endotoxemia and secondary bacteremia can occur in severe cases, which is more common in infections with no prior vaccine. If the quarter comes back, it may take until next milking system for her to start lactating again. Long term will probably have low production.

Who is susceptible?

Immune suppression (old, postpartum/early lactation), very dirty pens

Coliform mastitis treatment

NO intramammary tubes! Systemic abxs (broad spectrum like ceftiofur) are best for the endotoxemia/bacteremia. #1 treatment is PO/IV fluids. Can also give banamine cause maybe helps w the endotoxemia effects

Coliform mastitis control

Vaccines work very well!! Reduces the severity of the disease but does NOT prevent the disease. Most people do the E coli one and not really the klebsiella one

Pre-dip

reduces environmental contaminants

Strip

stimulates oxytocin, allows ID of clinical mastitis, and removes high SCC and bacteria laden milk

Attachment

put all 4 cups on as quick and efficient as you can to have proper alignments

Post dip

controls contagious mastitis while teat sphincter closes

Where things go wrong with milking protocol

bimodal milk let down. Even 30-60 seconds of no milk flow due to inadequate oxytocin release can cause teat damage, hyperkeratosis, and increased mastitis risk

What abnormalities require surgical correction?

lacerations, lactoliths, fistulas, stenotic teat canal, spider teat, ST mass, supernumerary teats

Hyperkeratosis

o Due to overmilking where machine is attached and no milk flow is occuring

o Early signs are teat ringing and discolored teats

o Increases mastitis risk, possibly stenosis of canals

Ulcerative mammalitis

-BHV-2

-Typically seen in heifers but can affect any animal of any age

-Fall to winter outbreaks

-No cure, lesions can cause teat necrosis and mastitis

Papillomas

-Flat rice grain fibropapilloma

-Very contagious, spread via fomites

-Can trim or freeze them

Pseudocow pox

-Large painful papules and cesicles that typically heal in 2-3 weeks but may become chronic

-ZOONOTIC

VS

-Clinical signs similar to foot and mouth disease

-Supportive treatment

-Painful and raw tissue

Goat mammary anatomy

2 teats with 1 gland on each side

Goat SCC vs dairy cows

Have a higher SCC than cows (1 million grade A). Goats shed more epithelial cells in their milk and gradual involution

Major mastitis pathogens in hoats

CNS staph (subclinical) and staph aureus (clinical)

Blue bag

staph aurues, M haemolytica, clostridium, coliforms

Hard bag

CAE/OPP. No treatment, isolate and cull. Herd level outbreaks usually right around kidding. Antibody testing can be used but negative does not rule it out.

Mastitis goat treatment

Always culture and then use the cattle IMM antitbiotics if animal is stable. If systemically ill, go ahead with IMM and supporitve care or cull. If gangrenous mastitis, so IMM +/- systemic antibiotics (naxcel ceftiofur), fluids, NSAIDs.

More goats vs cows

• Higher protein and fat that cows

• 80/20 cisternal:parenchyma ratio, cows are opposite

Precocious udder

most commonly occurs in young goats and causes can include puberty, progesterone, estrogen, seasonality. Rule out mastitis, neoplasia, abscess. Treatment is limited, benign neglect usually the way to go

Beef cows median suspensory ligament

plays important roles in keeping the udders tucked up. Can droop over time and is a hereditary thing

Beef cows common pathogens

staph aureus, CNS, pasturella/mannheimia, coliforms

Beef cows treatment

IMM, oxytetracycline, macrolides (draxin), forfenicol (nuflor)

Pigs anatomy

6-7 teats per side with one gland but 2-3 ducts per teat

Pigs mastitis

• Coliforms (E coli, klebsiella, enterobacter, citrobacter) — severe, acute, necrotizing, systemically ill, occurs in outbreaks

• Staph and strep are sporadic and moderate

• Treatment: oxytocin, systemic abx (ceftiofur, macrolides, oxytetracycline)

Horses anatomy

Anatomy — 2 teats with 1 gland per teat but 2-3 openings per teat end

Horses mastitis

not very prevalent and commonly occurs during the dry off. Strep zooepidemicus very important pathogen, may present with HL lameness and swollen mammary vein

Horses fescue grass toxicosis

dopamine agonist that can cause agalctia. Treat with dopamine antagonist