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Flashcards in Clincal Mastitis Deck (38):

Clinical v. Subclinical 

  • Mastitis is a bit of a continuum in that there is subclinical infection, clinical, etc. (same thing, but it is a gauge on the presentation and levels of signs that you are able to pick up) 
  • but remember: all the different strains will cause different types of mastitis
  • In aims to control the disease, we need to know if it is environmental or contagious in order to direct our treatments correctly as well as prevention plans
  • Clinical- you will see clots AND the cow is affected by the infection, there will be an element of *redness* around it (fever in severe grades, or just a blown up quarter where the swelling/redness is noticeable)
  • Subclinical- goes completely under the radar until we check for it. Doesnt mean S. aureus is causing the subclinical and E.Coli is causing the clinical. Need to see as a spectrum! some cows respond differently to the same pathogen as well
  • subclinical can be occurring in different cows at the same time even when there are notable clinical cases 
  • Also, some cows will present with clinical mastitis and then after treatment, subclinical mastitis continues to be the case 
  • There will often be cases that are subclinical that were clinical in the past and possibly missed by the farmer by not checking for signs (clinical mastitis needs to be checked in the parlor and if the farmer is not payin attention sufficiently then these clinical cases are reported as 0)
  • In order to know what the prevalence/incidence of the disease is on the farm, we need to know how the testing is taking place
  • Subclinical is usually marked on a sheet in the milking quarter from taking the SCC (get a linear score of cell counts) and then clinical should be marked upon noting signs 




  • many of our mastitis cases will occur in dry period
  • some will occur in the lactation period
  • These are important to differentiate when you are trying to control the situation 


Number of Cases of Clinical Mastitis

  • Cases of clinical mastitis marked in 50 day brackets of being "in milk"
  • Can tell that it is a dry period mastitis
  • The clinical cases are detected in the lactation period meaning they were likely infected in the dry period
  • So doesnt mean that all the cows were infected day 1 after calving, could have been 30 days after calving, 50, and some even include 60 
  • Cow has been coping with it for a period to a degree and then eventually you see clinical mastitis 
  • If you can better control the mastitis in the dry period then the large peak at the start of days in milk will decrease - end up with way less of a distribution of clinical mastitis through the lactation period 
  • Seems that there is very little cross-over in the milking parlor, but they may dry off with the mastitis or they are picking up the mastitis when they are being housed 


Subclinical Cases Cell Count Graph 

  • this is a classic way of presenting 
  • white: clean at dry off and calf down with low cell count
  • yellow: clean at dry off, but had a high cell count at calving down so there would be a clear cut dry period mastitis occurring 
  • green: girls that cure during the dry period (want to see green as big as possible to the red one) - in this case, you can see there was a very subclinical mastitis going on through the lactation cows which is actually more favorable (white is way bigger and there is a bigger proportion of whites and greens to yellows and reds)
  • this tells us if there is subclinical dry mastitis occurring




  • plug that can be put into cows and prevents dirt coming into the teats
  • has other trade names, but orbeseal was the first on the market 
  • only 1/2 of the teats will close off in the dry period, half will have communication to the outside world
  • orbeseal is a way to close off from exterior and keep external bugs out of the teat system during the dry period 




  • very important to know in order to be able to treat properly


Dirty Cows (in rain) 

  • Not very acceptable to keep cows this way and milk them in this condition 


Cubicle issues

  • Milking cow did not want to lie in her cubicle and therefore lies in the dirty passage way (also low straw)
  • Bad design will cause the cow to lie down in passage ways
  • at risk for mastitis and makes the teats very dirty
  • cleaning these teats would take a lot of time and therefore doesnt happen properly in these cases- can lead to clinical env'tal mastitis 


'Host Adapted' v. 'oppportunistic' Pathogens


  • These are the 5 different main pathogens we discussed
  • steptococcus agalactiae (SAG) 
  • ECO- E.Coli
  • Traingle represents the sliding slope that these pathogens are on 
  • Contagious mastitis is mainly for SAG, not a clinical mastitis but a subclinical (which is discovered by cell counts), can be really difficult for farms to detect because it goes under the radar and spreads quite well in the milking parlor (so major proponent of SAG is that it is contagious and host adapted)
  • E.Coli is mainly environmental and there are E.Coli's out there that will behave like SAG (so it is a spectrum)
  • additionally there will be E.Coli bugs that are not environmental (some can be contagious) - we need to look at the behavior of the pathogen, not put a label on the spread due to the name of that pathogen (these pathogens are in fact quite diverse!)



(env't vs. milk) 

  • good example of a pathogen being diverse
  • klebsiella is typically seen as an environmental bacteria that loves wet conditions (leaky water troughs)
  • They took some samples of the environment (the bedding and the flooring)
  • can see massive variation in the DNA profile on the agar
  • In the mastitis cases (milk agar) they all look identical (DNA fragments)- these would be identical cases
  • typically envt'al masitis (Klebsiella) this has a very contagious behavior, there is one strain causing the infection for all the different cows
  • Don't need to do DNA sequencing on all our samples of mastitis cases, but it does show that we need to read the behavior of the pathogen rather than say "Oh it is Klebsiella-->so it is environmental"
  • Same for E.Coli, same for S. uberis (sometimes they behave environmentally and sometimes they behave contagious)
  • Need to note that difference and appreciate it to monitor our control better 


Clinical Cases 

  • Multi factorial disease: clinical cases that occur in the dry period will be incubating in these cows for days and sometimes multiple weeks. So, thus it is not just the infection moment, but other factors occurring as well ot a degree and then they tip over the edge and become clinical 
  • Other factors include: immunity (high producing cows are challenged in their E drains and some require glucose as well to perform)- so there is a competition b/w milk yield and immunity. There are many other factors involved as well 
  • There are risk factors as well that make them more susceptible to infection 


Clinical Cases; incidence

  • Some strains will be more pathogenic than others. there are also minor pathogens that are well infectious but don't cause any clinical disease (e.g. corynebacterium bovis)
  • Over the past ten years the clinical cases have been similar/slightly increasing which is a concern (barely a change in the amount of clinical cases) - it is fine if there is an increase due to the farmers being more vigilent about picking up the disease
  • now seeing that higher performing herds are having mastitis at about 40% - apparent that they are picking up the mastitis in the milking parlor
  • we should be concerned if we go to the farm and the mastitis rate is only 10% (means likely that the mastitis rate is not being picked up) - farmer in parlor or the miling hands could be being a bit sloppy in practice 
  • farmers are legally required to strip milk and detect infection (to check for clinical mastitis)
  • Need to make a difference between a cow infection and quarter infection (infection in a different quarter or after a week in the same quarter after treatment - according to some is a "new" mastitis) and recurrence (happens in same quarter in recent terms) 
  • Always check the quarters that it is occurring in and host factor is quite important in these cases 
  • twice as many quarter cases than the number of clinical cows, then that means each cow will get about two cases of clinical mastitis (magnifies the importance of the host in this case)
  • In SE england has a high prevelance as they are on straw based pastures and it is difficult to control (lime is just not enough), farmers need to be vigilent about picking up mastitis in these cases 
  • but bulk tank SCC amount has changed over the past 10 yrs


  • shows the impact and the financial incentive for farmers
  • typically the threshold for a penalty would be about 250 (some lower it to 200)
  • If you go over that, you get a half a pence per L less ( that is a massive difference for a farming business)- this has had a massive impact on the average SCC
  • get a bonus if you go below 150 cell in your bulk tank - milk will last longer if there is a lower SCC bc even though it is pasteurized (won't be pathogens in it) but due to enzymes of the these pathogens breaking down milk comp. (lower shelf life)
  • Worth it for there to be incentive for these farmers to recieve a bonus
  • If we have cells in the bulk tank of less than 100,000/ml (not too bad) - will see fewer cases, but they will be more severe. Due to a level of innate immunity that has been triggered- If that pathogen does enter the teat cistern and ever slightly heighten the count, then these cases tend to be more severe. Inflammation process will be dramatic adn they will have a massive clinical infection of mastitis.
  • Individual cow percentage has improved as well (at any one time, 19% of cows will have a SCC of 200k/ml...10 yrs ago was about 30%)--> financial incentive 
  • farming is a margin business, it will have a massive impact 
  • There has been improvement in recent years for lowered cell count 


Mastitis, why bother?

  • Residues: if we do indeed try and treat the mastitis with AB's
  • There is also the potential loss of milk yield which would lead to a loss in quantity as well as potential milk which is a big concern in preventing mastitis 
  • about 100 gbp per case of mastitis (that is a big number!) - and this doesn't include prevention, teat dips, etc.


Clinical Entry of MAstitis

  • (picture) - teat canal has been popped out for long enough during milking, there has been keratosis of the teat canal.
  • Doesn't hurt as such but when the barrier has been reduced and slightly damaged (too long, too much pressure, Automatic Cluster Remover not set the right way, teat exposed to too much vacuum for too long) and that barrier has been reduced after exposure, it is therefore easier to cross for the pathogens
  • increases the chance for mastitis.
  • this is a milking parlor setting issue
  • stripping milk let down can help cows with the intensity of milking process and make it less traumatic
  • This picture can be a big indicator of farms not doing the job just


Clinical Mastitis

  • From the cistern into the other tissue and this is why the clinical changes occur
  • inflammary response
  • Clinical will always see changes in the milk - sometimes will see systemic as well


Grades of Clinical Mastitis 

  • Grade 1: only changes to the milk (clots in the milk, more serous, not as visible, milk won't curdle in cheese making tub), decreased yield at that time already. can use device (picture) to milk out clots of mastitis by placing on to milking tube, filter out the lage clots --> you need to pre-strip though! (farmer should know they have clincal mastitis prior)
  • Need to clean as well between each cow and maybe direct a treatment to prevent further spread
  • Grade 2 (acute): changes in the milk AND udder. quarter may be hanging lowered or ever slightly so red.
  • Grade 2 (chronic): as above, biggest loss in milk yield from persisitent changes and loss in functionality of alveoli. persistent changes don't always give you clinical mastitis (changes in the milk) but sometimes when it flares up 
  • grade 3: systemically sick cow- BAD. sloughing. demarcations. will likely need to be put down. If you let them be, the quarters will slough off (arteries will be exposed--> bleeding). Can find this in sheeps and goats as well, not always contagious, can be environmental.
  • we do have toxic mastitis by E.Coli that doesnt give this quarter changes, see more sickly cow than sloughing off quarter 


The Players of Acute/ Clinical Mastitis

  • S. agalactiae will give contagious mastitis, but its not always a clinical mastitis. Therefore, its only high cell content they will give --> so not really clinical. the rest definitely are
  • Mycoplasma mastitis is common in California. doesn't really grow on the plate, so we tend to miss it in our sampling. Will likely become more prevalent in the UK over time 


Sub-clinical Mastitis

  • these are completely off the radar
  • only can tell by using CMT or cell count test of the milk
  • only half of the cows in the UK are being tested for milk cell count
  • For sure we have reducced milk yield, and that might be the biggest cost for mastitis on milk farms 



  1. wipe teats clean first (avoid dirt falling into your wells)- any dirt in the wells will not make it positive (as it tests for SC's)
  2. pre-strip teats into bucket (or on the floor- not ideal): stagnant milk will have more cells formed at the bottom --> inaccurate results of test. Improve specificity of your test (avoid false positives).  
  3. Remember which quarter fed into which well! 
  4. look at wells: check for milk clots (yellowish). Reagent will add color and once you add that you cannot see the clots anymore - need to pick up clinical mastitis. If you don't pick this up, you are just as bad as the farmers who don't pre-strip
  5. add reagent (as much as milk there is in each well): soap is opening up the membranes and matching pairs of DNA from opened cells will link up and the viscocity of the liquid will be higher. thick --> positive
  • the bottom right would be over 1 million (tipping out), the others are normal and would be 100, 100, 100 . --> this cow would only have on average 300,000 cells/ml/cow.


In-line SCC

  • takes a cow sample rather than a quarter sample
  • bacteria produce ATP (like cells do) and our somatic cells elevation is related to the ATP elevation
  • basically measuring ATP in that sample
  • downside, we do need to have reagents (casettes), so it is relatively expensive to run 



  • NIR: Near Infra Red
  • NIR spectrum will bounce it to the milk and some of it will be reflected while some of it goes through the sample 
  • the refraction being reflected: will determine many many things
  • There is algarithms for cheese yield that you can use 
  • cheese yield will depend on the type of pathogen causing the mastitis - may be able to discover the type of pathogen this way by checking the cheese yield 


Players of Chronic/Sub-clinical Mastitis 

  • similar to the clinical
  • Corynebacterium bovis is found when we submit our cultures, but is considered a minor pathogen - not causing any clinical signs, not a very pathogenic bacterium. Good indicator that your post milking teat dip isn't working



  • need to take a history!
  • especially Cell Counts in the NMR records


Clinical Examination of Cow

  • check for kicking before you look at udder 
  • check for swollen quarters
  • kicking while palpating?
  • palpate lymph nodes



  • generally the treatment is based on a farm level rather than a cow level
  • one example: tetra-delta
  • based on farm level or cow- level 
  • there are a few different drivers for choice of tube 



  • a fluoroquinolone
  • not something you typically first use in mastitis cases
  • don't mistake as being best as it is high up on NOAH list, that is just becasue it starts with a "B" 


Intramammary Treatment 

  • we can give AB's systemically or in the mammary gland
  • tubes are generally intramammary, but consider systemic treatment as well 
  • downside of intramammary, be careful that you don't insert bacteria as you are treating!
  • don't mix lactation tubes with the dry tubes. the pharmacokinetics of both are completely different!
  • lactation duration is short and treated as directed
  • dry cows: only treated once and be there for 6-8 weeks total.
  • you are going to waste a lactating cow if you give it a dry cow tube during lactation 
  • costs becomes a player: mastitis medication is the biggest in sales for cow treatment


Other Treatment than Antimicrobials

  • Need to think about NSAIDs for pain relief
  • drain of the milk IS part of the treatment, oxtocin is useful (even 10x a day) - can help them get over mastitis if frequent enough, even if no AB's are given. when the udder is painful bc of mastitis, the cow is able to supress her milk let down and oxytocin will help us override that and get the milk out properly
  • Corticosteroids: slim evidence base for it, some tubes will contain corticosteroids (Prednisolone)- local treatment of that quarter with corticosteroids. can be good for cows with toxic mastitis - the cascade of inflammation can be the biggest damaging factor and not necessarily the pathogen 
  • Last 3 options are good for toxic mastitis: when they become hypoglycemic, can't get to trough anymore, dehydrated, hypocalcemic due to infection of pathogen



  • In terms of usage
  • Intramammary is not as big as in feed/water (which is usually dominated by pig and poultry industry)
  • There is pretty much an even split between dry cow tubes and lactating tubes
  • Farmers are getting more selective in the dry cow tube usage, cows are being selected whether they need AB's at dry off or not, or whether they can be dried off with just the Orbeseal - we want to reduce Antimicrobial use and use wisely!


Why Culturing?

  • very useful, we can get an antibiogram of these samples - can't tell off clinical presentation what this bug is going to be
  • select samples wisely! - $$$
  • about 10gbp a sample, 20 gbp a sample if you do PCR
  • sample recurrent cases or persistent cases, or rise in SCC (need for A. galactiae)
  • take a sample before you start treating, freeze and then treat the cow, see what response will be. by the time you get the result of that culture (3-4 days) you may have treated them before they get worse in that time (cow will be cured or killed, need to treat before knowing what pathogen it is)
  • Need to know AB resistance is on each particular farm as it is very farm specific!



  • Bulk tank sample for every farm available - can also use this sample for culture, quick summary of that herd
  • milk recording on about 50% of the cows
  • also can have pooled sample of one cow
  • Or individual quarter sample which can be preferable 
  • Don't contaminate sample with teat skin microflora or else get new sample - need to keep teat end sterile! (swab the teat ends until no dirt comes off)
  • remember to pre-strip!! 


Some issues with culturing

  • Downside is that about 40% of these cultures will return negative, S.aureus is difficult to culutre for example
  • If you have contaminated samples (more than 10%) you need to reassess your procedures
  • prolapsing teat ends are more prone to mastitis!
  • don't stick teat in the pot, you will culture teat floar not milk flora that way 
  • PCR is a bit less time sensitive, but it can still take a few days for it to be sampled 


  • likely grade 2 mastitis


  • Likely grade 3 mastitis


Electrical Conductivity

  • Will strip the milk and measure the resistance of that milk
  • If there is a cell count, the resistance will go down because there is more minerals
  • minerals will increase conductivity and you can then infer the cell count in these wells
  • Not completely full proof, but relatively cheap to run as it takes no reagent



  • Prevention will be different per farmer and different per bug
  • Need records in order to investigate the proper treatment



  • Good treatment to consider for cows with clinical mastitis