Bovine Mastitis Pathogens Flashcards
How are samples collected for diagnosing mastitis?
- Swab the parenchyma of the udder
- Take a udder parenchyma biopsy
- Teat cistern swab
Compare environmental and contagious routes of infection of mastitis
- Contagious pathogens
o Milking equipment/hands of the milker/contaminated cloths
o Colonize teat end
o Mycoplasma can spread systemically to the udder - Environmental
o Contamination of the teat canal from manure/bedding/soil/plant/water
Compare the pathogens types that cause environmental and contagious mastitis pathogens
contagious
Strep. Agalactiae
Strep dysgalactiae
Staph aureus (coagulase positive)
Coagulase negative staphylococci
enviro
Strep uberis (other strep spp.)
Coagulase negative staphylococci
Truperella pyogenes
Coliform bacteria: E. coli/Klebsiella/Enterobacter)
Compare clinical and subclinical mastitis
Disease manifestation
* Clinical: abnormal milk +/- signs (swollen quraters/fever/systemic signs)
* Subclinical: normal milk but elevated SCC (>200,000 cell/ml) +/- bacteria
List the mastitis pathogens in ascending severity
- E. coli (most severe)
- Klebsiella
- Strep uberis
- Strep dysgalactiae
- Stap aureus
- Strep agalactiae
What is the main causative agent of subclinical mastitis?
o Mainly non- staph aureus staphylococci bacteria 950% = S. chromogenes)
What type of mastitis pathogen is S. agalactiae? What does it infect?
S. agalactiae
* Contagious – infect the cisterns and ducts of mammary gland
What are the clinical signs of S. agalactiae
- Clinically: no signs but high SCC (> 1,000,000)
o Can cause scarring/fibrosis of the quarter and reduce production
What type of mastitis pathogen is S. aureus? How does it compare to S. agalactiae?
S. aureus
* Contagious
* More difficult to eradicate vs S. agalactiae
What is the pathogenesis of S. aureus mastitis
- Pathogenesis
o Colonize teat skin lesions/teat canal
o Bacteria damage the duct system
o Form deep pockets of infection = abscess formatioin
o Bacteria walled off by fibrosis
o Early stages = minimal damage/reversible
o Later stages = abscesses/irreversible
How is S. aureus treated? What evidence of it is there in milk?
- Not high bacterial count in bulk milk
- Tx: poorly treated by abx
Why might a mastitis culture be negative? 5 Reasons
Culture negative
* Anaerobic bacteria
* Fastidious bacteria (mycoplasma)
* Improper transport
* Low amounts of bacteria in the sample (E. coli – by th time clinical signs appear the infection of almost over)
* Abx tx before sampling
What does Intra-mammary infection mean?
- Intra-mammary infection: can be caused by inflammation/mastitis
What are the clinical signs of mycoplasma mastitis
- Clinical mycoplasma mastitis
o Abnormal secretions with tan/brown discolouration
o Sandy/flaky sediment in watery/serous fluid
o Loss of production from affected quarters
o Severe mastitis in affected quarters
o Can spread between quarters on the same side (then move to other side)
What is the causative agent of clinical mycoplasma mastitis? How are they transmitted?
Mycoplasma bovis
contagious
What animals are mainly affected by mycoplasma mastitis?
- Target: cows in any stage of production cycle
What type of pathogen iis Klebsiella? Where is it found? What kind of mastitis does it cause?
Klebsiella
* Environmental – ubiquitous
o Causes opportunistic infections
* Mainly subclinical mastitis
What are risk factors for klebsiella infection
- Risk
o Influenced by management practices
o more common in free stall vs tie stall
o sawdust/wood shavings bedding are more susceptible
low moisture/inorganic (sand/limestone) is better
Straw: low coliforms but higher streptococci
Explain why it is important to identify the pathogen causing mastitis. How does it influence prognosis/treatment?
- Strep. Agalactiae: obligate pathogen = can eradicate (abx)
- Staph. Aureus: chronic infection that persist in lactation (reduce the number of infected cows)
- Mycoplasma: no treatment
o Control disease by identifying infected animals and culling
When are mastitis infections most common? Why
At the beginning of the dry period and at the beginning of lactation
- moving to new location
- not being milked (more pressure on the mammary glands and less disinfection of the glands)
- immunosuppression
- negative energy balance
List 5 common pathogens causing foot root
- Fusobacterium
- Dichelobacter
- Bacteroides
- Prevotella
- Porphyromonas
What are 3 tests used to diagnose mastitis
- California mastitis test
- Delaval direct cell counter
- On-farm culture
List 3 contraindications for antibiotic trreatment for mastitis
- No abx if…
o E. coli mastitis
o Chronic clinical or recurrent mastits
o Subclinical mastitis in lactation - Use C/S
Where is fusobacterium necrophorum located? What is the route of infection? What are the pathogen characteristics?
- Located: mouth/GI commensal = f. necrophorum
o Endogenous route of infection - Obligate symbiotic facultative pathogen
List the lesions caused by fusobacterium necrophorum
- Lesions:
o Abscess/necrosis in local infection
o Necrotic stomatitis/metritis/mastitis
o Bovine foot rot
o Liver abscess
What is the pathogenesis of foot rot caused by fusobacterium necrophorum
- Cause foot rot when combined with Dichelobacter nodosus
- Pathogenesis
o Trauma/microtrauma to the foot
o Bacteria enter
o Necrosis and vascular damage by exotoxins
Leukotoxin – cause local tissue damage and immune cell damage
Protease
Hemolysin
o Edema/fluid loss
o Spread to tendon sheath/tendon/ligament/joints
o Septicemia spread to organs
What is the pathogenesis of liver abscess caused by fusobacterium necrophorum
o Grain overload
o Acidosis/poor rumen motility
o Ruminal wall damage
o Infection in rumen wall
o Enter portal circulation
o Spread to liver and cause abscess/septic thrombi
Proteases and dermonecrotic toxins contribute to damage
How is fusobacterium necrophorum diagnosed
- Diagnosis
o See gram (-) fusiform rods
o Post mortem/slaughter = liver abscesses
What type of pathogen is Dichelobacter nodosus? What disease does it cause?
Dichelobacter nodosus
* Obligate pathogens
* Disease: infectious interdigital dermatitis
What animals does Dichelobacter nodosus target
- Target: sheep mainly
o Economically significant
What are risk factors for Dichelobacter nodosus
- Risk factor
o Poorly maintained hooves
o Warm/wet environment
What are the clinical signs f Dichelobacter nodosus
- Clinically: develop after 28d oof infection
o Recumbency
o Unable to feed/weight loss
o Reduced milk production
What is the virulence factor of Dichelobacter nodosus
- Virulence: extracellular protease
How is Dichelobacter nodosus diagnosed
- Diagnose: clinical and gross lesions
o Interdigital areas = moist/red/invasion of horny tissue
o Require culture to confirm
How is Dichelobacter nodosus prevented
- Prevent
o Don’t buy sheep from infected herds
o Transport in clean vehicles
o Quarantine
o Regular hoof trimming
o Zn sulfate and Cu sulfate and detergent use
What kind of bacteria is Bacteroides? What kind of pathogen is it? Where is it found?
Bacteroides
* Gram (-) rod, obligate anaerobe (no spores)
* Obligate symbiotic facultative bacteria in GI
What disease does bacteroides cause?
- Bacteroides genus commonly causes many infections
o Soft tissue/periodontal/lung/liver abscess
o Cellulitis/peritonitis/pyometritis/osteomyelitis/mastitis
o Watery non-hemorrhagic d+ in livestock and children
list 2 main bacteroides?
o Prevotella melaninogenica
o Bacteroides fragilis
What is the main clinical outcome of bacteroides infection
o Purulent necrotizing infection/abscess
List 5 alternate names for digital dermatitis
- Aka. slurry heel/hairy eel warts/strawberries/mortellaro’s disease
List the lesion stages of digital dermatitis
- Lesion Stages
1. M0: Healthy
2. M1; < 2 cm
3. M2: > 2 cm
a. Treatable stage
4. M3: healing after tx
5. M4: chronic proliferation
a. M4.1: chronic proliferation and <2cm lesions (M4 + M1) - Reactive epidermal proliferation
What is digital dermatitis caused by?
- Caused by bacteria (because it spreads rapidly/microscopic investigation of the lesion/response to abx)
- Polymicrobial disease:
o Commonly have spirochete bacteria (Treponema spp.) in lower layer of dermis
How is digital dermatitis treated?
- Treat
o Individual: systemic or topical abx or other topic treatment
o Group: either abx or non-abx treatment
How is digital dermatitis prevented
o Footbaths (formalin/copper sulfate/peroxide/peracetic acid/Zn sulfate)
What is the causative agent for anthrax? What are the characteristics of the bacteria? What do they look like?
Anthrax
* Agent: Bacillus anthracis
- Gram (+) rod
o Bamboo like appearance
o Form spores (in high CO2 environment – no spores in un-opened carcass)
o Obligate pathogen
o Exotoxigenic bacteria
List 2 notable features about Bacillus anthracis
- Reportable
- Zoonotic
What is the virulence factor for Bacillus anthracis
- Virulence factors
o capsule made of polyglutaminic acid = aantiphagocytic
o tripartite anthrax toxin (3 subunits)
PA: protective antigen = cell binding protein that ddelivers the LF and EF into host cells
LF: lethal factors = enzyme that inhibits kinase = cell death
EF: edema factor = enzyme that increases cAMP and impairs homeostasis in cells = edemaa
Cause necrosis/oxygen depletion/shock/organ failure/death
List 3 clinical forms of Bacillus anthracis? What is a common consequence
- Clinical forms
o Cutaneous anthrax
o Intestinal anthrax
o Inhalation anthrax
o All can cause septicemia
Compare anthrax manifestation in ruminants/horses and cat/dogs/pigs
- Species
o Ruminant/horse: acute septicemia due to GI exposure to spores
o Cat/dog/pig: chronic disease in throat/intestine
What is the pathogenesis of Bacillus anthracis?
- Pathogenesis
o Germination in enterocytes
o Local edema and necrosis
o Phagocytosis and germination of spores
o Movement to regional LN
o Hemorrhagic lymphadenitis
o Bacteremia and toxemia
o Death
How to prevent Bacillus anthracis?
- Prevention
o Don’t open carcasses
Allows vegetative cells to sporulate
Environmental contamination
o Do not bury carcasses – spores will rise to the surface (they are buoyant and earthworms will carry them
How to diagnose Bacillus anthracis?
o Identify bacteria in peripheral blood smear (bacilli in chains with pink stained capsules)
o Confirm via culture/PCR
What is the causative agent for Anaplasmosis? What are the bacterial features? Where is it found?
- Agent: anaplasma marginale
o Obligate intraRBC
o Located: tropical/subtropic
o Economically significant
What are the clinical signs of Anaplasmosis?
- Clinically
o Progressive anemia (low RBC/PCV/Hgb) = thin/watery blood
o Icterus
o Peracute = acute death
o Low milk production
o Inappetence
o Ataxia
o Breathlessness
o Bounding pulse
What are the gross lesions of Anaplasmosis?
o Spleen: enlarged and soft/prominent follicles
o Liver: mottles/orange
o Gallbladder: distended/thick brown/green bile
What are the pathogenesis of Anaplasmosis?
- Pathogenesis
o Extravascular destruction in liver and spleen
How is Anaplasmosis diagnosed?
o Cytology with Giemsa stain: see bacteria in RBC
