Bovine Pathogens Flashcards
What are the bacterial features of Clostridia bacteria
- Gram (+) obligate anaerobe
- Spore forming
- Exotoxin forming
List 12 common ruminant bacterial diseases
- 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
What is the hallmark feature of histotoxic Clostridia
- Hallmark = enthusiastic toxogenesis
List 4 types of Clostridia, their associated toxin and what disease they cause
o C. perfringens type A = alpha and theta toxin
Gas gangrene/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
6 common ‘themes’ of clostridia infection
o Acquisition from environment
o Entry after trauma/ingestion
o Local multiplication
o Toxin production
o Tissue damage
o Rapid death
List the toxins associated with C. septicum
Alpha = hemolysin
* Most important
Beta = leucocidin
Gamma = hyaluronidase
Delta = hemolysin
Where is C. septicum found and how does it infect animals
o Located: soil and GI (ingested)
o Transmit: contamination of wounds with soil/feces
What are the 2 different clinical manifestation of C. septicum
malignant edema
Braxy – lambs
What are the main lesions of malignant edema? How does it spread?
C. septicum
myonecrosis due to toxigenesis
* Hemorrhage/edema/necrosis
* Spread rapidly through muscle
* Death in 24h
How does braxy spread? What are the lesions? What causes it?
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)
What are the main clinical signs of C. septicum
41-42C fever
Depression/weakness/muscle tremor/lame
Soft doughy swelling/erythema around infection site
What are the main lesions of C. septicum
Gangrene
Malodorous
Exudate in SC/IM
Serosanguinous fluid in body cavities
Dark red muscle (no gas)
How to differentiate C. septicum from blackleg
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)
List 4 histotoxic Clostridium
o C. septicum
o C. novyi
o C. perfringens
o C. chauvoei
List the 2 types of toxin of C. novyi? What do they do
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
What disease is caused by C. novyi type A? What are the hallmark lesions?
o Type A
Gas gangrene aand wound infection
Lesions
* Hallmark = edema (bighead - young ram)
What disease is caused by C. novyi type B? What animals are affected? What are the lesions?
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
What is the pathogenesis of C. novyi type B?
Associated with liver fluke associated damage in liver (focal hepatic necrosis)
What disease is caused by C. novyi type D? What animals are affected? What are the lesions?
o Type D (aka C. haemolyticum)
Bacillary hemoglobinuria aka redwater disease
Similar to type B
* But more beta toxin
Signalment: well nourished animals >1yo
What is the pathogenesis of C. novyi type D?
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
What are the clinical signs of C. novyi type D?
Clinically
* Fever
* Icterus/pale MM
* Anorexia
* Abd pain
* Hemoglobinuria
What disease is caused by C. chauvoei? What are the 4 associated toxins
- C. chauvoei
o Causes black leg
o Toxins
Alpha = leucocidin
Gamma = hyaluronidase
Delta = hemolysin
Neuraminidase
What is the pathogenesis of C. chauvoei?
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
What are the lesions associated with C. chauvoei?
o Lesion: necrotizing emphysematous myositis (gas in muscle)
Primarily affect hind end muscle/myocardium/tongue/diaphragm
Stinky
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)
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
What are the lesions of C. chauvoei?
Laying on side with legs sticking out
Bloating
Dark red-black muscle
Bubbly muscle
How is C. chauvoei diagnosed?
o Dx: tissue sample (cardiac or skeletal muscle) and fluorescent antibody teest or IHC
What are 4 ddx for black leg
o Ddx:
Other clostridial infection (bacillary haemoglobinuria)
Anthrax
Poisoning
Lactation tetany
How is black leg prevented
Vaccine – blackleg bacterin = effective
Antibiotic not effective
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)
List 3 GI bacteria that affect calves
Digestive System
Calf
* E. coli
* Salmonella
* C. perfringens
List 4 GI bacteria that affect adults
Adult
* Actinbacillus ligneresii
* Actinomyces bovis
* Salmonella
* Mycobacterium avium paratuberculosis
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)
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
What are the risk factors for Actinobacillus ligneresii? Where is the bacteria found
o Commensal of oropharynx/rumen
o Risk: trauma predisposes
What are the lesions of Actinobacillus ligneresii?
o Lesions
granulomas contain odorless pus
Granulomatous lesions
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
Where is Actinomyces bovis found
o Commensal of oropharynx/rumen
Enter via wounds in oral mucosa
How to diagnose and treat Actinomyces bovis?
o Diagnose
Sulfur granules on H and E stain
What are the lesions of Actinomyces bovis?
o Lesions
Pyogranulomatous infection and proliferation of connective tissue
Can impact bone (periostitis)
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)
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
How is Coxiella burnetii transmitted?
- Transmit: inhaled (+/- ticks or ingestion)
o Very low infectious dose
o Excrete in milk/feces/abortus/vaginal discharge
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
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
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
What animals does Mycobacterium avium paratuberculosis target
- Target: adult animals
o Usually get infected within 1yo – but clinical signs take a long time
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
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
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
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
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
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
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
How is johnes treated
- Tx: no cure
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
