Staphylococcus aureus – Epidemiology, Pathogenesis & Treatment

Introduction

The genus name Staphylococcus refers to the gram-positive cocci that grow in a pattern resembling a cluster of grapes.
The cell wall of staphylococci is rich in peptidoglycan similar to a typical gram-positive cell wall.
- Have ribitol-teichoic acid interspersing the peptidoglycan molecules.
- Have antigenic property.
Other than peptidoglycan, surface proteins such as protein A are present.
- It uniquely binds to the Fc portion of the IgG antibody, and the antigen reacting Fab region is left externally. which interferes in the process of opsonization.
On blood agar, S. aureus forms white color colonies, which later turn into golden in color.
- Most strains show hemolysis.
Coagulase Positive (S. aureus).

- These proteins are secreted by all staphylococcal strains, the exception is coagulase-negative ones.
- It gets inserted in the lipid bilayer and forms pores which cause lysis of cytoplasmic membranes,
  - It leads to cell death.

The skin epidermal layer has intercellular junctions, exfoliatin disrupts these junctions splitting the epidermis between stratum granulosum & stratum spinosum.

These secreted proteins produced by staphylococci trigger systemic symptomatic effects.
Strongly mitogenic (protein inducing mitosis) for T cells.
They associate themselves with MHC II molecules, externally and show specificity for T cell’s V β region.
It triggers the large production of cytokines such as interleukins-1, and tumor necrosis factors by T cells & macrophages.

It targets the gastrointestinal tract and induces related symptoms such as vomiting.
Several antigenically variants are known such as enterotoxin A, B, C; they are low molecular weight proteins.
Toxins are stable even after getting exposed to acidic gastric & jejunal enzymes and also even after boiling.
They directly act on neural receptors present in the upper gastrointestinal tract, leads to vomiting.

It’s a leading cause of staphylococcal toxic shock syndrome, and its properties are very similar to staphylococcal enterotoxins.
Triggers the release of the cytokines, here superantigens mechanisms are involved.
It also causes hypotension, capillary leakage & shock.

S. aureus is a common microorganism present in normal human microbiota of the skin, nasal carriers.
They are opportunistic pathogens.
Community outbreaks are usually seen where there is poor hygiene maintained, even fomite transmissions between individuals are the source of infection.
Even nosocomial infections are recurrent can be spread from hospital personnel.

Colonization is mediated by surface proteins, which binds to the host elements, which can be tissues or foreign parts like catheters.
- Proteins bind to collagen, fibronectin & fibrinogens.
The initiation of infection is induced by any trauma, foreign matter.
There are some factors such as protein A that interfere in phagocytosis.
- It binds to the Fc region of IgG, competes with phagocytes, by which opsonization is interrupted.
Coagulase production, retard the migration of the phagocytic cells & lysosomal killing is resisted.
The lesion is formed due to an acute inflammatory response. or maybe due to fibrotic reactions of the host cells to the toxins.
- The process depends on localization by the host which varies with tissues involved.
- On the skin, it may appear as a boil which may include fibrosis & granulation.
- On other organs such as lungs, kidneys, it may spread with a small focus area then may involve broad areas.
Cytotoxins involved are more destructive, which causes massive necrosis.
In severe cases, infections may enter the bloodstream and cause more damage.
- Organisms may shed its component, which leads to massive complement activation, septic shock syndrome, leukopenia.

The primary infection serves as the initial site of toxin absorption.
As it is seen in staphylococcal food poisoning, pyrogenic exotoxins are the cause of illness rather than the microorganisms involved.
The exfoliative toxin, cause blister-like epidermal separation, localized at the skin region.
In Staphylococcal scalded skin syndrome, it is caused by a toxin, by which epithelial desquamation occurs.
In Staphylococcal, TSS (Toxic Shock Syndrome), is a pyrogenic exotoxin TSST-1, which stimulates the release of superantigen-mediated cytokine. e.g., Menstruation related TSS, a combined effect of menstruation and high absorbing tampon, which favors the growth of staphylococci and toxin production is enhanced.

Disease	Manifestations
Primary Infections	Manifestations
Furuncle and Carbuncle	Furuncle or boils develops in hair follicles, sweat glands, infections are only restricted to superficial skin. Carbuncle, involved in subcutaneous tissues, may invade the bloodstream.
Chronic Furunculosis	Reoccurrence of the boils, may involved inflammation & necrosis, suppress host immunity.
Impetigo	Skin pustules. Large blisters are formed in the superficial layer of the skin. If Exfoliatin is involved, which forms bullous impetigo, also known as localized scalded skin syndrome.
Deep Lesions	Skin lesions caused by S. aureus may invade the bloodstream causing bacteremia. Acute osteomyelitis in children is caused by S. aureus. Deep tissues lesions in pneumonia are highly destructive.
Toxin mediated disease
Scalded Skin Syndrome	It’s due to the production of exfoliatin in lesions caused by staphylococcus. Desquamation of epidermal skin and erythema is observed. Children and neonates are more prone to it.
Toxic Shock Syndrome	Involve symptoms like vomiting, high fever, sore throat, & muscle pain. After 48 hrs, it may progress into a severe form that involves hepatic & renal damage. Severe skin desquamation.
Staphylococcal Food Poisoning	Acute vomiting & diarrhea in 1- 5 hrs of consumption of food containing the toxin.

Pyogenic infections by staphylococcal can be detected by microscopy.
In nonselective media, S. aureus grows rapidly, but to obtain this microorganisms from the contaminated specimens, mannitol salt agar is used, which is a selective media.
Even blood agar can be used for isolation of S. aureus.

Localized skin infection is managed by minor incision & drainage.
Oral Therapy includes doxycycline, minocycline, trimethoprim-sulfamethoxazole, vancomycin (intravenous therapy).
Proper cleaning of the infected wounds by disinfectants.
Hand Washing & covering exposed wounds are preventative measures that can be followed.

https://www.researchgate.net/publication/11386423_Staphylococcal_Exfoliative_Toxin_B_Specifically_Cleaves_
Desmoglein_1
https://acikders.ankara.edu.tr/mod/resource/view.php?id=59091
https://www.researchgate.net/publication/14643895_Localization_of_biologically_important_regions_on_toxic
_shock_syndrome_toxin
https://microbenotes.com/staphylococcus-epidermidis/
https://www.ncbi.nlm.nih.gov/books/NBK8477/
http://www.textbookofbacteriology.net/staph.html
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923430/

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