01. Introduction
02. Gram-Positive Cocci
03. Gram-Positive Bacilli
04. Gram-Positive Branched Filaments
05. Gram-Negative Diplococci
06. Gram-Negative Bacilli
07. Gram-Negative Coccobacilli
08. Additional Bacteria
09. RNA Viruses
10. DNA Viruses
11. Fungi
12. Opportunistic Fungi
13. Protozoa (single-celled eukaryotes - small parasites)
14. Helminths (parasitic worms - large macroparasites)
15. Prions

2.03 Streptococcus pyogenes

Streptococcus pyogenes – Audio and Lecture Notes – Click to Expand

Streptococcus pyogenes is a catalase-negative, beta haemolytic gram-positive cocci. Strep pyogenes is a Lancefield Group A Streptococcus. They appear as gram-positive cocci in chains. 

Another beta haemolytic gram-positive coccus is Streptococcus agalactiae, we differentiate the two by the fact that Strep pyogenes is bacitracin sensitive, whilst Strep agalactiae is bacitracin resistant.


Its virulence factors include:

    • Streptolysin O (oxygen labile): form pores in host cells including immune cells such as macrophages, neutrophils as well as epithelial cells; ultimately leading to the death of these cells.

Anti-streptolysin O (ASO) antibodies are an important part of identifying Strep pyogenes. As an ASO positive titre helps to confirm prior Strep pyogenes infection.

    • Streptolysin S (oxygen Stable) - causes the destruction of red blood cells, white blood cells and platelets as well as epithelial cells; it is thought to be responsible for the beta-haemolytic phenotype of Strep pyogenes.
    • M protein - aids in strep pyogenes’ resistance to phagocytosis, in the formation of its micro-colonies, and its attachment to keratinocytes and invasion of various epithelial cells. 
    • DNase - plays a role in degrading DNA. Immune cells e.g. neutrophils are responsible for trapping and destroying bacteria. One of the ways this is done is through the production of extracellular traps - mainly composed of DNA. DNase allows Strep pyogenes to disarm such traps. 
    • Streptokinase - enables the conversion of plasminogen to plasmin, which ultimately causes clot breakdown aka fibrinolysis. 
    • Hyaluronidase - facilitates bacteria invasion by breaking down the host connective tissue

Strep pyogenes can be found as part of the normal flora of the oropharynx or the skin. Transmission is via respiratory droplets or direct contact (through a break in the skin barrier).


Strep pyogenes may cause harm through 3 avenues: these are direct infection, toxin release, or via a delayed immune-mediated pathology.  


Focusing on direct infection.

Strep pyogenes may infect the pharynx via respiratory or food transmission, resulting in pharyngitis aka Strep throat; this infection can then spread to the ears, causing otitis (aka ear infection), or to the CNS causing - meningitis (aka inflammation of the meninges).

Strep throat is a common infection in children. 

Strep pyogenes may also directly infect the skin, gaining entry via any breaks in the skin. This results in: 

    • Cellulitis - is a bacterial infection of the lower dermis and subcutaneous tissue, 
    • Erysipelas - which is a superficial form of cellulitis, affecting the upper dermis, it presents with sharper borders around inflamed skin area, 
    • Impetigo - is a superficial skin infection often described as honey coloured crusted plaques; non-bullous impetigo is typically caused by Staph Aureus and Streptococcus pyogenes and presents on the face. 

It’s important to remember that Strep pyogenes pharyngitis or skin infections may self-limit; without leading to the pathologies of toxin release or the immune system.


Focusing on diseases caused by toxin release. The three major diseases associated with toxin release are: scarlet fever, necrotising fasciitis and toxic shock syndrome. 

Scarlet fever may follow Strep throat (aka Strep pyogenes pharyngitis) in which exotoxin A, B and C have been released. Clinical presentation includes:

    • Fever, 
    • A diffuse ‘sandpaper’ rash that blanches on pressure. The rash spreads from the trunk outwards, usually sparing the palms, soles and face. The rash may persist for around 1 week.
    •  Once the rash resolves, palm and sole desquamation (peeling off) may occur. 
    • The face may flush, with the pallor observed around the mouth - termed circumoral pallor. 
    • Initially, the tongue may be covered in a yellowish-white coating with red papillae (i.e. red dots on a white tongue); this will eventually disappear, leaving a ‘strawberry tongue’ appearance (i.e. multiple raised circular areas on a red tongue).

Scarlet fever typically occurs in children under the age of 10, as many adults would have developed immunity from their own childhood exposure.

Necrotising fasciitis may occur when the bacteria are introduced into the fascia surrounding muscles. This is done either through surgery or trauma. The toxin which causes this, is a protease exotoxin B. 

Necrotising fasciitis causes rapid necrosis of the fascia planes, it typically presents with muscle preservation (although remember that necrotising fasciitis may also be caused by compartment syndrome, in which case myonecrosis/muscle involvement is prominent). 

Toxic shock syndrome may follow Strep pyogenes skin infection; where the toxin involved is exotoxin A. Clinical presentation includes fever, rash, shock; and subsequent organ hypoperfusion and failure. 


Focusing on delayed immune-mediated pathologies, previous Strep pyogenes infection may result in the formation of antibodies 2-3 weeks following the original infection. 

Antibodies are generated by the body against Strep pyogenes, following Strep throat or skin infection; these antibodies can come together to generate immune complexes that deposit at the glomerular basement membrane of the kidneys. Therefore leading to renal pathologies that include glomerular inflammation and ultimately glomerulonephritis. 

Glomerulonephritis presents as haematuria, hypertension and periorbital oedema.


Untreated, Strep throat may also result in anti-streptococcal antibodies attacking host tissue, mistaking the body’s antigens for those of invading pathogens. This leads to inflammation of the attacked host tissue i.e. joint tissue, heart tissue. This is termed Rheumatic fever, and can be diagnosed using the ‘Jones Criteria’.

‘Jones’ is also a mnemonic for the most common presentations of Rheumatic fever. It stands for:

    • Joints involvement
    • Heart valvular damage, and carditis
    • Nodules (subcutaneous)
    • Erythema marginatum
    • Sydenham chorea

Remember that attacks on heart tissue and the subsequent valvular damage, can later be exploited and colonised by other bacteria, such as Streptococcus Viridans and Enterococcus bacteria, to cause endocarditis.


Strep pyogenes is treated using penicillin, alternatively, antibiotics include azithromycin or clindamycin.

Additionally, in necrotising fasciitis, clindamycin may be added to penicillin treatment to reduce further toxin release and reduce bacterial load. 

Early, and prompt surgical debridements play a crucial role in treating necrotising fasciitis (along with medical treatment). 


Finally, with immune-related pathologies of Strep pyogenes, preventing further cardiac complications is key to managing the condition, as such, penicillin is given prophylactically to Rheumatic Fever patients - or those with a history of Rheumatic Fever. 


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