17. corynebacterium, erysipelothrix, pseudomonas

corynebacterium gram stain

positive, small rods (can appear pleomorphic)

what is the most clinically relevant species of corynebacterium?

c. pseudotuberculosis

sources of c. pseudotuberculosis

soil and gut commensal (normal microbiota)

c. pseudotuberculosis virulence factors

• exotoxin phospholipase D (PLD) → increases vascular permeability and bacterial dissemination

• high content of cell wall lipids → survive inside macrophages → dissemination

c. pseudotuberculosis pathogenesis

killing of immune cells → new wave of immune recruitment → kill immune cells → recruit …. → create lamellar (layered) pyogranulomas

how is c. pseudotuberculosis transmitted?

• penetration through breaks in the skin or mucous membranes

• contact with purulent draining lesions

• + biting flies (horses)

• (less common: inhalation or ingestion)

what disease is associated with c. pseudotuberculosis in small ruminants?

caseous lymphadenitis

c. pseudotuberculosis clinical signs (small ruminants)

• external abscesses

• internal infection/abscesses → chronic weight loss, failure to thrive; organ-specific symptoms

diagnosing c. pseudotuberculosis (small ruminants)

• definitive diagnosis by culture when accessible

• serological tests available, but limited interested in diagnostics (neg. Ab test does not rule out infection)

c. pseudotuberculosis treatment (small ruminants)

• lancing and draining

• surgical excision

• antibiotics (intralesional and/or systemic)

• inform on recurrent-chronic nature of disease and contagious risk

  • culling option

c. pseudotuberculosis prevention (small ruminants)

• culling infected animals

• careful disinfection

• vaccination → commercial vaccines available to decrease incidence

what diseases are associated with c. pseudotuberculosis in horses?

• equine ulcerative lymphangitis

• chronic abscesses

(aka pigeon fever or breast-bone fever or dryland distemper)

clinical signs of c. pseudotuberculosis (horses)

• external abscesses

• internal abscesses → fever, weight loss, depression, lameness

• ulcerative lymphangitis (rare)

diagnosing c. pseudotuberculosis (horses)

• definitive diagnosis by culture when accessible

• PCR testing from abdominal fluid

• serological tests can help with suspected infection (keep in mind neg test is inconclusive)

treatment/prevention of c. pseudotuberculosis (horses)

treatment

• open drainage of external abscesses usually sufficient

• internal abscesses and ulcerative lymphangitis require long-term treatment (weeks) with systemic antibiotic cocktail

prevention

• isolation of infected animals & fly control

• conditionally licensed vaccine available

erysipelothrix rhusiopathiae gram stain

positive rods (can appear pleomorphic)

• can be filamentous

e. rhusiopathiae sources

• widespread in the environment and in animals

• pigs are important reservoir

• external slime of fish

e. rhusiopathiae virulence factors

• capsule

• neuraminidase → leads to vascular damage

how does immunity status of the host affect e. rhusiopathiae pathology?

• partial immunity → more superficial and less systemic

• no immunity → systemic and multi-organ 

e. rhusiopathiae hosts

• most important:

  • pigs

  • chickens

• sporadic (rare) disease:

  • sheep

  • dogs

diagnosing e. rhusiopathiae

• based on clinical signs and culture

• PCR & other molecular tests

• no serology test available

treatment/prevention of e. rhusiopathiae

• treatment: penicillin effective (early stage of disease)

• prevention: vaccines available (limited immunity — 6-12 months); proper sanitary conditions (e.g. shearing)

e. rhusiopathiae transmission in swine

• ingestion of contaminated feed (e.g. bird and rodent feces)

• wound infection

e. rhusiopathiae predisposing factors

anything that weakens the immune system (stress, diet change…)

e. rhusiopathiae clinical signs (swine)

• diamond skin disease (common; good prognosis) → skin lesions (red to purple rhomboids) from vasculitis and thrombosis, can progress to necrosis

• septicemia (high mortality if untreated)

• chronic:

  • arthritis

  • endocarditis

e. rhusiopathiae transmission (poultry)

wound infection, most likely from fighting

e. rhusiopathiae clinical signs (poultry)

• septicemia (high mortality if untreated): cyanotic skin and snood; vasculitis and thrombosis, can lead to sudden death

• chronic:

  • arthritis

  • endocarditis

e. rhusiopathiae transmission (sheep)

• skin breaks

• wound infection

• via umbilicus

• lambs are most susceptible

e. rhusiopathiae clinical signs (sheep)

arthritis

e. rhusiopathiae transmission/predisposing factors (dogs)

1. transmission: ingestion of contaminated food

2. predisposing factor: state of immunosuppression

e. rhusiopathiae clinical signs (dogs)

• septicemia → non-specific signs such as lethargy, anorexia, and pyrexia

• skin lesions

• (other cases: arthritis, endocarditis)

erysipeloid disease in humans

• self-limiting disease of the hands

• occupational disease: veterinarians, fish handlers, slaughter-house works, butchers

pseudomonas aeruginosa gram stain

negative rods

sources of p. aeruginosa

• ubiquitous in the environment

• not commensal

predisposing factors to p. aeruginosa

• anything that weakens the immune system/kills microbiota

• wounds

• contaminated medical equipment

p. aeruginosa transmission

constant exposure → very broad spectrum of infections and infection sites

• can cause many different diseases in a number of hosts

major diseases associated with p. aeruginosa

• canine otitis externa (very common)

  • breeds with long ears are high risk

• pyoderma (dogs/cats)

• equine corneal ulcers

• hospital-acquired (frequent)

notable p. aeruginosa virulence factors

has many virulence factors

• type 3 secretion system → inject exotoxins that are good at killing cells

• type 6 secretion system → kills other (resident) bacteria; important for colonization

• biofilm formation

equine melting corneal ulcer risk factor/pathogenesis

• application of corticosteroid preparation (inducing immune suppression) in eye with damaged cornea

• bacterial proteases degrade cornea

• invades damaged cornea and thrives

what is a challenge associated with treating p. aeruginosa?

high levels of antibiotic resistance → sensitivity profile essential