Group A Strep: the Flesh-Eating Bacteria Living in our Throats

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Group A Streptococcus is a gram positive bacterium that resides in our nose, throat and skin. It can cause a wide range of health complications from minor infections like pharyngitis to exacerbations, such as the fastest moving form (type II) of necrotising fasciitis. [1]

Necrotising: causing the death of tissue and the failure of blood supply

Fasciitis: inflammation of muscle/organ fascia

   Necrotising fasciitis is a rare invasive infection affecting approximately 500 people a year. It occurs when the bacteria living in your throat embed themselves in deep tissue through a break in the skin e.g. an insect bite or even an injection site. It is important to note that the bacteria cause no harm where they colonise, but only when introduced to the new environment of deep tissue. Whilst presenting itself as harmful for all, those suffering from conditions weakening their immune system are more susceptible to necrotising fasciitis. Subsequently the elderly, the young and those suffering from diabetes, kidney disease, HIV or cancer must take more pre-emptive measures to avoid contracting the infection – treat wounds promptly and wash hands frequently and regularly. [2] [3]

   Necrotising fasciitis is often known as the ‘flesh-eating disease’, however, the name is thought of as misleading; group A Streptococcus does not literally eat your flesh but instead releases toxins and enzymes that result in thrombosis in the blood vessels – destroying soft tissue, subcutaneous tissue (beneath skin) and fascia. This ischaemia leads to eventual necrosis of the tissue. As the infection begins in the fascial layers, the initial spread is horizontal – it cannot be seen; it is not apparent. It is then followed by vertical spread down to deep tissue and up to the skin, making the infection obvious to the human eye. [4] [5]

   Due to the unapparent physical symptoms at the site of the wound, diagnosis can be delayed. However, in the initial hours of contracting the infection, other classic symptoms develop – a high fever and severe pain disproportionate to the wound. These progress into swelling, redness, blisters and diarrhoea in the following couple of days. At this point, prompt medical attention is required, but if still untreated the symptoms deteriorate further to dizziness, weakness and confusion.

   Diagnosis of the infection is difficult; especially in the early stages as it mimics cellulitis. As a result, it can only be confirmed by a tissue biopsy to identify grey necrotised tissue and thrombosis in the vessels. However, with a high degree of suspicion, presence of bullae (sac of fluid – blister) in an x-ray can be diagnostic, yet surgical exploration must be undergone to clear conjecture.

   The infection can also present itself as a secondary form of varicella (chicken pox), developing in 1% of children. Despite being extremely rare, the monobacterial infection is developed in immunocompetent children after group A Streptococcus invades the skin lesions. Necrotising fasciitis as the cause of fever in children with chickenpox is suspected when the child does not respond to orally ingested antibiotics that treat cellulitis. [6]  

   Treatment of the infection takes the form of IV antibiotics that directly attack the effected bloodstreams. However, this is sometimes inadequate, as too much tissue in the effected areas has been killed – reducing blood flow, and so perfusion of the antibiotics. Subsequently, the patient has to undergo surgery to remove the blockades of decayed tissue. There are many cases that result in amputations due to the large amounts of affected tissues that must be removed in order to avoid further spread. Necessary surgery to remove all traces of the infection is later followed by additional surgeries to alter the appearance of damaged areas. The patients are subsequently left with long-term disabilities and need to undergo continuous rehabilitation courses. Despite spread between people being very rare (most cases occur randomly), patients are still isolated from others immediately after treatment to avoid any risk of further destruction.

   However, despite copious surgeries, necrotising fasciitis carries a high mortality rates of 20-40% for previously healthy patients, and sometimes even higher for those that had a delayed diagnosis or suffered from diabetes. The fast progressing infection can often lead to sepsis or organ failure. An example of this is a case in Florida; a man had 25% of his skin removed after 3 consecutive surgeries to prevent spread, but still died in hospital 8-9 days later. Patients that simultaneously contract streptococcal toxic shock syndrome (low blood pressure and multiple organ failure as the body goes into shock) as a result of the group A Streptococcus infection have a 4/10 chance of survival. [7]  

  Despite the small chance of contracting this rare infection, it is important to educate ourselves to its existence due to the severe complications it causes – awareness can only be beneficial.


References

  1. “Necrotizing Fasciitis: All You Need to Know”, Centers for Disease Control and Prevention, https://www.cdc.gov/groupastrep/diseases-public/necrotizing-fasciitis.html , Dec. 31, 2019
  2. Dr. Colin Tidy, “Necrotising Fasciitis”, Patient, https://patient.info/doctor/necrotising-fasciitis-pro , Jul. 29, 2015
  3. “Necrotising Fasciitis”, NHS, https://www.nhs.uk/conditions/necrotising-fasciitis/ , Apr. 10, 2019
  4. Vanesa Ngan, “Necrotising Fasciitis”, DermNet NZ, https://dermnetnz.org/topics/necrotising-fasciitis/ , 2003
  5. “Necrotising Fasciitis (Soft Tissue Inflammation)”, Healthline, https://www.healthline.com/health/necrotizing-soft-tissue-infection
  6. Dr. Rose Xavier, “Early diagnosis of post-varicella necrotising fasciitis: A medical and surgical emergency” , NCBI, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4955452/ , Mar. 2016
  7. Rachael Rettner, “Man Has 25% of His Skin Removed to Treat ‘Flesh-Eating’ Infection”, Live Science, https://www.livescience.com/flesh-eating-bacteria-skin-removed.html , Aug. 27, 2019

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