Gram positives Flashcards
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)
cornyebacterium
truperella
nocardia
rodococcus
actinomyces
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
Nocardia
Strictly aerobic
aerial hyphae
widely distributed in soil, water, air and sewage
ACID FAST
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
Corynebacterium
diverse genus, small pleomorphic gram positives
look like chinese letters on stain
pyogenic
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
Prevention strategies of CLA
diagnosis/vax
PLD is found to be a protective antigen.
Diagnosis: ABs against PLD common in infected animals; detection of anti-PLD abs is a marker of infection.
Listeria species
L. monocytogenes: meningoencephalitis, septicemia, abortion, pyogenic infection
L. ivanovii: abortion, systemic infection
Epidemiology of listeria
Common commenal (tonsils, intestine) and enviromental organisms. Grow at temps from 4-45 degrees C, ph 6-9.6
Incidence relates to mgmt/husbandry, silage feeding, seasonally
Predisposed by trauma, immunocompromise, hormonal alterations
Listeriosis in Ruminants- symptoms/clinical signs
Meningoencephalitis
common=circling disease (small rums.)–circles in one direction only
Unilateral facial paralysis, difficult swallowing, fever, blindness, headpressing, paralysis, death in 2-3 days.
Infection happens through cutting of mouth through silage. Bug goes into CN V–> brain.
Listeria in pregnant animals
may loclaize in placentomes: cross-over aniotic fluids, multiples; ingested by fetus–> fetal death/abortion
Listeria in milking cows
Mammary gland can be involved: subclinical mastitis, contamination of milk, may survive low temp pasteruization inside milking tanks; lengthy survival in nature
Modes of access of listeria
entry also by nasal mucosa, conjunctiva
direct access to CNS via dental plates of CN V ganglia
Can survive within macrophages–> can serve as source of infection for humans
Pathogenesis of listeria
1) tooth loss/cutting–> oral inoculation–> CN V—> brain stem–> meningoencephalitis
2) naive/neonatal animals–> epithelial invasion –> bacteremia–> neonatal septicemia
3) pregnancy –> epithelial invasion –> bactermia –> placentitis –> abortion
Pathogenic mechanisms
facultative intracellular parasites surviving in macrophage and epithelial cells
cell uptake by bacterial protein internalin
Inside the cell, they escape the phagolysosome, multiply in the cytoplasm and via actin based motility, spread laterally to adjacent cells
Escape epithelium and are taken up by polymorphonuclear neutrophils and macrophages. these cells are killed and the organism may spread systemically.
Listeria is non-motile, but it hijacks the cytoskeleton->polymerizes actin–>forms tail.
Virulence factor of listeria
Listeriolysin (LLO): thiol-activated toxin; mediates escape from phagocytic vesicle. Bacteria polymerize actin, form tails–> bacteria moves through cytoplasm, invade adjacent cells. Secreted actin nucleating factor (ActA), localized at one of the bacterium
Food products associated with listeria
raw, unpasteurized milk products
feta, camembert, blue cheese
raw, cooked ready to eat meat and poultry, undercooked hotdogs and chicken
fresh, frozen and processed seafoods.
Cutaneous listeriosis in vets
most develop lesions 1-4 days after attending congenitally infected bovines.
Erysipelothrix rhusiopathiae- general characteristics
commensal, widespread in animals and infects man
grows at 4-37 degrees C
infection in pigs, sheep, turkeys and other
smooth and rough forms associated with the disease
E. rhusiopathiae smooth and rough form- diseases caused
Smooth: acute septicemia in pigs, turkeys, sub-acute skin lesions in pigs
Rough: chronic arthritis in sheep, endocarditis in pigs
Pathogenesis of E. rhusiopathiae
in Pigs: commensal in tonsils, RES, bone marrow and many other organs
Depression of host defenses
Multiplication of virulent strains (reversion to smooth)
Entry via tonsils or cuts/abrasions
Invades n’phils
Acute: septicemia- fever, anorexia, DIC, hemorrhage, lymphadenitis, fatal
Sub-acute (utricarial form): malaise, fever, DIC, diamond-shaped epidermal lesions
Chronic: arthritis/endocarditis: persistent, erosive, chronic inflammation, ill-thrift
