Staphylococcus and Streptococcus. Nightmare bacteria. Super bugs. Flesh eating bacteria. Streptococcal necrotizing fasciitis. MRSA. Common characteristics. Staphylococcus. Streptococcus. Gram positive cocci Facultative anaerobes Non-sporing, non-motile Important pathogens
Flesh eating bacteria
DNAse agar. Not definitive
S. aureus Infections
Impetigo: A contagious skin infection that is characterized by the eruption of superficial pustules and the formation of thick yellow crusts, commonly on the face.
Septicaemia: blood poisoning caused by pathogenic microorganisms and their toxic products in the bloodstream
Osteomyelitis: infection of bone and bone marrow in which the resulting inflammation can lead to a reduction of blood supply to the bone
Interferes with phagocytosis
2. Staphylococcal complement inhibitor (SCIN) inhibits complement activation -
3. Capsule production
Inhibits all complement (C’)
Activates and binds complement, but not opsonised or phagocytosed
4. Fibrinogen binding protein -surface bound fibrinogen
5. Haemolysins and leukocidin
Inhibit or lyse phagocytesStaphylococcal resistance to phagocytosis
Pyogenic infections following penetration of skin, boils etc –many species.
Exfoliative skin diseases.
Scalded skin syndrome
Greasy pig disease
Stimulate 2-20 % of T cells
Stimulate < 0.01% of T cells
Massive release of pro-inflammatory cytokines
Superantigens (SAgs) are a class of antigens which cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release. SAgs can be produced by pathogenic microbes as a defense mechanism against the immune system.
S.aureus and Streptococcus pyogenes produce many SA
Toll-like receptors (TLRs)
Toll-like receptors (TLRs) are a class of proteins that play a key role in the innate immune system. They recognize structurally conserved molecules derived from microbes. Once these microbes have breached physical barriers such as the skin or intestinal tract mucosa, they are recognized by TLRs which activates immune cell responses.
LPS, lipid A
Juliane Bubeck Wardenburg, Wade A. Williams, and Dominique MissiakasHost defenses against Staphylococcus aureus infection require recognition of bacterial lipoproteinsPNAS 2006 103: 13831-13836
S.aureus mutant can not make lipoproteins
Infection of mice
S.aureus mut 20%
Superficially grouped based on their growth on blood agar plates into:
Lansfield serologic typing – place streptococci in 22 (Lansfield) groups (A-V), based on differences in carbohydrate antigen in cell wall. Use antisera against different antigens to type.
Host cross-reactive epitopes
Factor H binding
(destroy C3 convertase and preventing opsonization)
S. agalactiae 2%
S. dysgalactiae 7%
S. uberis 28%
Staphylococcus aureus 25%
E. coli 25%
Opportunistic e.g. 2° respiratory infections; wound; metritis; etc.
Infects various host species: cattle, sheep, dogs, etc.
Fever, swollen lymph nodes, discharge - STRANGLES
Septicaemia (fatal) - BASTARD STRANGLES
Quarantine & antibiotic treatment
Two M-like proteins-SeM, SzPSe
SzPSe present in S.zooepidemicus
SeM more important
Hyaluronic acid capsule
Streptolysin S (SLS)-like toxin, anti-phagocytic
Virulence factors of S.equi
Intervet Equilis StrepE.
Live genetically modified S.equi vaccine, S.equi aro mutant
Administer inside upper lip.
Canine toxic-shock syndrome. An emerging disease?
Symptoms of toxic shock syndrome vary depending on the underlying cause. Typically characterized by high fever, accompanied by low blood pressure, malaise and confusion, which can rapidly progress to coma, and multi-organ failure.