Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

VETM 423 Bacteriology > Bovine Pathogens > Flashcards

Bovine Pathogens Flashcards

(58 cards)

Start Studying
1
Q

What are the bacterial features of Clostridia bacteria

A
  • Gram (+) obligate anaerobe
  • Spore forming
  • Exotoxin forming
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List 12 common ruminant bacterial diseases

A
  • Clostridium
    o Malignant edema
    o Braxy
    o Black disease
    o Black leg
  • Wooden tongue
  • Johns disease
  • Mastitis
  • Foot rot
  • Digital dermatitis
  • Anthrax
  • Q-fever
  • anaplasmosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the hallmark feature of histotoxic Clostridia

A
  • Hallmark = enthusiastic toxogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List 4 types of Clostridia, their associated toxin and what disease they cause

A

o C. perfringens type A = alpha and theta toxin
 myonecrosis

o C. septicum = alpha
 Abomasitis

o C. chauvoei = alpha and beta
 Black leg

o C. novyi (novyi type d is same as haemolyticum) = alpha and beta toxin = infectious necrotic hepatitis/bacillary hemoglobinuria /Gas gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

6 common ‘themes’ of clostridia infection

A

o Acquisition from environment
o Entry after trauma/ingestion
o Local multiplication
o Toxin production
o Tissue damage
o Rapid death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

List the toxins associated with C. septicum

A

 Alpha = hemolysin
* Most important
 Beta = leucocidin
 Gamma = hyaluronidase
 Delta = hemolysin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is C. septicum found and how does it infect animals

A

o Located: soil and GI (ingested)
o Transmit: contamination of wounds with soil/feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 2 different clinical manifestation of C. septicum

A

 malignant edema
 Braxy – lambs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the main lesions of malignant edema? How does it spread?

A

C. septicum
myonecrosis due to toxigenesis
* Hemorrhage/edema/necrosis
* Spread rapidly through muscle
* Death in 24h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does braxy spread? What are the lesions? What causes it?

A

C. septicum
* Bacteria get into lining of abomasum and cause abomasitis
o Hemorrrhagic/necotic/fatal bacteremia
o Enter via hardware dz or eating frozen food (damge mucosa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the main clinical signs of C. septicum

A

 41-42C fever
 Depression/weakness/muscle tremor/lame
 Soft doughy swelling/erythema around infection site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the main lesions of C. septicum

A

 Gangrene
 Malodorous
 Exudate in SC/IM
 Serosanguinous fluid in body cavities
 Dark red muscle (no gas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How to differentiate C. septicum from blackleg

A

o VS blackleg
 Horse and pig can get malignant edema – not blackleg
 Confirm with fluorescent Ig stain
 Require lab testing to differentiate
 If >24 after death – samples unreliable (post mortem artifact)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

List 4 histotoxic Clostridium

A

o C. septicum
o C. novyi
o C. perfringens
o C. chauvoei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List the 2 types of toxin of C. novyi? What do they do

A

o Toxins: alpha and beta (expressed differentially in each type)
 Alpha = affect cytoskeleton by binding host regulatory proteins

 Beta = phospholipase with lethal necrotizing and hemolytic activities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What disease is caused by C. novyi type A? What are the hallmark lesions?

A

o Type A
 Gas gangrene aand wound infection
 Lesions
* Hallmark = edema (bighead - young ram)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What disease is caused by C. novyi type B? What animals are affected? What are the lesions?

A

o Type B
 Necrotic hepatitis/black’s disease

 Sheep and cow

 Acute death after alpha toxin dissemination
 Lesions
* Cardio/neuro/histo/hepatotoxic effects
* Darkening (black) skin and liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the pathogenesis of C. novyi type B?

A

 Associated with liver fluke associated damage in liver (focal hepatic necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What disease is caused by C. novyi type D? What animals are affected? What are the lesions?

A

o Type D (aka C. haemolyticum)
 Bacillary hemoglobinuria aka redwater disease

 Similar to type B
* But more beta toxin

 Signalment: well nourished animals >1yo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the pathogenesis of C. novyi type D?

A

 Path:
* Ingest > deposition of typ D spores in GI/liver
* Immature flukes migrate in liver = liver necrosis
* Germination of spored in kuppfer cells
* Beta toxin causes hepatic necrosis and dissemination through bloodstream = intrraavascular hemolysis and hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the clinical signs of C. novyi type D?

A

 Clinically
* Fever
* Icterus/pale MM
* Anorexia
* Abd pain
* Hemoglobinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What disease is caused by C. chauvoei? What are the 4 associated toxins

A
  • C. chauvoei
    o Causes black leg

o Toxins
 Alpha = leucocidin
 Gamma = hyaluronidase
 Delta = hemolysin
 Neuraminidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the pathogenesis of C. chauvoei?

A

o Pathogenesis
 Entr via ingestion
 Located in intestines of cattle and sheep
 Enter bloodstream and travel to organs
 Stay dormant until injury
* Tissue hypoxia triggers germination of bacterial cells/toxin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the lesions associated with C. chauvoei?

Study These Flashcards
A

o Lesion: necrotizing emphysematous myositis (gas in muscle)
 Primarily affect hind end muscle/myocardium/tongue/diaphragm
 Stinky

25
What is the typical signalment of animals affected by C. chauvoei?
o Signalment: well fed animals >3yo  Grass fed > stall fed animals (more exposure in environmental soil)
26
What are the clinical signs of C. chauvoei?
o Clinically  41C fever  Depression/anorexia  Dry/cracked skin  Lameness  Crepitus on hips and shoulders  Sudden death = common
27
What are the lesions of C. chauvoei?
 Laying on side with legs sticking out  Bloating  Dark red-black muscle  Bubbly muscle
28
How is C. chauvoei diagnosed?
o Dx: tissue sample (cardiac or skeletal muscle) and fluorescent antibody teest or IHC
29
What are 4 ddx for black leg
o Ddx:  Other clostridial infection (bacillary haemoglobinuria)  Anthrax  Poisoning  Lactation tetany
30
How is black leg prevented
 Vaccine – blackleg bacterin = effective  Antibiotic not effective
31
What does the Clostridium vaccine protect against
* Clostridial vaccine = 7 way o C. chauvoei o C. septicum o C. sordelli o C. novyi o C. perfrinigens (3 types)
32
List 3 GI bacteria that affect calves
Digestive System Calf * E. coli * Salmonella * C. perfringens
33
List 4 GI bacteria that affect adults
Adult * Actinbacillus ligneresii * Actinomyces bovis * Salmonella * Mycobacterium avium paratuberculosis
34
How to differentiate Actinobacillus ligneresii and Actinomyces bovis
* Actinobacillus ligneresii o Gram (-) soft tissue inf can treat more effectively * Actinomyces bovis o Gram (+) bone inf can't fix (b/c bone involvement)
35
What are the clinical signs of Actinobacillus ligneresii
o Clinically  granuloma formation in tongue = dysphagia  Weight loss  Soft tissue infection in head/neck/skin/LN/heart/stomach/liver
36
What are the risk factors for Actinobacillus ligneresii? Where is the bacteria found
o Commensal of oropharynx/rumen o Risk: trauma predisposes
37
What are the lesions of Actinobacillus ligneresii?
o Lesions  granulomas contain odorless pus  Granulomatous lesions
38
How to diagnose and treat Actinobacillus ligneresii?
o Diagnose  Biopsy or exudate  Gram stain * club-like granules with H and E stain o Tx: surgery/iodide/abx
39
Where is Actinomyces bovis found
o Commensal of oropharynx/rumen  Enter via wounds in oral mucosa
40
How to diagnose Actinomyces bovis?
o Diagnose  Sulfur granules on H and E stain
41
What are the lesions of Actinomyces bovis?
o Lesions  Pyogranulomatous infection and proliferation of connective tissue  Can impact bone (periostitis)
42
What are the bacterial features of Coxiella burnetii? What disease does it cause?
Coxiella burnetii = Q fever * Gram (-) * Obligate intracellular (difficult to grow – use serology) * Resistant to low pH * 2 forms: small variant (spore-like, transmitted) and large variant (cause disease)
43
What are the clinical signs of Coxiella burnetii? What is an important consideration?
* Clinically o Ruminants: abortion  Lots of bacteria in the abortion fluid/tissue/vaginal discharge = can dry out and become aerosolized * Humans = zoonotic o Endocarditis
44
How is Coxiella burnetii transmitted?
* Transmit: inhaled (+/- ticks or ingestion) o Very low infectious dose o Excrete in milk/feces/abortus/vaginal discharge
45
What is the pathogenesis of Coxiella burnetii?
* Pathogenesis o Small variant are the extracellular form  Metabolically inactive  Released by infected cells (lysis/exocytosis) o Invade and replicate in host cells – bind to monocytes  Phagocytosed and phagolysosome fuse = large vacuole o Slow intracellular multiplication = no host cell damage
46
How do you diagnose Coxiella burnetii?
* Diagnose o 2 antigenic phases 1. Phase 1 a. Chronic: higher Ig to phase 1 2. Phase 2 a. Acute = higher Ig level to phase 2 in second week of illness o Type 1 and 2 antigens persist for months – years o Indirect immunofluorescence o Cytology o Serology o PCR o Modified Ziehl Nielsen from placental tissue/vaginal discharge
47
What are the bacterial features of Mycobacterium avium paratuberculosis
Mycobacterium avium paratuberculosis * Obligate pathogen with rough/waxy cell wall * Facultative intracellular (invade macrophages) * Difficult to grow in lab * Environmentally/disinfection resistant
48
What animals does Mycobacterium avium paratuberculosis target
* Target: adult animals o Usually get infected within 1yo – but clinical signs take a long time
49
How is Mycobacterium avium paratuberculosis transmitted
* Transmit: oral ingest (young) o Shed lots (10^12 cells/d) o Found at low concentration in milk o Transplacental
50
What is the pathogenesis of Mycobacterium avium paratuberculosis?
o Transplacental * Pathogenesis o Ingest feces o Infect ileum o Inflammation over 2- 5 years  Host T cells recruit lymphocytes and macrophages  Survive in macrophage by inhibiting maturation of phagolysosome o Low shedding  When low shedding = may not detect with ELISA o Weak immune response = high shedding  ELISA effective to detect o Emaciation
51
What are the clinical signs of Mycobacterium avium paratuberculosis?
* Clinically: months – years before clinical signs o Progressive/emaciating o Chronic non responsive diarrhea + good appetite o Muscle wasting o Bottleneck edema (due to PLE) o Usually get culled before reaching later stages of disease
52
What are the histo signs of Mycobacterium avium paratuberculosis?
* Histo: o Ziehl Nielsen acid fast stain o Thickened corrugated intestine o Diffuse granulomatous histiocytic enteritis +/- necrosis/fibrosis o Swollen LN
53
What are the financial consequences of Mycobacterium avium paratuberculosis?
* Financial consequences o Less milk/weight at slaughter o Delayed conception o Annually = 1500-2500/cow
54
What are the 4 stages of johnes dz and why is it important?
o Types  Non-infected  Infected/no shed  Infected/shed  Clinical/shed There is a spectrum of infected animals on the farm may not detect the majority of cases
55
How is johnes diagnosed?
 Rectal/fecal smear > acid fast * Not used – only for clinical animals  Fecal culture * Long time  Tissue culture * Best way to ID – grow from ileum biopsy  PCR * Pool sample and detect DNA  Serology  Skin test  Interferon gamma release assay
56
How is johnes treated
* Tx: no cure
57
How is johnes controlled
* Control: difficult (test and cull mainly) o Notifiable o Reduce contact between infected and susceptible young animals o Environmental clean up o Cull infected o Segregate calves o Control herd additions o Colostrum management and pasteurization
58

VETM 423 Bacteriology (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions