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VETM 423 Bacteriology > Bovine Mastitis Pathogens > Flashcards

Bovine Mastitis Pathogens Flashcards

(57 cards)

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1
Q

How are samples collected for diagnosing mastitis?

A
  • Swab the parenchyma of the udder
  • Take a udder parenchyma biopsy
  • Teat cistern swab
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2
Q

Compare environmental and contagious routes of infection of mastitis

A
  • 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
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3
Q

Compare the pathogens types that cause environmental and contagious mastitis pathogens

A

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)

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4
Q

Compare clinical and subclinical mastitis

A

Disease manifestation
* Clinical: abnormal milk +/- signs (swollen quraters/fever/systemic signs)
* Subclinical: normal milk but elevated SCC (>200,000 cell/ml) +/- bacteria

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5
Q

List the mastitis pathogens in ascending severity

A
  • E. coli (most severe)
  • Klebsiella
  • Strep uberis
  • Strep dysgalactiae
  • Stap aureus
  • Strep agalactiae
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6
Q

What is the main causative agent of subclinical mastitis?

A

o Mainly non- staph aureus staphylococci bacteria 950% = S. chromogenes)

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7
Q

What type of mastitis pathogen is S. agalactiae? What does it infect?

A

S. agalactiae
* Contagious – infect the cisterns and ducts of mammary gland

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8
Q

What are the clinical signs of S. agalactiae

A
  • Clinically: no signs but high SCC (> 1,000,000)
    o Can cause scarring/fibrosis of the quarter and reduce production
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9
Q

What type of mastitis pathogen is S. aureus? How does it compare to S. agalactiae?

A

S. aureus
* Contagious
* More difficult to eradicate vs S. agalactiae

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10
Q

What is the pathogenesis of S. aureus mastitis

A
  • 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
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11
Q

How is S. aureus treated? What evidence of it is there in milk?

A
  • Not high bacterial count in bulk milk
  • Tx: poorly treated by abx
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12
Q

Why might a mastitis culture be negative? 5 Reasons

A

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

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13
Q

What does Intra-mammary infection mean?

A
  • Intra-mammary infection: can be caused by inflammation/mastitis
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14
Q

What are the clinical signs of mycoplasma mastitis

A
  • 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)
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15
Q

What is the causative agent of clinical mycoplasma mastitis? How are they transmitted?

A

Mycoplasma bovis

contagious

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16
Q

What animals are mainly affected by mycoplasma mastitis?

A
  • Target: cows in any stage of production cycle
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17
Q

What type of pathogen iis Klebsiella? Where is it found? What kind of mastitis does it cause?

A

Klebsiella
* Environmental – ubiquitous
o Causes opportunistic infections
* Mainly subclinical mastitis

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18
Q

What are risk factors for klebsiella infection

A
  • 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
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19
Q

Explain why it is important to identify the pathogen causing mastitis. How does it influence prognosis/treatment?

A
  • 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
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20
Q

When are mastitis infections most common? Why

A

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
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21
Q

List 5 common pathogens causing foot root

A
  • Fusobacterium
  • Dichelobacter
  • Bacteroides
  • Prevotella
  • Porphyromonas
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22
Q

What are 3 tests used to diagnose mastitis

A
  • California mastitis test
  • Delaval direct cell counter
  • On-farm culture
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23
Q

List 3 contraindications for antibiotic trreatment for mastitis

Study These Flashcards
A
  • No abx if…
    o E. coli mastitis
    o Chronic clinical or recurrent mastits
    o Subclinical mastitis in lactation
  • Use C/S
24
Q

Where is fusobacterium necrophorum located? What is the route of infection? What are the pathogen characteristics?

Study These Flashcards
A
  • Located: mouth/GI commensal = f. necrophorum
    o Endogenous route of infection
  • Obligate symbiotic facultative pathogen
25
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
26
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
27
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
28
How is fusobacterium necrophorum diagnosed
* Diagnosis o See gram (-) fusiform rods o Post mortem/slaughter = liver abscesses
29
What type of pathogen is Dichelobacter nodosus? What disease does it cause?
Dichelobacter nodosus * Obligate pathogens * Disease: infectious interdigital dermatitis
30
What animals does Dichelobacter nodosus target
* Target: sheep mainly o Economically significant
31
What are risk factors for Dichelobacter nodosus
* Risk factor o Poorly maintained hooves o Warm/wet environment
32
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
33
What is the virulence factor of Dichelobacter nodosus
* Virulence: extracellular protease
34
How is Dichelobacter nodosus diagnosed
* Diagnose: clinical and gross lesions o Interdigital areas = moist/red/invasion of horny tissue o Require culture to confirm
35
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
36
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
37
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
38
list 2 main bacteroides?
o Prevotella melaninogenica o Bacteroides fragilis
39
What is the main clinical outcome of bacteroides infection
o Purulent necrotizing infection/abscess
40
List 5 alternate names for digital dermatitis
* Aka. slurry heel/hairy eel warts/strawberries/mortellaro’s disease
41
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
42
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
43
How is digital dermatitis treated?
* Treat o Individual: systemic or topical abx or other topic treatment o Group: either abx or non-abx treatment
44
How is digital dermatitis prevented
o Footbaths (formalin/copper sulfate/peroxide/peracetic acid/Zn sulfate)
45
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
46
List 2 notable features about Bacillus anthracis
* Reportable * Zoonotic
47
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
48
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
49
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
50
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
51
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
52
How to diagnose Bacillus anthracis?
o Identify bacteria in peripheral blood smear (bacilli in chains with pink stained capsules) o Confirm via culture/PCR
53
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
54
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
55
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
56
What are the pathogenesis of Anaplasmosis?
* Pathogenesis o Extravascular destruction in liver and spleen
57
How is Anaplasmosis diagnosed?
o Cytology with Giemsa stain: see bacteria in RBC

VETM 423 Bacteriology (18 decks)

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