Role of group A streptococcal virulence factors in adherence to keratinocytes. Hyaluronic acid capsule and the role of streptococcal entry into keratinocytes in invasive skin infection. Characterization of a mouse-passaged, highly encapsulated variant of group A streptococcus in in vitro and in vivo studies. Molecular analysis of the role of the group A streptococcal cysteine protease, hyaluronic acid capsule, and M protein in a murine model of human invasive soft-tissue infection.
Hyaluronic acid capsule modulates M protein-mediated adherence and acts as a ligand for attachment of group A streptococcus to CD44 on human keratinocytes. CD44 as a receptor for colonization of the pharynx by group A streptococcus. Group A Streptococcus tissue invasion by CDmediated cell signalling. Critical role of the group A streptococcal capsule in pharyngeal colonization and infection in mice. Rheumatic fever-associated Streptococcus pyogenes isolates aggregate collagen.
Molecular characterization of hasA from an operon required for hyaluronic acid synthesis in group A streptococci. A response regulator that represses transcription of several virulence operons in the group A streptococcus.
Spontaneous mutations in the CsrRS two-component regulatory system of Streptococcus pyogenes result in enhanced virulence in a murine model of skin and soft tissue infection.
Virulence control in group A streptococcus by a two-component gene regulatory system: global expression profiling and in vivo infection modeling. The association of lipoproteins with the inhibition of streptolysin S by serum.
Cytocidal effect of Streptococcus pyogenes on mouse neutrophils in vivo and the critical role of streptolysin S. Environmental regulation of virulence in group A streptococci: transcription of the gene encoding M protein is stimulated by carbon dioxide. Use of DNA arrays to identify a mutation in the negative regulator, csrR, responsible for the high virulence of a naturally occurring type M3 group A streptococcus clinical isolate.
Longitudinal analysis of the group A streptococcus transcriptome in experimental pharyngitis in cynomolgus macaques. Temporal changes in streptococcal M protein types and the near-disappearance of acute rheumatic fever in the United States. Protective immunity evoked by locally administered group A streptococcal vaccines in mice.
Bacterial determinants of persistent throat colonization and the associated immune response in a primate model of human group A streptococcal pharyngeal infection. Studies of the carrier state following infection with group A streptococci.
Effect of climate. Infectivity of streptococci isolated during acute pharyngitis and during the carrier state. Safety and immunogenicity of valent group A streptococcus vaccine in healthy adult volunteers. The epidemiology of invasive group A streptococcal infection and potential vaccine implications: United States, — Issue Section:.
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Physician-Scientist Faculty Position. Infectious Disease Physician. Senior Clinician. Infections of the skin are only associated with the acute glomerular nephritis Streptococcal infections should be treated to limit secondary complications Outbreaks of pharyngitis and impetigo in school-age children or in group settings are common There has also been more recent interest in healthcare-associated clusters in the long-term care facility setting, where there have been growing cases identified 8, 9, Given the infrequency of these infections and the lack of a clearly effective chemoprophylaxis regimen, the available data do not support a recommendation for routine testing for GAS colonization or for routine administration of chemoprophylaxis to all household contacts of persons with invasive GAS at this time.
However, in some situations, prophylaxis may be recommended for someone who is exposed to someone with an invasive group A streptococcal infection i. That decision should be made after individual patients talk with their doctors 7, 11, Given the rise in cases in those 65 years of age and older and living in long-term care facilities, additional controls in these populations, including larger scale prophylaxis, may warrant discussion but is now not common practice 7, The global strategies for prevention of GAS on a larger scale remain complex HCWs should wear gloves and gowns for contact with the skin of patients with major lesions, wounds, and purulent discharge.
Place the patient in a private room. When a private room is not available, place the patient in a room with a patient s who also has infection with Streptococcus pyogenes cohorting. Discard the gloves after use and wash hands thoroughly between patient contacts. Contact isolation may be discontinued after 24 hours of directed antistreptococcal therapy For GAS infections that involve the pharynx and respiratory tract, such as pneumonia and scarlet fever in infants and children, HCWs should use standard and droplet precautions, including use of a surgical mask when working within 3 feet 1 meter of the patient.
Logistically, some hospitals may want to implement the wearing of a mask to enter the room of affected patients. When a private room is not available, cohorting should be used.
When a private room is not available and cohorting is not achievable, maintain spatial separation of at least 3 feet 1 meter between the infected patient and other patients and visitors. Special air handling and ventilation are not necessary, and the door may remain open 7, 12, HCWs who are known or suspected to have infection or colonization of their respiratory tract with Streptococcus pyogenes should wear a mask to reduce respiratory spread of their organism Newer typing modalities, including whole — genome sequencing compared to traditional pulsed field gel electrophoresis [PFGE] may be needed to elucidate epidemiology in some clusters.
Even though the Lancefield M protein serotyping system over the past 60 years has been very valuable, in recent years the inherent difficulties encountered in expanding this system through conventional serologic procedures have become increasingly evident.
Using a less demanding sequence based system that is predictive of Lancefield M serotypes emm typing , specialized labs such as the U. It can be carried in the pharynx, skin, vagina, and rectum asymptomatically. There are a wide variety of clinically presentations of GAS. Although the most common GAS infections are mild i. Patients who do not respond to antimicrobial therapy or who have impaired respiratory function may require surgical incision and drainage under general anesthesia.
Duration of therapy should be 10 days. O titis Media and Sinusitis: Otitis media and sinusitis due to group A streptococcus normally are secondary to direct extension from a streptococcal infection occurring in the upper respiratory tract. Appropriate therapy for both is amoxicillin. In patients allergic to amoxicillin, erythromycin or clindamycin is an acceptable alternative. Oral cephalosporins can be effective as well in patients who have not had immediate hypersensitivity reactions to penicillin.
U vulitis : Uvulitis can occur alone or in association with acute pharyngitis or epiglottitis Long known to be primarily a complication of H. However, uvulitis can occur secondary to group A streptococcus, usually as a complication of an acute pharyngitis Parenteral therapy should be used, directed against both group A streptococcus and H.
Patients can be discharged on an oral antibiotic to complete a 10 day course of therapy. C ervical Lymphadenitis: Cervical lymphadenitis secondary to group A streptococcus infection can result from direct extension from an acute pharyngitis or direct inoculation.
Since the etiologic agent is not always known, therapy is initially directed against the most common organisms, which include S. If the infection persists or the patient develops signs of systemic toxicity, parenteral antibiotics should generally be used. First generation cephalosporins such as cefazolin , nafcillin , or clindamycin are also appropriate choices. M eningitis and Brain Abscess: Meningitis and brain abscesses are rare complications of group A streptococcus that can occur either from direct extension of acute pharyngitis or sinusitis or from bacteremic spread.
Penicillin is still the drug of choice for treatment of known group A streptococcal meningitis or brain abscess Antimicrobial therapy should be given parenterally for 10 to 14 days Patients allergic to penicillin can be treated with a third generation cephalosporin such as ceftriaxone or cefotaxime A rthritis: Post-streptococcal reactive arthritis PSRA is a recognized complication of group A streptococcal infections. Antibiotic therapy aimed at the underlying focus of infection is generally all that is required.
However, anti-inflammatory drugs may aid patient comfort. Of concern, is the risk that a subset of patients with PSRA may develop rheumatic heart disease. This has led some to suggest that patients with PSRA, like patients who have had ARF, may require antimicrobial prophylaxis to prevent the occurrence of rheumatic heart disease It has been recommended that these patients receive prophylaxis for 1 year, and then if no evidence of rheumatic heart disease develops, prophylaxis could be discontinued Septic arthritis secondary to group A streptococcal infection can result from direct inoculation or bacteremic spread.
Therapy consists of parenteral antibiotics given for 10 to 14 days. Choices include a third generation cephalosporin, such as ceftriaxone and cefotaxime , or beta lactams such as nafcillin or penicillin.
In addition, surgical drainage of purulent material from the joint space is required. E ndocarditis: Endocarditis due to group A streptococcus was relatively common during the preantibiotic era. However, it is now rarely seen. Therapy aimed at the most common organisms in endocarditis also provides coverage for group A streptococcus and should be continued for 4 to 6 weeks. Patients with known GAS endocarditis have been treated successfully with 6 weeks of parenterally administered penicillin O steomyelitis : Like septic arthritis, osteomyelitis secondary to group A streptococcal infection is known, but rare.
Therapy consists of appropriate antimicrobials given parenterally to control the infection. If group A streptococcus has been identified as the etiologic agent, penicillin can be used. Patients allergic to penicillin can be treated with clindamycin , vancomycin , or cefazolin. L iver Abscess: Liver abscesses secondary to group A streptococcal infection generally result from hematogenous spread. Therapy consists of long term parenterally administered penicillin and surgical drainage.
Initially, until an etiologic agent has been determined, a combination of a penicillinase-resistant penicillin, such as nafcillin , and an aminoglycoside should be used. Treatment should consist of 2 to 4 weeks of parenterally administered antibiotics followed by oral antibiotics to complete a 4 week course.
Patients allergic to penicillin can be treated with clindamycin , vancomycin , or an appropriate first generation cephalosporin. Non-Suppurative Complications. A cute Rheumatic Fever: Treatment of patients with acute rheumatic fever is generally directed toward decreasing acute inflammation, decreasing fever and toxicity, controlling cardiac failure, preventing episodes of recurrent ARF after significant streptococcal upper respiratory tract infections, and preventing rheumatic heart disease.
The mainstays of treatment are salicylates and corticosteroids. Neither of these agents prevents or modifies the development of rheumatic heart disease. Patients clinically diagnosed with ARF who have not received antimicrobial therapy for a recent episode of GAS pharyngitis should receive a 10 day course of penicillin. P rimary prevention of ARF depends on accurate diagnosis of an antecedent streptococcal infection as well as adequate therapy.
Penicillin given orally for 10 days or intramuscularly one time will prevent rheumatic fever. Erythromycin is considered the drug of choice f the treatment of GAS pharyngitis in penicillin-allergic patients, but it has not been shown to prevent ARF Approximately one third of patients who develop ARF have streptococcal infections that are either subclinical or too mild to be brought to medical attention; as a result, they receive no antibiotic therapy for the infection.
In contrast, in the past, preceding streptococcal infections were noted to be severe Of even more concern are reports of patients who develop ARF despite receiving adequate therapy for GAS pharyngitis Possible explanations for this include poor patient compliance with antibiotic therapy, a shorter latency period, documented streptococcal infections were not the cause of the resultant episodes of ARF, or currently recommended therapies for GAS pharyngitis have become inadequate for prevention of ARF The last is of greatest concern.
These studies were conducted during the s on army recruits at Fort Warren, Wyoming. Penicillin G suspended in oil, administered parenterally in a placebo-controlled study, decreased the incidence of ARF Following these studies, researchers compared orally administered penicillin with parenterally administered penicillin and found equivalent bacteriologic effects.
It was then assumed that bacterial eradication from the pharynx was the necessary step in prevention of ARF. As a result, penicillins as a class were assumed to be efficacious in preventing ARF.
This has never been studied. No study has investigated the efficacy of other antibiotics in prevention of ARF. P atients who develop ARF require continuous prophylaxis to prevent intercurrent and recurrent streptococcal infections and recurrent episodes of ARF. The preferred regimen consists of penicillin G benzathine, 1. The recurrence rate of ARF with this regimen was reported to be 0. Both of these regimens are considered less effective than penicillin G benzathine.
This is thought to be due to lack of patient compliance with an oral regimen. Patients who are allergic to penicillin can be treated with erythromycin stearate mg, twice a day 8. Considerable debate has arisen over the optimal duration of prophylaxis. Some investigators previously recommended lifelong prophylaxis.
However, the risk of recurrence of ARF decreases with patient age and the number of years since the last attack and increases with the presence of rheumatic heart disease or previous recurrences. The physician must take into account all factors when deciding when to discontinue prophylaxis. In general, it is recommended that prophylaxis continue until patients are in their early twenties and at least 5 years have passed since the most recent episode of ARF. The committee recommended that patients who had rheumatic fever without rheumatic carditis should receive prophylaxis until the age of 21 or until at least 5 years had passed since their last attack.
Patients who had rheumatic fever with carditis but no valvular disease should receive prophylaxis until adulthood and until at least 10 years had passed since their last attack of ARF.
Patients with valvular disease should receive prophylaxis until age 40 and until at least 10 years had passed since their last attack Patients with residual rheumatic valvular disease must receive antibiotic prophylaxis whenever they undergo a surgical or dental procedure that may potentially evoke bacteremia.
This is done to prevent the occurrence of bacterial endocarditis. Antimicrobial regimens recommended for the prevention of bacterial endocarditis are entirely distinct from regimens used in the prevention of ARF Currently, investigators are attempting to develop a polyvalent M-protein vaccine for the prevention of streptococcal infection and ARF.
A cute Glomerulonephritis: Unlike rheumatic fever, post-streptococcal acute glomerulonephritis AGN has shown no increase in incidence.
Indeed, nephritogenic strains particularly serotype M type 12 have decreased in prevalence Treatment strategies in the approach to post-streptococcal acute glomerulonephritis are directed toward management of acute problems. All patients should be treated with penicillin to eradicate the nephritogenic strain regardless of culture results of group A streptococci or immunologic tests.
Paralleling the recent changes in the pathogenesis of ARF, a substantial number of patients who develop post-streptococcal AGN do not have a history of a preceding pharyngitis or soft tissue infection. Penicillin-allergic patients can be treated with erythromycin in doses adequate for treatment of streptococcal pharyngitis.
It is generally recommended that family members be cultured for group A streptococcus. Family members with positive cultures should be treated appropriately. Treatment of patients with post-streptococcal AGN or of family contacts is for epidemiologic purposes only. Therapy will not alter pre-existent post-streptococcal AGN or prevent the disease in patients who are in the latent period. Some data suggest that antibiotic therapy may have a small effect on prevention of post-streptococcal AGN, but this has not been substantiated.
However, antibiotic therapy is effective in epidemiologic efforts at eradicating nephritogenic strains of group A streptococcus. In high risk settings during an acute epidemic of AGN, universal penicillin prophylaxis can be considered. Recurrent episodes of AGN are rare, and continuous anti-streptococcal prophylaxis is generally not recommended.
C ombination Therapy. In general, combination antimicrobial therapy offers no added benefit in the treatment of known GAS infections.
Antimicrobial agents possess sufficient activity in vitro to GAS and, when initiated promptly, are effective in the treatment of such infections. However, in clinical situations in which GAS is suspected but has not been identified e.
Invasive Streptococcal Infections: For necrotizing streptococcal infections, early and aggressive surgical debridement of the site of infection as well as appropriate antimicrobial therapy is required.
The patient with StrepTSS also requires intensive management of hemodynamic abnormalities and vital functions. Some investigators have suggested use of hyperbaric oxygen therapy HBO in treatment of necrotizing fasciitis reviewed in 7 , however, HBO therapy is not without risks, and its use has not been well studied. O ther proposed therapeutic interventions include the use of intravenous immunoglobulin IVIG and monoclonal antibodies. Investigators are studying the use of monoclonal antibodies against specific group A streptococcal toxins and the neutralization of circulating cytokines in managing invasive streptococcal disease caused by toxin-producing strains.
I t was recently suggested that the use of nonsteroidal antiinflammatory drugs NSAIDS in the treatment of fever in patients with GAS infections may predispose the patient to a more severe invasive infection.
NSAIDs may inhibit neutrophil function and enhance cytokine production In addition, their use may mask some of the early signs and symptoms of invasive GAS infections and has been associated with episodes of necrotizing fasciitis and toxic shock syndrome in patients with varicella P haryngitis : Tonsillectomy may help reduce the number of acute infections in children with recurrent GAS pharyngitis and is generally recommended for children who have 6 to 7 documented GAS infections in a given year or 3 to 4 infections in each of 2 years 8.
It may also be desirable as a method to eliminate the carrier state in a select group of patients such as those with a family history of rheumatic fever. The latter has not been well studied. Roos et al. A cute Rheumatic Fever: Salicylates and steroids are very effective in suppressing the acute manifestations of rheumatic fever, but neither has been shown to proven chronic valvular rheumatic heart disease Corticosteroid therapy is only for patients with significant carditis, especially cardiomegaly or congestive heart failure.
After 2 - 3 weeks, a slow taper may begin, decreasing the daily dose at the rate of 5 mg every 2 - 3 days. The problem of bacteriologic and clinical failures in the treatment of GAS pharyngitis has led some investigators to suggest that all patients should receive a test of cure at the end of treatment.
The patient who is symptomatic and culture positive at the end of treatment for acute pharyngitis may represent either failed treatment or acquisition of a new strain of GAS and should receive further treatment. Clearly, patients with previous rheumatic fever who have symptoms of strep throat should be re-cultured at the end of treatment.
Development of an effective group A streptococcal vaccine continues to be of interest; currently, none are commercially available. Researchers have looked at the conserved region of the M protein since this region is shared by all serotypes of GAS and because long-term exposure to group A streptococci results in acquired immunity A vaccine incorporating the conserved region of the M protein of group A streptococcus may stimulate a rapid rise in protective antibodies, but may also stimulate development of cross-reactive antibodies that recognize heart tissue.
Because of these potential safety issues, recent efforts have been directed at developing a vaccine against certain epitopes of the M protein that do not cross-react with myocardial tissue, providing a safer vaccine for immunizations This strategy is not without its problems. To provide immunity against the or so known M-types of GAS, the vaccine would need to be polyvalent. Further, the vaccine composition would likely need to be changed periodically to reflect those M-types prevalent in the population.
Group A streptococci are highly contagious and epidemics of pharyngitis, impetigo, scarlet fever, rheumatic fever, post-streptococcal glomerulonephritis, bacteremia, puerperal sepsis, streptococcal toxic shock syndrome and necrotizing fasciitis have been described reviewed in The acquisition of GAS in the family environment poses problems for individuals in that environment who may have previously acquired rheumatic fever.
This issue is discussed in section III. In the hospital environment, group A streptococcus can spread rapidly to patients with surgical wounds, burns or chicken pox or post-partum patients. Strict adherence to infection control measures is crucial. Because there are over different M-types of GAS this means that nosocomial isolates should be saved for subsequent epidemiologic comparisons should additional cases be identified. Performing M-typing or comparing RFLP patterns is extremely important to determine if these cases originated from a common source such as an employee who is a carrier of GAS.
Strict isolation procedures should be employed in patients who are admitted to hospitals with GAS infections.
Close contacts of primary cases of severe invasive GAS infections are at greater risk than the general population for development of colonization or superficial infection. The risk for invasive infection is less, but still higher than the general population. The clinician managing such cases should consider the risk and safety of these contacts and may wish to prescribe penicillin V K or, in penicillin allergic patients, clindamycin.
Likewise, invasive infections of soft tissues can be severe e. Whereas host genetic susceptibility plays a key role in modulating disease manifestation, variations in bacterial virulence properties contribute to infection severity. Pharyngitis: GAS is a major cause of pharyngitis and remains the only agent of this syndrome requiring etiologic diagnosis and treatment. The burden and economic costs of GAS pharyngitis are great.
It has been estimated that in the United States alone more than seven million cases of acute pharyngitis are diagnosed by pediatricians annually. On clinical grounds, streptococcal pharyngitis is strongly suggested by the presence of fever, tonsillar exudate, tender enlarged anterior cervical lymph nodes and absence of cough Figure 4. Since the s, the incidence of GAS pneumonia declined dramatically. Small outbreaks of GAS pneumonia have been described in chronic care facilities and within families, as well as sporadic cases occurring in the community.
GAS pneumonia now occurs with a frequency similar to that of other causes, such as Staphylococcus aureus or Klebsiella pneumoniae. Genitourinary tract infections and maternal sepsis:GAS is an uncommon cause of urinary tract infections. Although GAS is an uncommon cause of peripartum infection, it is an important cause of puerperal maternal sepsis. Cesarean section is a risk factor for serious puerperal infection. Prophylactic antibiotics in women undergoing caesarean section both elective and emergency have substantially reduced the incidence of febrile morbidity, wound infection, endometritis and serious maternal infectious complications.
Scarlet fever:Scarlet fever is a diffuse erythematous eruption that generally occurs in association with pharyngitis. Development of the scarlet fever rash requires prior exposure to GAS and occurs as a result of delayed-type skin reactivity to pyrogenic exotoxin erythrogenic toxin, usually types A, B or C produced by the organism.
It usually starts on the head and neck and is accompanied by circumoral pallor and a strawberry tongue. Subsequently the rash expands rapidly to cover the trunk followed by the extremities and ultimately desquamates; the palms and soles are usually spared.
The rash is most marked in the skin folds of the inguinal, axillary, antecubital, abdominal areas, and about pressure points. The definitive diagnosis is based on clinical findings that usually include a sharply demarcated shiny erythematosus plaque associated with pain, swelling and fever. A female predominance exists, except in young patients. Risk factors include disruption of the cutaneous barrier leg ulcer, wound, fissured toe-web intertrigo, and pressure ulcer , lymphedema, chronic edema, or local surgical operations lymph node dissection, saphenectomy.
Toe-web intertrigo appears to be a major portal of entry whether due or not due to dermatophyte infection. Erysipelas is less commonly caused group B, C or G streptococci and rarely by staphylococci. Bulla formation is considered as a relatively severe but frequent local complication of the disease. Pasteurella multocida following cat or dog bites, Aeromonas hydrophila following immersion in fresh water,Vibrio species after saltwater exposure, orHaemophilus influenzae in periorbital cellulitis in children.
Measures to reduce recurrences of erysipelas include treatment of any predisposing factor such as toe-web intertrigo or wound, or reducing any underlying edema. If frequent infections occur despite such measures, prophylactic antibiotics may be warranted. Impetigo:Impetigo is a highly contagious infection of the superficial epidermis that most often affects children two to five years of age, although it can occur in any age group.
Impetigo is classified as bullous or non-bullous impetigo. Bullous impetigo simply means that the skin eruption is characterized by bullae blisters. Non-bullous impetigo is the most common form of impetigo. The infection usually heals without scarring, even without treatment. GAS causes fewer cases, either alone or in combination with S. The diagnosis usually is made clinically and can be confirmed by Gram stain and culture, although this is not usually necessary.
Culture may be useful to identify patients with nephritogenic strains of GAS during outbreaks of poststreptococcal glomerulonephritis. Impetigo usually is transmitted through direct contact. Patients can further spread the infection to themselves or others after excoriating an infected area. Infections often spread rapidly through schools and day care centers. There is good evidence that the topical antibiotics, mupirocin and fusidic acid, are equal to or possibly more effective than oral antibiotic treatment.
Oral antibiotics may have a role for more serious and extensive forms of impetigo. Penicillin is not as effective as most other antibiotics. Cellulitis: Bacterial cellulitis refers to a diffuse, spreading skin infection. Associated regional lymphadenopathy and lymphatic streaking are variable, and local complications abscesses, necrosis are more frequent than in erysipelas.
Petechiae and ecchymoses with frequent bullae may develop in inflamed skin resulting in hemorrhagic cellulitis. Cellulitis usually refers to a more deeply situated skin infection than erysipelas which is considered to be a more superficial.
However, the distinction between these entities is not clear cut, and the two conditions share the typical clinical features including sudden onset, usually with a high fever, and the tendency to recur. The predominant infection site for cellulitis is on the lower extremities.
Lymphedema and disruption of the cutaneous barrier, which serves as a site of entry for the pathogens, are risk factors for infections. Necrotizing fasciitis is historically divided into 2 types.
Type I results from mixed infection with anaerobic species in combination with facultatively anaerobic organisms such as streptococci non-group A , enterococci, and Gram-negative rods, whereas type II involves GAS either alone or in mixed infections.
Early diagnosis is difficult as there is no single clinical laboratory test, imaging technique, or pathognomonic physical exam finding available. Patients with GAS necrotizing fasciitis commonly present with nonspecific symptoms such as fever, exquisitely tender skin lesions, vomiting, diarrhea, and toxemia. It is noteworthy that a substantial number of invasive streptococca infections have no known portal of entry.
Transient bacteremia originating from the oropharynx has been suggested as the source in such cases. Anecdotal reports have suggested an association between the use of nonsteroidal anti-inflammatory drugs NSAIDs and the progression or development of GAS necrotizing infection, although this has not been found in prospective studies. In a matter of hours to days, the infection can progress from an apparently non-descript pain or benign appearing skin lesion, to a highly lethal disease.
Of patients with necrotizing fasciitis, more than half have concomitant myonecrosis. Not infrequently, the patient will have sought medical care prior to the diagnosis being made.
One of the clinical clues early in the course of the disease is pain out of proportion to the history or physical findings. He had sought medical care two days earlier for flu like symptoms and severe axillary pain. A prospective population-based surveillance for invasive GAS infections in Ontario from to identified patients with invasive GAS disease corresponding to an annual incidence of 1. The clinical spectrum of disease may vary from mild to severe, resulting in streptococcal toxic shock.
Streptococcal cellulitis tends to develop at anatomic sites in which normal lymphatic drainage has been disrupted such as sites of prior cellulitis, the arm ipsilateral to a mastectomy and axillary lymph node dissection, a lower extremity previously involved in deep venous thrombosis, or chronic lymphedema, or the leg from which a saphenous vein has been harvested for coronary artery bypass grafting.
The organism may enter via a dermal breach some distance from the eventual site of clinical cellulitis. For example, some patients with recurrent leg cellulitis following saphenous vein removal stop having recurrent episodes only after treatment of tinea pedis on the affected extremity. Fissures in the skin presumably serve as a portal of entry for streptococci, which then produce infection more proximally in the leg at the site of previous injury.
Streptococcal cellulitis may also involve recent surgical wounds. GAS is among the few bacterial pathogens that typically produce signs of wound infection and surrounding cellulitis within the first 24 hours after surgery. These wound infections are usually associated with a thin exudate and may spread rapidly, either as cellulitis in the skin and subcutaneous tissue, or as a deeper tissue infection.
Streptococcal wound infection or localized cellulitis may also be associated with lymphangitis, manifested by red streaks extending proximally along superficial lymphatics from the infection site. Varicella is a risk factor for invasive GAS disease in all age groups, but in children it is the most important risk factor for the acquisition of invasive GAS infection.
Clindamycin is recommended for the treatment of streptococcal toxic shock syndrome STTS and necrotizing fasciitis. The rationale for clindamycin is based on in vitro studies demonstrating both toxin suppression and modulation of cytokine i. Prompt and aggressive exploration of suspected deep-seated GAS infections is currently advocated in order to determine the presence or absence of necrotizing fasciitis.
Despite only anecdotal evidence, the current medical literature as well as standard surgical and medical reference textbooks advocates an early and aggressive surgical approach for patients with suspected or proven necrotizing fasciitis.
Delaying surgery may decrease morbidity by allowing the development of a line of demarcation separating necrotic from vital tissue, thereby limiting the extent of tissue resection. It may also decrease mortality by allowing the patient to stabilize hemodynamically prior to surgery. Early versus late surgical debridement has been a matter of debate also in acute necrotizing pancreatitis, where a common therapeutic approach in the past was early surgical intervention and debridement.
Thus, the concept that the existence of infected tissue in the acute stages of pancreatitis worsens the outcome may not be true, and in fact the more crucial process may be the inflammatory response that results. However, any necrotic tissue should eventually be removed, but if the use of an immunomodulating agent such as intravenous polyspecific immunoglobulin G IVIG that neutralizes the toxins and the pathological levels of pro-inflammatory cytokines allows for the tissue debridement to be performed at a later stage, this may be beneficial for the patient Figure 8.
This women had STSS and widespread evidence of severe soft tissue disease, with the presence of bullae.
The original surgical plan was to debride all involved tissue, however because of being unstable it was decided to wait and observe. She was treated with IVIG.
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