Staphylococci are gram +ve cocci that form irregular bunches of cocci that resembles bunches of grapes. They occur as commensals of skin and mucosa, and some act as opertunistic pathogen causing pyogenic infections. Staphylococci are non motile and catalase positive. They do not form spores and is stable in the environment.
In the laboratories staphylococci are represented by opaque and rich creamy colonies. One can do a catalase test to distinguish staphylococci from streptococci. Staphylococci are resistant to bile salts and therefore grow on macconkey agar. Staphyolococci will grow on simple media (nutrient agar) and survive well in the environment outside the host. Staphylococcus make cytokines so some will produce a diffuse zone incomplete beta haemolysis.
Staphylococci diseases in domestic animals include mastitis, tick pyaemia, exudative epidermitis, botryomycosis and pyoderma. There are a lot of different species, most important in the veterinary field is S.aureus which is the most important of pathogens and has the widest host range. S.aureus is the most common cause of mastitis in cattle, but can also cause thick pyaemia in sheep and dangerous dermatitis in poultry. S.pseudintermedius cause pyoderma I n dogs. S.hyicus cause exudative epidermis in pigs (greasy pig disease) or s.epidermidis cause skin commensal in all species.
Staphyolococci has a range of virulence factors to help them avoid the host immune system and maintain in the host. Coagulase will prevent phagocytosis. Protein A bind to Fc portion of IgG to inhibit opsonization and produces a capsule. Leukocidin will destruct the phagocytes of some species. Alpha and beta toxins will demage cells. Exfoliative toxin will cause desquamation (scaly skin syndrome in humans). And enterotoxins which is a heat stable toxin.
For the majority the pathogenesis is multifactorial so its is difficult to determine precisely the role of any given factor. However there are correlations between strains isolated from particular diseases and expressions of particular virulence determinants that suggest the role they had. Normally the host response to staphylococci is inflammation with swelling, accumulation of pus and necrosis of tissue. Around inflamed areas fibrin clots might form, walling off the bacteria and leukocyutes as characteristic pus filled boil or abscess. If the bacteria invade the blood stream this could cause septicemia which might be fatal. Bacteremia may result in seeding other internal abscesses, other skin lesions, or infections in the lung, kidney , heart, skeletal muscles or meninges.
Binding of the Fc portion of antibody to protein a will interfere with phagocytosis. because it binds the wrong way around which interferes with phagocytosis and therefore its not able to bind to white cell receptors. Staphylococcus have a molecule that has complement inhibitor (SCIN) which will inhibit all complement activation pathways. By producing a capsule it prevents the cell interacting with white cells and therefore wont be opsonized and phagocytosed. Fibrinogen binding protein are surface bound proteins that inhibits opsonisation (hiding it from phagpcytosis)
Haemolysins and leukocidin toxins are produced to kill (lyse) or inhibit phagocytosis.