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Actinobacteria- general characteristics

related group of gram-positive organisms- form branching structures similar to fungi
non-spore forming, non-motile
ubiquitous in environment (commensals of plants and animals)
pharmacologically active metabolites- found in ABX and MSG
some genera are pathogenic for humans and animals
mycobacterium (TB)
All have mycolic acids in cell walls--> resist phagocytosis


Actinobacterial diseases

some are opportunistic, some are highly host-adapted pathogens. Pathology is often similar: chronic inflammation, focal lesions or dissemination (within macs); granulomatous lesions (abscessed, pyelonephritis, lymphadenitis, osteomyelitis)


Immune protection to actinobacterial disease

CMI is natural host-response to infection; vaccine induced humoral immunity is effective as well.


treatment with ABX

in vitro, sensitive to many abx.
in vivo, poor response due to intracellular location



Strictly aerobic
aerial hyphae
widely distributed in soil, water, air and sewage
non-motile, non-spore forming
12 species: pathogenic to a variety of species


Nocardia species

N. asteroides: most frequent nocardial pathogens- SQ infections in dogs acquired through environmental contact
N. brasiliensis: pneumonia in horses
N. otitidis caviarum: bovine mastitis (not very frequent cause), ear infection in guinea pigs.
N. farcinica- common isolate (genome)


Nocardia epidemiology

Organism are inhaled, ingested or get in via wound
Direct or hematogenous spread
Resist phagocytosis due to acid-fast cell wall.
Chronic invasive pyogenic infections (no production of sulphur granules)
3 clinical forms: cutaneous, respiratory (pyothorax), and systemic (pyrexia, cough, neurological)
Dogs- 3x more common in males
Cats- mainly thoracic infection
Tx is difficult and prolonged (not penicillin--> not great for intracellular infections).


Trueperella (arcanobacterium)

T. pyogenes- first described in 1946
commensal but opportunistic
causes non-specific purulent lesions
focal or disseminated abscesses
wound infection
septic arthritis- esp. in pigs
secondary respiratory infections
reproductive impairment: increase frequency in repro tract- big cause of metritis--> perhaps symbiosis with e. coli.
Often secondary/mixed infections.
Broad host spectrum


Viruelnce factors of t. pyogenes

protease (necrosis/suppuration)
hemolytic exotoxin (dermonecrotic)
neuraminidase- allows it to adhere to host cell
Pyolysin- resembles thiol-activated toxins. Thiol activated toxins have 2 cys residues that form disulfide bridge. PLO doesn't form bridge. punches a hole between cholesterol residues of cell membrane to allow leakage of cytoplasm resulting in eventual lysis.


diseases caused by t. pyogenes

bovine abortion, porcine abscesses (caseous lesions) and porcine polyarthritis.


Actinomyces species

A. bovis, A. viscosus, A. suis
Most non-acid fast, branching
Non-motile, Non-spore forming
Microaerophilic or anaerobic
Produce pyogenic, granulomatous reactions with production of sulphur granules.


A. bovis

Component of normal mouth flora- anaerobic
Thick, yellow pus (sulphur granules)
Causes actinomycosis/lumpy jaw in cattle
Invasion through wound/rough feed/damaged mucosa- osteomyelitis (granulomas form in bone) animal stops eating
other soft tissue infection- i.e. in GI tract
mastitis: perhaps from suckling damage.


A. viscosus

Mainly dogs (but also pigs, goats, cats, cattle and horses)
Virulence factor: fimbriae- adherence to teeth- plaque?
Similar lesions to Nocardia (but nocardia doesn't produce sulphur granules)
Localized, pyogranulomatous lesions
Two main conditions: thoracic lesions and osteomyelitis


A. suis

Mastitis in pigs due to suckling trauma



diverse genus, small pleomorphic gram positives
look like chinese letters on stain
common commensals


C. renale group

C. renale, C. pilosum, C. cystitidis- all cause cystitis and pyelonephritis in cattle


C. renale group

C. renale, C. pilosum, C. cystitidis- all cause cystitis and pyelonephritis in cattle


Diphtheria group

C. diphtheria, C. ulcerans, C. pseudotuberculosis
cause various diseases of cats, cattle horses, small ruminants and humans


Diphtheria group

C. diphtheria, C. ulcerans, C. pseudotuberculosis
cause various diseases of cats, cattle horses, small ruminants and humans


C. renale group

C. renale most frequently encountered, followed by C. cystitis and c. pilosum
opportunist- highly adapted-->when stressed, cause disease
Causes cystitis, pyelonephritis and balanoposthitis (inflammation of glans and foreskin)
Pre-disposing factors: pregnancy, parturition, post-mating.
90% of bulls have c. cystitidis in prepuce- means by which organism can be transferred.


Virulence factors of C. renale group

Pili- adherence
Renalin- cell lysis--> causes clots
Urease--> breaks down urea- provides N source for which to grow
Caseinase--> proteolytic enzyme allows organism to obtain nutrients.


Pathogenesis of C. renale

adhere to urogenital mucoas; proliferation during stress; ascending infection (through bladder into kidney); inflammation; cystitis/pyelonephritis


Diphtheria group

C. diphtheria, C. ulcerans, C. pseudotuberculosis


Diseases caused by diphtheria group

C. diphtheria- URI in humans
C. pseudotuberculosis- various pyogenic infections
C. ulcerans- nasal congestion in cats, mastitis in cows


Cornyebacterium pseudotuberculosis-general characteristics

facultatively anaerobic, non-encapsulated, non-spore forming, non-motile, catalase-positive, non-acid fast


2 biotypes of corynebacterium

1) ovis: non-nitrate reducing; infects sheep and goats (caseous lymphadenitis)
2) equi: nitrate-reducing; predominantly infects horses.
Evolution of these two strains by horizontal gene transfer (phage)


Caseous lymphadenitis

Introduced into UK in 1989
Leads to fibrous, encapsulated lesions at various sites.
Significant financial loss to producers- v. chronic disease, doesn't seem to kill animals outright.
Carcass condemnation at slaughter, decreased wool, milk production, repro performance


Pathogenesis of CLA

C. pseudotubrculosis gainst entry to host through wounds
Normally transfer of pus (direct contact or flies)
Drains from point of entry to local LN and spreads within animal from there.


Virulence factors of C. pseudoTB

Phospholipase D: sphingomyelinase- causes vascular permeability, antichemotactic lethal for neutrophils, complement depletion
Mycolic acid (cell wall): toxicity, survival within macrophages
Serine protease: undefined function, possibly survival within macrophages
Siderophore: acquistion of iron from host--> animal tries to decrease iron availability via transferrin and lactoferrin


Diagnosis of C. pseudoTB

cAMP test: synergistic lysis between S. aureus and group B. strep (strep agalactiae)
cAMP inhibition test: inhibition of synergistic lysis between S. aureus and group B strep