Pathogenesis and Aetiology of Mastitis Flashcards
1
Q
Disease Process Involving the Mammary Gland
A
- Mastitis
- Neoplasia of Mammary Gland
- Diseases of the SKin of teats and mammary gland–> Gangrene (Wet/Dry)
- Trauma (and subsequent mastitis)
- Teat Blockage (mastitis or loss of function)
- Pathogen Transmission to young
2
Q
Mastitis
A
- Considered one of the big 3 diseases of dairy cattle
- Very Expensive as there is an issue with loss of function, treatment, cost of culling, etc.
- Has a significant impact on animal welfare: can die overnight from toxic mastitis and is it also very painful!
- Can often prevent this though which is good and do something about it
3
Q
Big Disease Processes in Dairy Cattle
(3 main)
A
- Mastitis
- Lameness
- Fertility Decrease
4
Q
Mycoplasma Bovus in the Herd
A
- Clotting/curtled appearance often associated with the pathogen Mycoplasma bovus
- If it persists it can cause persistent mastitis within the herd and lead to mass culling
- can also see lameness in these cows
- Big issue when in the herd
- causes significant issues
5
Q
Mammary Gland Structure
A
- Its like an apocrine gland of the skin
- milk producing alveoli –> leading into glandular ducts –> leading into lactiferous sinus–> then into the papillary duct and through the teat
- majority of disease entry will be through the teat
- Galactophoresis refers to all the ducts
- where as mastitis then refers also to the tissues and alveoli affected
- will spread along the sinuses and then the ducts before reaching the alveoli and affecting the milk producing tissue (if the pathogen enters from an external source)
6
Q
Mammary Gland Histo
A
- Immature gland or inactive (not induced to grow by prolactin or estrogen)
- Lactating can see the milk within the alveoli being produced
7
Q
Entry of Microorganisms into the Mammary Gland
A
- galactogenic or ascending infection - organisms somehow gain entry via the teat canal (most common)
- or bloodstream going directly into alveoli (where major blood supply is)- often diseases where we don’t see the mycoplasma associated with it
- trauma can result in damage in the teat and pathogens getting directly into the papillary duct
8
Q
Defence Against Mastitis
A
- Try to control pathogen entry and pathogen proliferation
- Whether these cases will present as mastitis - depend on host immunity, pathogen itself and env’tal conditions
9
Q
Resistance to Infection
A
- How does the mammary gland protect itself? (fight or prevent infectious disease from manifesting itself)
- Keratin block from epithelium - the teat itself prevents infection itself. Need to try and keep the teat in good function and health to act as main protection. whole of the teat is basically anitbacterial
- Main mode of protection is the teat itself so often don’t get infection - protecting the teat is a major factor. If they bypass the teat and get into the lactiferous sinus, there will be an infection no matter what
- Furstenberg Rosette - prevent the entry of bacteria, mucosal folds with a lot of blood supply so it gets a lot of plasma cells there helping with the immunity
- these are physical factors that are part of the innate immunity, but also… milking them out can be really helpful!
10
Q
Resistance to Infection
(innate Immunity)
A
- there are soluble and cellular factors to this innate immunity as well
- If you get bacteria in there, you will get neutrophils in there very very quickly
- Unfortunately, neutrophils are much more efficient in the blood than in the milk (in the milk they often don’t manage to kill the bacteria fully)
- You tend to get this inverse cycling of high numbers of neutrophils and then the neutrophils kill other neutrophils and you seen get high numbers of bacteria and low neutrophil count and keeps on going
- hard to control
- followed on by macrophages
11
Q
Resistance to Infection
(adaptive)
A
- In particular IgA on the immunoglobulin side has been the local Ig
12
Q
Mammary Tissue Damage
A
- damage/issues is therefore not only caused by the pathogens but by the inflammation
- neutrophils die off and release cytokines, host proteases that can all dmage the tissue and result in longer term damage and shorter term as well
- even repair can damage- fibrosis
13
Q
Categorization of Mastitis by “time”
A
- Traditional way of separating mastitis is: contagious and environmental, but this is a way to identify by timing
- If acute isn’t treated and hasnt reached complete resolution, then you could end up with chronic mastitis
- Chronic mastitis can lead to progressive loss of secretory ability, which can often lead to eventual culling - and the chronic is usally following subclinical infections or acute infections
- Type of Pathogen does not define this: Staph Aureus could cause all of them (peracute, acute, chronic)
- Type of mastitis is not pathogen dependent
- Do not forget subclinical mastitis as it is the most common
14
Q
Peracute Mastitis/Severe Necrotising
A
- Usually associated with systemic disease and a lot of fertility disease
- severe necrotizing
- turns cold and blue
- Tends to be caused by S.aureus - alpha toxin causing vasoconstriction and ischemia
- but can also have a more severe ‘toxic mastitis”- due to coliform bacteria, E.Coli–> endotoxin release. Get severe vascular leakage and that can be seen by marked edema (gelatinous appearance) in the subcutaneous tissue. Often it is very watery fluid
- In severe cases, if they go recumbent, part of the udder can just slough off bc its blood supply has been cut off and it becomes gangrenous and they just lose it- but they can survive this!
- But the toxemia is the major problem
15
Q
Acute Mastitis
A
- much less toxin production/release and damage to the tissue
- much more local effects: oedema, fibrin, neutrophilic inflitration (when you are milking a cow and you see the clots come out- that is usually a sign of acute mastitis)
- when you look histologically: lots of neutrophils, edema, fibroplasia
- if you dont get under control at this point and get fully rid of it, may progress to chronic mastitis
16
Q
Chronic Mastitis
A
- If the acute mastitis doesn’t clear up, you may get local fibrosis around the milk ducts and there may be a block on the milk coming from healthy areas
- may get involution (temporary loss of secretorial function due to an obstruction) of the glands - can recover in the next lactation and come back into function
- permanent loss would then be fibrosis- the tissue will not be replaces, it can not be regenerated so the tissue is lost
17
Q
Acute Localised Clinical Mastitis - Initial Flare Up
A
- Get acute infection and then travels up the ducts to settle somewhere in the mammary gland
- starting to cause some lesion and then neutrophils will come in to repair
- get some fibrosis (obviously due to tissue being damaged somewhat, get necrosis replaced by fibroplasia) - not that big a deal, normally affects this little acinoid only
- but the neutrophils aren’t very good and effective (particularly in the periparturient period - they don’t migrate as well into the mammary gland)
- thus, may get a further infection/ flare up just adjacent to it, and the same immune/repair processes occur, but then that fibrosis may block up that whole area and there is blockage - when you get repair then by fibrosis of this, the whole area connot drain anymore
- may get involution or fibrosis of this area depending on how much it spreads around
18
Q
Subclinical Mastitis
A
- Much more common than clinical
- You don’t see clots, you don’t see watery appearance - looks pretty normal, feels pretty normal
- how do we know there is mastitis then? - CELL COUNT WILL INCREASE
- CMT will be your best estimate: will detect neutrophil cells and will result in the more viscous appearance of fluid (Note: will need to know how to do these for the OSCE’s)
- from a disease development of subclinical mastitis, it develops almost identically to acute mastitis and then into chronic mastitis (still get pathogen entry, but just doesn’t cause as much local damage or disease to result in obvious or systemic changes)
- Still need to interfere and treat even though it is a lower pathogenesis
- SCC should be less than 200,000 cells/ml of milk (can input for each quarter)
- can then make sure there is no inflammation going on
- Neutrophil numbers already rise quickly in infections, so you should be able to detect them early on
19
Q
Take Home Messasges on Mastitis
A
- This is not only an issue in dairy cows! - See it in sheep (gangrenous mastitis leading to early culls)
- most of your efforts will be based on preventing galactogenic entry
- immune response has a big effect (emphasis) on the clinical presentation of mastitis