Gram + aerobes Flashcards
Staphylococcus morphology & species (w diseases)
Gram + cocci in clumps
S. aureus = cows (mastitis)
S. pseudintermedius = dogs (pyoderma + others)
S. hyicus = pigs (greasy pig disease/exudative dermatitis)
Staphylococcus virulence factors
(true for all Staphylococcal disease)
(13)
Adhesins
Halotolerant/fatty acid tolerant
Antiphagocytic capsule
Staphyloferrin B siderophore
Chemotaxis Inhibiting Protein (CHIPS)
Protein A = binds Fc > inh opsonisation/complement
Clumping factor
Exoenzymes (staphylocoagulase, hylauronidase)
Exotoxins:
- α-toxin (haemolysin) + leucocidins > suppuration
- Exfoliative toxin > skin exfoliation
- Enterotoxins
- Toxic shock syndrome toxin (TSST) superAg
Staphylococcus - habitat (2)
Skin surface
Mucocutaenous jcn
Staphylococcus - host factors (3) & defence
Wounds
Hair follicles / skin glands
Hypersensitivity rxn (esp arthropod allergies)
Defence = phagocytosis (neut’s)
Pyoderma, otitis externa, abscesses, wound infections etc. in dogs
- Agent
- Pathogenesis
S. pseudintermedius
- Damage to skin integrity = wounds, allergies (flea bite/tick pyaemia), seborrhoea, maceration, glucocorticoids
- Suppuration + abscessation
Tick pyaemia
Staphylococcus spp. (esp S. pseudintermedius in dogs)
Staphylococcal bovine mastitis
- Forms (3)
- Transmission
Peracute = fatal in young cows > gangrenous dt α-toxin Subacute = heat/swelling/induration of affected quarter Subclinical = high ICCC + decreased milk prod'n
Transmission = via milking machines
Greasy pig disease (exudative epidermitis)
- Agent & virulence factors (3)
- Source of agent
- Predisposing host factors (2)
- Disease characteristics
Staphylococcus hyicus (fibrinolysin, exfoliative exotoxin, no α-toxin)
- Source = skin of pigs
- Predisposition = environmental stress, vit B deficit
- Acute, contagious, generalised, non-pruritic disease of young pigs (w high mortality)
Antibiotic tx for Staphylococcal disease
- Large animals vs small animals
Bo = Penicillin G (benzyl penicillin) Ca = ampicillin, amoxycillin
Streptococcus spp.
- Morphology
- Environment
Gram + cocci in chains
Mucous membranes (mouth/URT/GIT/genital tract)
Pyogenic pathogens
Virulence factors of Streptococcus (5)
Adhesins (lipotechoic acid + M protein) Capsules (hyaluronic acid or polysacch) = anti-phag M protein = anti-phagocytic Haemolysin (streptolysins O/S) Exoenzymes (proteinases, streptokinases)
Tx of Streptococcus
Tx = penicillin G (narrow spectrum, no resistance)
Tx = drain abscesses + isolate
Streptococcal bovine mastitis
- Source of infection
- Cause of dz
- Tx
Streptococcus agalactiae > S. dysgalactiae / S. uberis
- Source = obligate parasite of udder ductular tissue
- Acute cases = faulty milking machine, poor hygiene
- Tx required = benzyl penicillin (no resistance)
- Variable milk quality
Strangles
- Agent
- Source of agent
- Disease characteristics/progression
Streptococcus equi subsp equi
- Obligate parasite of equine nasopharynx/guttural pouch
Acute, contagious, purulent infection of pharyngeal mucosa > local lymphadenitis/LN abscessation > abscess rupture > recovery
Strangles VFs (3)
M protein = ↓ phagocytosis, adhesin
Hyaluronic capsule = ↓ phagocytosis
Streptolysin O (haemolysin) = damages phagocytes
Strangles defence + immunity
Defence = humoral anti-M protein Ab Immunity in 70% of recovered horses - Ab in colostrum = neonatal immunity - Cell-free vax available - Carrier animals = reservoir
Strangles transmission/infection route
Transmission = oral/nasal route
Infection = direct/indirect contact w infectious secretions
- feeding troughs, flies
- outbreaks in horses in close confinement
Agent persistent in pus/secretions in environment
Endometritis in mares
- Agent
- natural environment
- other dz’s
Streptococcus equi subsp zooepidemicus
- Commensal of skin/URT/genital mucous membranes
Dz = wound infections, secondary URT infection (after viral infection), genital infections in mare, neonatal infection > septicaemia/athritis
What causes S. equi subsp zooepidemicus to cause endometritis in mares?
Impaired bacterial clearance mechanisms of uterus (e.g. during luteal phase)
Zoonotic meningitis, arthritis, sepsis, pneumonia in young pigs
Streptococcus suis
- Commensal of tonsils/nasal cavity of all pigs
Feline/canine Streptococci
S. canis = dog/cat lymphadenitis + other inf’s =
Arthritis/polyarthritis in pigs
Streptococcus dysgalactiae ssp dysgalactiae
Streptococcus suis
Lymphadenitis in pigs
Streptococcus porcinus
Rattles (equine)
- Source of infection
- Dz characteristics
Rhodococcus equi (gram + cocci/coccobacilli)
- Soil/dust + multiplies in dung
- Pyogranulomatous bronchopneumonia + GI ulceration
Rattles VFs (4)
Polysaccharide capsule = ↓ phagocytosis
VapA gene > virulence associated protein = ↓ phagosome function
Facultative intracellular parasite (in alveolar MPS/PMNs)
No toxin
Rattles
- Susceptible animals
- Pathogenesis
- Tx
- Immunity
Young foals w waning maternal Ab
Infection via inhalation/ingestion > granulomatous abscess > suppuration/abscessation in bronchial LNs > cough/rattles > exhaled in aerosols
Tx = azithromycin
CMI + Ab immunity important
Zoonosis reported
Mycobacterium spp.
- Morphology
- Environment
Gram + rods
Obligate aerobes
Saprophytic or obligate intracellular parasites (RES)
Mycobacterium VFs (5)
Lipid-rich cell wall
Cell wall mycolipids/phospholipids = inhibit phag-lys fusion
Mycolic acid (cell wall) = protects against macroph killing
Tuberculoprotein = delayed type HS response
No toxin
Host factors in Mycobacterium infection (3)
Intracellular parasites TF CMI (macroph)
Breed-related susceptibility (Jersey > SE Asian)
Stress (calving, heavy lactation) > dz/shedding
Environmental factors of Mycobacterium (2)
Carrier animals = reservoir of infection
Resistant in environment (drying, pH)
Bovine tuberculosis
- Dz characteristics
Mycobacterium bovis
- Chronic granulomatous lesions of lung/GIT/other organs
- Tubercles are encapsulated + calcified > stress = shedding
Bovine TB infection route + resulting disease
Ingestion > GIT > mesenteric LNs > liver, lungs
Inhalation > alveolar macroph > lung lesions > local LN > lymphatics/blood > other organs
Bovine TB epidemiology
Extensive systems = inhalation > pulmonary TB
Intensive systems = ingestion > GI TB
Contaminated environment
Wildlife reservoirs (possums, pigs)
Eradicated from Aus
Is Mycobacterium bovis zoonotic?
Yes - cervical adenitis in children from drinking unpasteurised milk
Bovine TB tx
Macrolide AB (azithromycin) = gram + aerobes
Johne’s disease
Mycobacterium avium ssp paratuberculosis
Johne’s disease characteristics
JD route of infection
JD transmission
Chronic contagious enteritis (distal SI) of sheep/cattle
Infection early in life > long incubation period (>2y)
Faeco-oral route (ingestion > invasion of ileal mucosa)
Shedding by carrier animals
- High stocking density important
JD clinical signs
JD necropsy signs
Malabsorption > chronic wasting + (pea-soup) diarrhoea
Protein-losing enteropathy > hypoalbuminaemia > bottle jaw + ascites
PM = thickened intestinal mucosa w corrugations
JD parasite factors (3)
Intracellular parasite of macrophages
Depresses Th cell activity
Fe-dependent
JD host factors (3)
Infection early in life > prolonged incubation period
Infection as adult > no disease + shedding (TF reservoir)
Disease precipitated by stress (calving, heavy lactation)
JD environmental factors (3)
JD epidemiology (2)
Stress = climatic conditions/nutritional shortages
Climate = temperate regions
Stocking density = ↑ facilitates transmission
Contaminated environment important (resistant to dessication)
Endemic in Aus (NSW/Vic/SA/Tas)
JD vax
Live vaccine > ↓ clinical disease but doesn’t affect infection rate/shedding
JD zoonosis
Crohn’s disease - no causal link
Avian tuberculosis
Mycobacterium avium ssp avium
Avian TB disease & pathogenesis
Dz in pigs
Zoonosis?
Ingestion of contaminated food/water/soil
> caseous nodules in GIT, liver, spleen + GI ulceration
> emaciation, joint swelling
> shed in faeces (↑ numbers)
Causes submandibular LN abscesses in pigs
Zoonotic potential in immunocompromised (AIDS)
Avian TB epidemiology & environmental factors
Rare in birds < 1yo
Extended survival in environment > environmental contamination + reinfection
Worldwide distribution
Cat leprosy
Mycobacterium lepraemurium
- Nodular cutaneous lesions on heads/limbs of cats ± draining LNs
Cat leprosy - source of infection
Rat bites
Corynebacterium morphology
Gram + pleomorphic rods in palisade arrangements
Cheesy gland/caseous lymphadenitis agent
Corynbacterium pseudotuberculosis
- Sheep/goats
Ulcerative lymphangitis in horses agent
Corynebacterium pseudotuberculosis
Cheesy gland parasite VFs (3)
Leucotoxic surface lipid = destroys PMN WBCs > persistence in abscesses
Pyogenic factor = cell wall component
Phospholipase haemolytic exotoxin = ↑ vasc perm > early dissemination
Cheesy gland pathogenesis in sheep
Agent entry via skin wound (shearing)/macerated skin (wetting)
> localised skin lesion (heals quickly)
> dissemination to draining LNs (exotoxin important)
> phagocytosis, intracellular multiplication, PMN cell death (leucotoxin)
> chronic purulent abscesses
> continuing fibrosis = encapsulated abscess + layered appearance
May enter lymphatics/blood > generalised lymphadenitis, pyaemia, anaemia, cachexia
Cheesy gland pathogenesis in goats
Agent entry via oral abrasions (dt grazing habits of goats)
Cheesy gland epidemiology (2)
CG control (3)
↑ incidence with age (dt ↑ chance of exposure)
Discharge from abscesses > contaminate environment (soil, shears - esp wet/faeces-rich)
Shear/dip young sheep before old
Keep dips clear of organic matter
Toxoid vaccine
Is cheesy gland zoonotic? risk factors?
yes - lymphadenitis
Close contact w sheep
Cheesy gland tx
CG outcomes (2)
Penicillin (sensitive)
Encapsulated abscess = drug doesn’t penetrate
↓ morbidity/mortality
Carcasse condemnation
Bovine pyelonephritis
Ovine balanoposthitis/vulvitis (pizzle rot)
Corynebacterium renale
Pizzle rot/pyelonephritis VFs (3)
Tropism for renal medulla
Pili = attachment to UGT mucosa
Urease (urea > NH3) = necrosis/ulceration
Bovine pyelonephritis - pathogenesis
Commensal of lower UGT
> ascending UTI (F predisposed dt short/wide urethra + pregnancy)
> cystitis > ureteritis > pyelonephritis
> necrosis, congestion, chronic inflamm/fibrosis
Clin signs = lumbar pain, haematuria, pyouria, poor BCS
Older cows > young
Ovine pizzle rot/vulvitis risk factors (2) + pathogenesis
Commensal of lower UGT
Risk factors
- high pasture E2 > preputial swelling >
- ↑ dietary protein > ↑ [urea] of urine
> urine accumulation in poorly developed penis (retracted in prepuce)
ulceration/scabbing = balanoposthitis
urinary obstruction = extension of lesions
complete obstruction = toxaemia/sepsis
Trueperella pyogenes morphology
Gram + pleomorphic rod
T. pyogenes - examples of diseases
Commensal of mucosal surfaces
Non-specific suppurative lesions in catte/sheep/pigs (secondary infections)
- Liver abscesses (bo)
- Pyogenic mastitis (bo)
- HW disease (bo)
- Foot abscesses (ov) = footrot
- Pneumonia (po)
Mixed infection w Fusobacterium necrophorum
Trueperella pyogenes VFs (2)
Haemolytic exotoxin (pyolysin) Predilection for closed cavities (udder)
Tx of Trueperella pyogenes
Penicillin sensitive (doesn’t penetrate lesions though)
Anti-pyolysin Ab protective
No vax
Nocardia asteroides morphology
Environment
Location when pathogenic
Gram + filamentous rods
Saprophytic - soil, decaying organic matter
Facultatively intracellular parasite
Strict aerobe
Nocardiosis diseases (3)
Chronic suppurative/granular respiratory infections > haematogenous spread
Chronic granulomatouus skin lesions
Acute mastitis
Nocardia asteroides VFs (2)
No toxin
Virulent strains inhibit phag-lys fusion
Tx of Nocardiosis
Trimethoprim-sulfonamide
resistant to penicillin
Nocardiosis - host factors (3)
Immunity (2)
Dogs > other sp
M > F
Young (<2yo) > old
CMI important
Immunosuppression > systemic dz
Lumpy wool
Strawberry footrot
Cutaneous streptothricosis
Rain scald
Dermatophlius congolensis
- Obligate animal parasite in uncornified layers of epidermis
Lumpy wool (+ others) disease characteristics
Proliferative, exudative dermatitis + scab formation
Life cycle of agent causing lumpy wool
Dermatophilus congolensis
> Long branching filaments > broaden into wide filaments > septation into cocci > divide + become motile
Lumpy wool/strawberry footrot risk factors (8)
Chronic wetting (↑ rainfall in spring) ↑ ambient T/humidity Intercurrent disease (orf virus) Ectoparasites (hypersensitivity) Abrasions Wax content of fleece (TF waterproofing) Age (young > old) Carrier animals
Lumpy wool predisposes to fly strike
Lumpy wool pathogenesis
Transmission by direct/indirect contact
> proliferation in epidermis
> exudation + scab/crust formation
> regeneration of epidermal layers = layered scab (cornified epidermis/exudate)
> coalescing scabs = large areas affected
Is lumpy wool zoonotic
Yes - humans handling animals
Porcine pyelonephritis/UTI
Atinobaculum suis
Lumpy jaw agent + morphology + O2 requirement
Actinomyces bovis
Gram + branching filament
Obligate anaerobe
Lumpy jaw pathogenesis
Commensal of oral cavity
> Injury to buccal mucosa (coarse feed, shedding teeth) = pathogen entry
> local pyogranulomatous lesions in mandible/maxilla (at site of entry) w S granules
> pus discharge through fistulous tracts
> extension to soft tissues + bone
Lumpy jaw tx
Sensitive to penicillin (G)
Listeria morphology
Gram positive rod
Motile at low T
Forms of listeriosis (5)
Adult ruminants:
- Meningoencephalitis (via CN V)
- Abortion
- Keratoconjunctivitis
- Mastitis
Neonatal lambs: septicaemia
Listeria monocytogenes VFs (4)
Growth at low T Surface protein (internalin) = cell invasion Haemolysin = phagosome lysis Surface protein (Act A) = facilitates transfer
Facultative intracellular parasite
Listeriosis - host factors (5)
Subclinical infection common
CMI - macrophages
Immunocompromise/pregnancy = ↑ susceptibility
Oral wounds allow entry > CN V > brain
Meningoencephalitis/meningitis (circling disease) in ruminants
Listeria monocytogenes
Circling disease pathogenesis (ruminants)
Inhalation/conjunctival contamination > entry through oral wounds > ascending infection along CN V > localisation in brain > white matter granulomas + perivascular cuffing
Circling disease clin signs (ruminants) (6)
Unilateral facial paralysis Circling Deviation of the head Depression Head pressing Progressive paralysis > death
Listeriosis environmental factors (2)
Ubiquitous (cool climates/seasons)
Poorly fermented silage (pH > 5.5)
Pathogenesis of ruminant abortions - Listeria monocytogenes
Infection of pregnant animal > bacteraemia > localisation in uterus >invasion of foetal/placental tissue > foetal death > abortion (w RFM)
What are the risk factors for zoonotic listeriosis?
Food borne infection (milk/cheese)
> meningitis in neonates/elderly
> abortions in pregnant women
High infectious dose
Erysipelothrix morphology
Slender gram + rods in filaments
Erysipelas in pigs - agent
- Disease forms (3)
Erysepelothrix rhusiopathiae
Bacteraemia >
- arthritis and/or endocarditis
- skin lesions (diamonds)
Septicaemia
Tx of listeriosis
Ampicillin
Amoxy-Clav
Erysipelothrix VFs (4)
Virulent strains = invasive
Adhere to intestinal epithelium
Neuraminidase = vascular dmg/thrombosis
Antiphagocytic capsule
Tx of erysipelas
Penicillin
Host factors of erysipelas (4)
Carrier animals (pigs) < > environment Ag persists in avascular joints/heart valves > immunopathological rxns (arthus) Humoral immunity (macrophages) Age-related susceptibility (3mo-3y)
Erysipelas immunity/vax (2)
Humoral (Ab) immunity
Killed or live attenuated vax
Erysipelas environmental factors (4)
Resistant to dry/salt/pH etc.
Survive in environment
Extensive pig raising
Feeding fish meal
Swine erysipelas pathogenesis
Oral/percutaneous transmission
> adhere to GI epithelium
> bacteraemia + vasculitis/thrombosis
> localisation in heart/skin/joints or sepsis
Clinical manifestations of swine erysipelas (4)
Acute sepsis = febrile, bright red diamond skin lesions > death
Urticaria = mild, non-fatal, purple skin lesions
Chronic form = vegetative endocarditis, non-suppurative arthritis
WHat is erysipeloid?
Zoonosis via Erysipelothrix rhusopathiae
- Acute skin inflammation via skin wounds
- Animal handlers
Bacillus morphology, environment, key feature
Large gram + rods
Soil/water - multiply in environment
Endospore-forming = resistant, long lived
Anthrax VFs (2 - subparts)
Plasmid-encoded VFs:
Poly-D-glutamic acid capsule = antiphagocytic
Exotoxin - made of 3 proteins
- Protective Ag (PA) = binds receptors + forms channels
- Oedema factor (EF) = adenylate cyclase > electrolyte/fluid loss
- Lethal factor (LF) = metalloprotease > IL-1 release from macrophages
LF+PA = lethal toxin > cell death EF+PA = oedema toxin > cell death
Diseases caused by Bacillus spp.
B. anthracis = anthrax
B. cereus = acute mastitis/abortion in cattle
Anthrax - host factors (2)
Herbivores most susceptible
Overprod’n of IL-1/TNF > endothelial dmg > acute CV shock
Anthrax - immunity
anti-exotoxin Ab protective Attenuated vax (no capsule) available
Anthrax - environmental factors (4)
↓ pCO2 > endospore formation
Anthrax belt = west NSW
Seasonal = warm, humid weather
Outbreaks = scarce feed > oral abrasion
Septicaemic anthrax pathogenesis
Ingestion of spores > local multiplication + local LNitis > bacteraemia > cleared by spleen RES > exceeds splenic clearance capacity > multiplies in blood > death dt hypovolaemic shock
Septicaemic anthrax clin signs (
Enlarged, pulpy (strawberry jam) spleen
Rapid decomposition of carcass
Black exudate from body orifices
Zoonotic anthracosis
Cutaneous anthrax > spore ingestion > black eschars > local LNitis > death
