cocci

white/golden opaque colonies

form grapelike clusters by dividing in 2 dimensions

Gram Positive

facultative anaerobes (catalase positive)

non motile

salt resistant and fermentative (mannitol)

coagulase: positive tend to be more pathogenic; can also be negative

can be hemolytic

staph aureus: protein binds to prothrombin to form staphylothrombin

non proteolytic activation of prothrombin

catalyse fibrinogen -> fibrin

other Staph spp: non specific proteolysis or coagulase homologs

role of coagulase in virulence has not been proven; coagulase activity is associated w more pathogenic spp

s aureus

s pseudointermedius

s intermedius

s hyicus

s delphini

s epidermis

s hemolyticus

s simulans

 many more

NORMAL FLORA!

teichoic/lipoteichoic acid (same as all Gram +)

Ig binding protein: PROTEIN A

fibronectin/fibrinogen binding (attach to epithelium and endothelium)

heme binding proteins: sequester Iron (ties in w hemolysis)

capsule (not that much)

accessory gene regulators aka Quorum sensing (colonies and biofilms)

DNAase

phospholipase

staphylokinase (breaks up fibrin - keeps infections from being "walled off" by the body)

hyaluronidase (inc tissue permeability)

alpha toxin: hemolysin

leukocidin

exfoliative toxin (spreading)

pyrogenic endotoxins (fever)

TSS toxins: superantigen

enterotoxins: food poisoning

plasmid in s aureus, chromosomal in other spp

can't treat with penicillin, but could use other beta lactams

semisynthetic penicillin is also resistant to penicillinase

present in multiple species (not just s aureus)

chromosomal mecA gene (MEChanism of Aquisition unknown)

encodes penicillin binding protein PBP 2a

low binding affinity for ALL beta lactam subclasses

multi drug resistance in other classes can occur (MRSA)

dog, cat, occasionally others

used to be classified w s. intermedius

pigs, occasionally cattle

"greasy pig disease!"

endogenous infection

endogenous: common (opportunistic infection)

animal to animal

contaminated fomites

nosocomical: resistant strains

phage typing: some bacteriophages are specific to the level of the bacterial strain

molecular epidemiology (PCR)

acute pyogenic infections most common

usually involve the skin

can cause septicemia

chronic infections can also occur (osteomyelitis, botryomycosis - cattle)

thin layer of epithelial cells that constantly slough off

keratin

dryness

high salt content

lipids (toxic and seal the surface)

organic acids

resident flora compete for nutrients

antigen presenting cells, lymphocytes: local immune response

keratinocytes: produce cytokines

thicker

connective tissue

blood supply (immune)

hair follicles

sebaceous glands

sweat glands

pH 3-5 (low)

fatty acids

can be resident or transient

mostly gram positive bacteria and yeasts

break in epithelium

moisture retention: folds

exocrine or endocrine disorders (glands don't secrete)

altered microflora (lose competition)

keratinization defects

superficial pyoderma - impetigo, superficial folliculitis

deep pyoderma (folliculitis, BOIL, cellulitis, subcutaneous abcess)

hoof infections

outer ear (otitis externa)

mastitis

vascular compromise leading to skin issues

diffuse inflammation of subcutaneous layer

rapidly advances along tissue planes

associated w exotoxin producing bacteria

risks: thin stratum corneum

lack of follicular plug

epidermal barriers don't develop well enough

ex keratin, glands, acids, lipids, immune

drain abcess (ABx not very effective if abcess has formed)

treat topically or systemically with antimicrobials

culture

serology uncommon (bovine)