White blood cells, or somatic cells, are the body’s natural defence mechanism, key players in the immune system. Lacy-Hulbert said there were three somatic cell types that came into play to fight bacteria in the udder – macrophages, polymorphonuclear leukocytes or neutrophils, and lymphocytes.
Macrophages – the reconnaissance troops in Lacy-Hulbert’s army – are always present in the udder at low levels. When the somatic cell count (SCC) is sitting at about 20,000-40,000 cells/ml, it is the macrophages making up most of this number.
“These are the rubbish collectors of the udder, picking up bacteria as well as bits of old cells, and fat or casein structures that haven’t made it out of the udder.”
Lacy-Hulbert described the neutrophils as the foot soldiers of the somatic cell army.
“When bacteria do get to levels that start to wake up the immune system, and swamp the macrophages, the foot soldiers come in. They are the ones that really pile in and create those high numbers of somatic cells.”
These neutrophils are the key defenders and directly attack any bugs that trigger the response, gobbling them up in a process called phagocytosis.
Marshalling from the rear are the lymphocytes, the officers directing operations. As with macrophages, they are always present at low levels but multiply when the foot soldiers – the neutrophils – gather at the site of the infection.
“These lymphocytes cannot deal directly with the bacteria, but they can release other things that can kill bacteria.”
There are three main types of lymphocytes – T cells, B cells, and natural killer cells. T cells can summon macrophages, and release cytokines – messenger molecules that move around the body summoning the foot soldiers, the neutrophils, within an hour of recognition of infection. B cells are the antibody factories in the body and can also release cytokines. Natural killer cells also release cytokines, typically kicking in about three days post-infection.
“So between the somatic cells and the bacteria there is a bit of a battle going on. The bacteria want to grow in the milk and establish a nice, warm, cosy home, and it is the somatic cells’ job to prevent that from happening. When we see a clinical case of mastitis, we are really seeing the tip of that iceberg – it’s all been going on below it.”
Lacy-Hulbert said the iceberg theory could also be applied when thinking about clinical and subclinical mastitis in the herd.
“There might be 10% of cows that are affected by clinical mastitis during a lactation, but there could be 30-40% of the herd that will develop subclinical mastitis, indicated by raised cell counts.”
Industry best guesses put average clinical mastitis incidence within a herd at about 10%, though Lacy-Hulbert said it was difficult to get accurate figures.
“I think that once people actually start looking at it and measuring it, they find it may be nearer to 15%.”
Environmental versus contagious
Mastitis is not simply one organism making its presence felt in the udder – it could be the result of infection from any one of several different pathogens. Although all of the pathogens originate outside the cow, Lacy-Hulbert separates them into two main types – environmental and contagious.
Environmental mastitis, unsurprisingly, relates to organisms that survive in the cow’s surroundings (eg feedpads, soil, manure, water) but have special characteristics that allow them to thrive in the udder. Infection is opportunistic with the bacteria cashing in on some set of circumstance that makes the udder more accessible or susceptible.
Contagious mastitis is the spread of bugs from cow to cow, usually during milking. These bacteria usually live on or around the teat’s skin, drawn by the presence of lipids in the milk.
Approaches to treatment
Lacy-Hulbert said using antibiotics to treat clinical mastitis infections was simply giving the cow a boost.
“At the end of the day the cow has to get rid of the infection herself. So, where necessary and where we think it will work, we are trying to tip the battle in favour of the cow.”
Given the variety of pathogens involved, and the different factors that contribute to their risk of infection, treatment is not always straightforward.
“You can expect 70-80% of clinical cases to clear up with treatment. But you are still going to get a population of 20-25% that may not clear up. You should work through those on an individual basis with your vet.”
Taking sterile milk samples before treating cows and freezing the samples for later analysis if required – if the infection will not clear up – can be a good idea to help identify the pathogen involved.
The potential spread of contagious mastitis can be minimised though good milking hygiene, maintaining healthy teat ends, and ensuring the milking plant is operating well with the correct vacuum. Regular teat spraying with good coverage will also contribute.
With environmental mastitis infections, calving is a particularly risky time with the udder highly susceptible to infection and the cows’ immune system naturally depressed. Calving cows on dry, mud- and manure-free areas will minimise some of that risk. All bedding materials will have high pathogen counts once contaminated with manure.
For more information, go to dairynz.co.nz/mastitis.
Streptococcus uberis
Strep uberis is an environmental pathogen, with manure the key culprit or source. Live bacteria have been detected in the gut of a relatively small proportion of cows in a herd – 5-10% – and these may be the main offenders, responsible for shedding large numbers of the pathogen in their manure.
Strep uberis most frequently gets into the udder during calving, early lactation, and in the first two weeks after drying off, especially if there is teat end damage or udder oedema (fluid retention). Clinical symptoms run the gamut, from slightly abnormal milk to severe swelling of the udder.
Most infections by respond well to early treatment and are short-lived, but up to 10% may become longer-lasting and possibly chronic. The median length of subclinical infections sits at about 16 days but a cow could be infected with different strains of the pathogen within the same lactation, so may appear to be infected for a longer period of time.
Strep uberis infections can cause very high rises in SCC, with individual cows potentially rocketing up to 10,000,000 cells/ml or more, which can cause a spike in bulk SCC.
Escherichia coli
E coli is another bacteria that is widespread in the gut, and therefore in a cow’s environment. Clinical mastitis cases are rare in NZ though, but there is higher risk of infection associated for cows that are housed or spend time on feeding or calving pads, as well as cows on a high starch diet.
E coli bacteria can cause a severe form of mastitis, involving a sudden onset of toxaemia – in layman’s terms, blood poisoning – with the cow showing symptoms like a high temperature initially before plummeting, lying down (recumbent), and eventually, death.
With E coli it is not the bacteria itself that damages the udder tissue but the toxins, and the degree of inflammation released by the cow, that that can cause long-term problems.
Somatic cell count will rise quickly after infection – though not to Strep levels – and will persist for about two weeks.
Staphylococcus aureus
Staph aureus takes no prisoners, living on the surface of teat skin. All lactating cows are susceptible to the contagious pathogen and infections usually become chronic (persistent). Infection risk is increased if teat end damage is present or if teats are poorly disinfected post-milking. Faulty milking plant can also make infection more likely.
Staph aureus symptoms range from minor changes in the milk through to severe illness. Bacteria can be shed from clinical and subclinical quarters, transferred from cow to cow via contaminated milk on liners or hands. Preventing infection is critical as Staph aureus is hard to cure during lactation, with dry cow antibiotics the most effective treatment.
Somatic cell counts will vary over lactation post-infection, ranging from 200,000 cells/ml to more than 1,000,000 cells/ml, though are generally of a lower magnitude than those found in Strep infections and will rarely impact on bulk SCC.
Streptococcus agalactiae
Another contagious type of infection, Strep agalactiae, colonises teat canals and is particularly prominent in first-calving heifers though all lactating cows are susceptible. Hard, swollen quarters are the main symptom of a clinical infection with even subclinical quarters having a high SCC.
As with Staph aureus, SCC fluctuates from 200,000 cells/ml to in excess of 1,000,000 cells/ml and the high number of bacteria shed by infected cows mean bulk SCC may lift.
Strep agalactiae is very sensitive to penicillin so treatment has a relatively high cure rate. Because of this, it is rarely seen in NZ now.
‘Black’ mastitis
Though black mastitis has traditionally been associated with severe infections of Staph aureus, Lacy-Hulbert said that was not necessarily the case.
“You can get cases of black mastitis occurring with environmental bacteria – it’s a bit of an unanswered question as to what the underlying cause can be.”
It could be a particularly virulent strain that has flown under the radar of the cow’s immune system.
“I think you get a bit of a perfect storm come together, and we’re not quite sure of the factors that do come together to make it happen.”
“It is a situation where the inflammation has gotten so out of hand that the blood supply has been affected, and that means part of the udder – big or small – tends to go gangrenous. The blood supply slows down and it stops working properly.”
