Severe (Toxic) mastitis in cattle Flashcards
Classification of clinical mastitis - Toxic
- cow often recumbent and very sick, may occur before changes to milk
- high(er) likelihood of gram-negative aetiology (than mild/grade 1)
Recognition of severe clinical mastitis
- Systemically unwell
- Not eating
- Dull and may not present to the parlour
- Recumbent
You will hear many producers & vets refer to these “toxic” clinical mastitis events as “E. coli” mastitis, but coliform infections mostly cause MILD disease
Ddx
Toxic
- acute toxic mastitis
- metritis
- diffuse peritonitis
Metabolic
- hypocalcaemia
– not as depressed or dehydrated as with toxic mastitis
– will have dry mm, hard faeces and won’t have passed faeces (smooth muscle shuts down before the skeletal muscle)
– may have swan neck position
– cow may keep trying to stand up
- hypophosphataemia
MSK
- fractures (e.g. pelvis, femur)
- dislocations (e.g. hip, sacroiliac)
Nervous
- condition affecting the peripheral nervous system (e.g. obturator nerve paralysis)
Following a dystocia event
- usually bright (unless in severe pain or have concurrent disease)
- unable to stand or may try to stand and fail
- often have increased heart and respiratory rates (due to pain) but few other obvious clinical signs
- diagnosis often from history +/- signs of a difficult calving (e.g., bruising of vulva)
CE for down cow
- demeanour: bruxism, attempts to rise?
- vital signs: rectal temp
- hydration status: eyelid skin tend time
- presence of dung behind the cow?
- evidence of a difficult calving?
- always examine the udder
Prognosis
- ~50%
- poorer prognosis associated with higher PCV, longer eyelid skin tent time, lower rectal temperature
Pathogenesis
- Gram-negative infection
- Lipopolysaccharides (endotoxin)
– Release of “LPS”
-> Release of pro-inflammatory eicosanoids
…e.g., TNF-α and IL-1
…induce pyrexia
…acute phase response - Phospholipase enzyme A2
– Produces arachidonic acid
-> COX converts arachidonic acid into eicosanoids including prostaglandins and thromboxanes,
…act as inflammatory mediators - Endotoxin acting on vasculature,
- Hyperaemia, haemorrhage and oedema of udder tissue,
- Severity of disease related to speed of immune response (influx of neutrophils)
- Negative Energy Balance (NEB) in high yielding, periparturient cows very important
– study showed “the phagocytic and bactericidal capacities of neutrophils are reduced when these cells are acting in the presence of high concentrations of ketone bodies” - Low SCC during udder inflammation-free state are associated with increased risk of clinical mastitis
– These cows are not already infected with a major pathogen – therefore they are susceptible to opportunistic Gram-negative infection - Administering antibiotic dry cow therapy in LOW cell count cows at drying-off appears to increase the risk of coliform mastitis in the next lactation
– low SCC cows getting dry cow therapy -> dysbiosis caused within the udder
Severe clinical mastitis events in cows
This is NOT a common presentation of clinical mastitis for many herds
- <1% of all clinical mastitis events detected?
- in low yielding, higher cell count herds
but in SOME herds, the incidence rate of severe (“toxic”) mastitis events can be relatively high
- >5-10% of all clinical mastitis events detected?
- in HIGH yielding, LOW cell count herds
- but not all the time and it is not inevitable
Tx
- NSAIDs
- Fluid therapy
- Supportive therapy
- Good nursing care
- Antibiotics?
NSAIDs
- Most important part of the tx plan in these cases
- Inhibit cyclo-oxyenase (“COX”) enzyme
– inhibit the formation of prostaglandins and thromboxanes from arachidonic acid - Anti-inflammatory
- Anti-pyretic
- Analgesic
- Administer I/V or I/M
- SC not going to be effective - dehydrated, hypovolaemic, crashing animals - will be very poorly absorbed this way
Fluid therapy
- IV
– but remains unproven in field cases - choice of fluids is between hypertonic and isotonic saline
– generally hypertonic is easier in the field
-> rapid (within 10 mins)
-> raises bp (increases ventricular preload)
– need a drip for isotonic - water available for the cow to drink
- beware giving fluids orally in these cows
– Poor circulation
– Cow in shock
– very poorly absorbed from rumen
Supportive therapy
- Oxytocin (“Oxytocin-S”, MSD)
– Licensed to aid mastitis treatment
– 20iu (2ml) to 80iu (8ml) I/M to facilitate “stripping out” of the udder
– i.e. increases milk let down - Calcium IV
– Inappetant cow
– Concurrent milk fever
Good nursing care
- Loose yard “hospital”
- Access to water and feed
- Regularly checked
- Discuss and follow progress with client
- Regularly turn when recumbent
- If ongoing for a couple of days, euthanasia on welfare grounds is often necessary
Role of antibiotics in these cases
- controversial
- Are these cows bacteraemic?
– These cows are generally not bacteraemic, therefore antibiotic administered is not to improve chance of cure but instead to reduce risk of secondary infection due to compromise of gut barrier - What is causing the clinical signs – endotoxaemia or bacteraemia?
– Toxaemia - Are we expecting to remove coliforms from the udder?
– Probably not as likely to be long gone by this point - Are we administering antibiotic to cover for potential secondary infection in a very sick cow?
– Provide covering systemic antibiotic (for secondary infection)
-> Broad spectrum, Category “D”
–> oxytetracycline IV (e.g., “Engemycin 10% DD”)
–> sulphonamides IV (e.g., “Norodine 24”) - Category B (FQ’s) required?
– NO robust evidence that treatment with FQ & NSAID improves outcome compared with NSAID alone
Prevention
- environment management
- immune function support
Prevention - environmental management
- Reduce environmental infection pressure
– Reduce risk of opportunistic infection
– Transition period (pre-calving) (e.g. high stocking density)
– At calving
– Immediately post-calving
Example: reduce pathogen load, reduce pathogen survival = improve bedding management
