I found your profile and I hope that you can help me with my problem. I am preparing a presentation about Streptococcus pyogenes and while looking for sources I read that the agressive "flesh eating" GAS can kill tissue at a rate of 30cm/h. This seems extremely fast to me and thus I wanted to check some scientific sources. However I didn't find anything regarding this rate.
I hope you could help me here.
Thnx in advance for your answer!
Regards,
Roland (Austria)
Answer I do not know the rate of invasion exactly and I think it differ but you should do your search on articles under Necrotizing fasciitis
The majority of necrotizing soft tissue infections have anaerobic bacteria present, usually in combination with aerobic gram-negative organisms. They proliferate in an environment of local tissue hypoxia in those patients with trauma, recent surgery, or medical compromise.
Facultative aerobic organisms grow since polymorphonuclear (PMN) leukocytes exhibit decreased function under hypoxic wound conditions. This growth further lowers the oxidation/reduction potential, enabling more anaerobic proliferation and, thus, accelerating the disease process.
Carbon dioxide and water are the end products of aerobic metabolism. Hydrogen, nitrogen, hydrogen sulfide, and methane are produced from the combination of aerobic and anaerobic bacteria in a soft tissue infection. These gases, except carbon dioxide, accumulate in tissues because of reduced water solubility.
In necrotizing fasciitis, group A hemolytic streptococci and Staphylococcus aureus, alone or in synergism, are frequently the initiating infecting bacteria. However, other aerobic and anaerobic pathogens may be present, including Bacteroides, Clostridium, Peptostreptococcus, Enterobacteriaceae, coliforms, Proteus, Pseudomonas, and Klebsiella.
Bacteroides fragilis usually is noted as part of a mixed flora, in combination with Escherichia coli. It does not directly cause these infections, but it does play a part in reducing interferon production and the phagocytic capacity of macrophages and PMNs.
A variant synergistic necrotizing cellulitis is considered to be a form of necrotizing fasciitis, but some authorities feel that it is actually a nonclostridial myonecrosis. It begins in the same manner as necrotizing fasciitis, but it progresses rapidly to involve wide areas of deeper tissue and muscle at an earlier stage than might be expected. Severe systemic toxicity occurs.
Anaerobic streptococci, occasionally seen in drug addicts, cause many forms of nonclostridial myonecrosis. Some cases of necrotizing fasciitis can be caused by Vibrio vulnificus. This organism is seen more often in patients with chronic liver dysfunction, and it often follows the consumption of raw seafood. It may cause subcutaneous bleeding.
Necrotizing fasciitis can occur after trauma or around foreign bodies in surgical wounds, or it can be idiopathic, as in scrotal or penile necrotizing fasciitis.
Necrotizing fasciitis also has been referred to as hemolytic streptococcal gangrene, Meleney ulcer, acute dermal gangrene, hospital gangrene, suppurative fascitis, and synergistic necrotizing cellulitis. Fournier gangrene is a form of necrotizing fasciitis that is localized to the scrotum and perineal area.
Necrotizing fasciitis is a progressive, rapidly spreading, inflammatory infection located in the deep fascia, with secondary necrosis of the subcutaneous tissues. Because of the presence of gas-forming organisms, subcutaneous air is classically described in necrotizing fasciitis. This may be seen only on x-ray or not at all. The speed of spread is directly proportional to the thickness of the subcutaneous layer. It moves along the deep fascial plane.
These infections can be difficult to recognize in their early stages, but they rapidly progress. They require aggressive treatment to combat the associated high morbidity and mortality.
The causative bacteria may be aerobic, anaerobic, or mixed flora, and the expected clinical course varies from patient to patient
The patient usually appears moderately to severely toxic, but early on, the patient may look deceptively well.
Typically, the infection begins with an area of erythema that quickly spreads over a course of hours to days.
The redness quickly spreads, and the margins of infection move out into normal skin without being raised or sharply demarcated.
As it progresses, the infection gives way to dusky or purplish skin discoloration near the site of insult.
Multiple identical patches develop to produce a large area of gangrenous skin, as the erythema continues to spread.
The initial necrosis appears as a massive undermining of the skin and subcutaneous layer.
If the skin is open, gloved fingers can pass easily between the 2 layers and may reveal yellowish-green necrotic fascia. If the skin is unbroken, a scalpel incision will reveal it.
The normal skin and subcutaneous tissue are loosened from the rapidly spreading deeper necrotic fascia that is a great distance from the initiating wound.
Fascial necrosis is typically more advanced than the appearance suggests.
Anesthesia in the involved region may be detected, and it usually is caused by thrombosis of the subcutaneous blood vessels, leading to necrosis of nerve fibers.
Without treatment, secondary involvement of deeper muscle layers may occur, resulting in myositis or myonecrosis. Normally, however, the muscular layer remains healthy red with normal bleeding muscle under the yellowish-green fascia.
Usually, the most important signs are tissue necrosis, putrid discharge, bullae, severe pain, gas production, rapid burrowing through fascial planes, and lack of classical tissue inflammatory signs.
There is usually some degree of intravascular volume loss detectable on clinical exam.
There may be general signs, such as fever and severe systemic reactions.
Fournier gangrene begins with local tenderness, edema, and erythema of the scrotal skin.
This progresses to necrosis of the scrotal fascia. The scrotum enlarges to several times its normal diameter.
There can be local crepitation in more than one half of patients.
If the process continues beyond the penile-scrotal region to the abdomen or the upper legs, the normal picture of necrotizing fasciitis can be seen.
In males, the scrotal subcutaneous layer is so thin that most of the patients present after the skin is already exhibiting signs of necrosis.
In 2-7 days, the skin becomes necrotic, and a characteristic black spot can be seen.
Early on, this infection may resemble acute orchitis, epididymitis, torsion, or even a strangulated hernia.
In women, Fournier gangrene acts more like necrotizing fasciitis because of the thicker subcutaneous layers involving the labia majora and the perineum.
Causes:
Surgical procedures may cause local tissue injury and bacterial invasion, resulting in necrotizing fasciitis. These procedures include surgery for intraperitoneal infections and drainage of ischiorectal and perianal abscesses.
IM injections and IV infusions may lead to necrotizing fasciitis.
Minor insect bites may set the stage for necrotizing infections. Streptococci can be introduced into the wounds, but the bacteriologic pattern changes from hypoxia-induced proliferation of anaerobes.
Local ischemia and hypoxia can occur in patients with systemic illnesses (eg, diabetes).
Host defenses can be compromised by underlying systemic diseases favoring the development of these infections. Illnesses such as diabetes or cancer have been described in over 90% of cases of progressive bacterial gangrene.
The number of diabetic patients has been reported to be 20-40%. As many as 80% of Fournier gangrene cases occur in diabetics.
As many as 35% of patients were alcoholics in some series.
Recent studies have shown a possible relationship between the use of nonsteroidal anti-inflammatory agents (NSAIDs), such as ibuprofen, and the development of necrotizing fasciitis during varicella infections. Additional studies are needed to establish whether ibuprofen use has a causal role in the development of necrotizing fasciitis and its complications during varicella infections. This has not previously been described.
http://www.bact.wisc.edu:81/ScienceEd/stories/storyReader$89
good site with pict and references http://woundhealer.com/WndWebPlain/necrotizing_fasciitis.htm
Baker DJ: Selected aerobic and anaerobic soft tissue infections - diagnosis and the use of hyperbaric oxygen. Hyperbaric Medicine Practice 1994; 395-418.
Baracco GJ, Bisno AL: Therapuetic Approaches to Streptococcal Toxic Shock Syndrome. Curr Infect Dis Rep 1999; 1(3): 230-237[Medline].
Brothers TE, Tagge DU, Stutley JE: Magnetic resonance imaging differentiates between necrotizing and non-necrotizing fasciitis of the lower extremity. J Am Coll Surg 1998 Oct; 187(4): 416-21[Medline].
Cullen TS: A progressively enlarging ulcer of abdominal wall involving the skin and fat, following drainage of an abdominal abscess apparently of appendiceal origin. Surg Gynecol Obstet.
Demello FJ, Haglin JJ: Comparative study of experimental Clostridium perfringens infection in dogs treated with antibiotics, surgery, and hyperbaric oxygen. Infect Surg 1983; 73: 936-941.
Eke N: Fournier's Gangrene: A review of 1726 cases. BrJ Surg 2000; 87(6): 718-28[Medline].
File TM, Tan JS: Group A steptococcus necrotizing fasciitis. Compr Ther. 2000; 26(2): 73-81[Medline].
Fink S, Chaudhuri TK, Davis HH: Necrotizing fasciitis and malpractice claims. South Med J 1999 Aug; 92(8): 770-4[Medline].
Fournier A: Gangrene foudroyante de la verge. Semaine Medicale 1883; 3: 345-347.
Fujisawa N, Yamada H, Kohda H: Necrotizing fasciitis caused by Vibrio vulnificus differs from that caused by streptococcal infection. J Infect 1998 May; 36(3): 313-6[Medline].
Hart GB, Lamb RC, Strauss MB: Gas gangrene. J Trauma 1983; (11): 991-1000[Medline].
Hirn M, Niinikoski J, Lehtonen OP: Effect of hyperbaric oxygen and surgery on experimental gas gangrene. Eur Surg Res 1992; 24(6): 356-62[Medline].
Holmstrom B, Grimsley EW: Necrotizing fasciitis and toxic shock- like syndrome caused by group B streptococcus. South Med J 2000; 93(11): 1096-8[Medline].
Hsiao GH, Chang CH, Hsiao CW: Necrotizing soft tissue infections. Surgical or conservative treatment? Dermatol Surg 1998 Feb; 24(2): 243-7; discussion 247-8[Medline].
Jones RB, Hirschman JV, Brown GS: Fournier's syndrome: necrotizing subcutaneous infection of the male genitalia. J Urol 1979; 122: 279-282[Medline].
Kaul R, McGeer A, Low DE: Population-based surveillance for group A streptococcal necrotizing fasciitis: Clinical features, prognostic indicators, and microbiologic analysis of seventy-seven cases. Ontario Group A Streptococcal Study. Am J Med 1997 Jul; 103(1): 18-24[Medline].
Lamerton AJ: Fournier's gangrene: non-clostridial gas gangrene of the perineum and diabetes mellitus. J R Soc Med 1986; 79: 212-215[Medline].
Mader JT: Mixed anaerobic and aerobic soft tissue infection. In: Problem Wounds: The Role of Oxygen. 1988: 173-186.
McGeehan DF, Asmal AB, Angorn IB: Fournier's gangrene. S Afr Med J 1984; 66: 734-737[Medline].
Meleney FL: Hemolytic streptococcus gangrene. Arch Surg 1924; 9: 317-364.
Mohammedi I, Ceruse P, Duperret S: Cervical necrotizing fasciitis: 10 years' experience at a single institution. Intensive Care Med 1999 Aug; 25(8): 829-34[Medline].
Niinikoski J, Aho A: Combination of hyperbaric oxygen, surgery and antibiotics in the treatment of clostridial gas gangrene. Infect Surg 1983; 2: 23-27.
Nomikos IN: Necrotizing perineal infections (Fournier's disease): old remedies for an old disease. Int J Colorectal Dis 1998; 13(1): 48-51[Medline].
Reyzelman AM, Armstrong DG, Vayser DJ: Emergence of non-group A streptococcal necrotizing diabetic foot infections. J Am Podiatr Med Assoc 1998 Jun; 88(6): 305-7[Medline].
Riseman JA, Zamboni WA, Curtis A: Hyperbaric oxygen therapy for necrotizing fasciitis reduces mortality and the need for debridements. Surgery 1990 Nov; 108(5): 847-50[Medline].
Somers WJ, Lowe FC: Localized gangrene of the scrotum and penis: a complication of heroin injection into the femoral vessels. J Urol 1986; 136: 111-113[Medline].
Sriskandan S, Kemball-Cook G, Moyes D: Contact Activation in shock caused by invasive group A Streptococcus Pyogenes. Crit Care Med 2000; 28(11): 3684-91[Medline].
Stephenson H, Dotters DJ, Katz V: Necrotizing fasciitis of the vulva. Am J Obstet Gynecol 1992; 166: 1324-1327[Medline].
Stevens DL, Bryant AE, Adams K: Evaluation of therapy with hyperbaric oxygen for experimental infection with Clostridium perfringens. Clin Infect Dis 1993 Aug; 17(2): 231-7[Medline].
Wysoki MG, Santora TA, Shah RM: Necrotizing fasciitis: CT characteristics. Radiology 1997 Jun; 203(3): 859-63[Medline].
Zamboni WA, Mazolewski PJ, Erdmann D: Evaluation of penicillin and hyperbaric oxygen in the treatment of streptococcal myositis. Ann Plast Surg 1997 Aug; 39(2): 131-6[Medline].
Zerr DM, Alexander ER, Duchin JS: A case-control study of necrotizing fasciitis during primary varicella. Pediatrics 1999 Apr; 103(4 Pt 1): 783-90[Medline].
Zerr DM, Rubens CE: NSAIDS and necrotizing fasciitis [In Process Citation]. Pediatr Infect Dis J 1999 Aug; 18(8): 724-5[Medline].
Zurawski CA, Bardsley M, Beall B: Invasive group A streptococcal disease in metropolitan Atlanta: a population-based assessment. Clin Infect Dis 1998 Jul; 27(1): 150-7[Medline].
sorry I do not have the rate of extention but when it is an emmergency and critical usually who cares of the rate we know that the patient can die within the 24h
thanks
dan
