When was streptococcus discovered

The distinctive bacteria was diesovered in by an European scientist, Fehleisen. Thi discovery proved that there is a different kind of bacteria which causes different kind of problems but it was still a part of the Streptococcus Pyogenes Group. This was a chain-like bacteria which was causing throat problems. Later in this year, they linked the bacteria which they had found with the Streptococci Bacteria.

Jun 29, Following infection with a particular M-type, specific antibody confers resistance to challenge with viable GAS of that M-type Recently, Boyle has shown that GAS protease cleaves the terminal portion of the M-protein, rendering the organism more susceptible to phagocytosis by normal serum but more resistant to phagocytosis in the presence of type specific antibody While M types 1 and 3 strains have accounted for the vast majority of strains isolated from cases of StrepTSS, many other M types, including some non-typeable strains, have also been isolated from such cases.

M types 1 and 3 are also commonly isolated from asymptomatic carriers, and patients with pharyngitis or mild scarlet fever 45 , M echanisms of Fever Induction: Pyrogenic exotoxins induce fever in humans and animals and also participate in shock by lowering the threshold to exogenous endotoxin Pyrogenic exotoxin C has been associated with mild cases of scarlet fever in the United States author's observations and in England S treptococcal Toxic Shock Syndrome.

The net effect is induction of T cell proliferation via an IL-2 mechanism with concomitant production of cytokines e. Kotb 49 has shown that a digest of M-protein type 6 can also stimulate T cell responses by this mechanism.

C ytokine production by less exotic mechanisms may also contribute to the genesis of shock and organ failure. Finally, a cysteine protease formed from cleavage of SPEB may play an important role in pathogenesis by the release of bradykinin from endogenous kininogen and by activating metalloproteases involved in coagulation T he mere presence of virulence factors, such as M-protein or pyrogenic exotoxins, may be less important in Strep TSS than the dynamics of their production in vivo.

Recently, Cleary has proposed a regulon in GAS that controls the expression of a group of virulence genes coding for virulence factors such as M-protein and C5-peptidase Using DNA fingerprinting, differences were shown in M-1 strains isolated from patients with invasive disease compared to M-1 strains from patients with non-invasive GAS infections Multi-locus enzyme electrophoresis demonstrates two patterns that correspond to M-1 and M-3 type organisms which produce pyrogenic exotoxin A, a finding that fits epidemiologic studies implicating these strains in invasive GAS infections 64 in the United States.

P athogenic Mechanisms in Acute Rheumatic Fever: The pathogenesis of acute rheumatic fever involves an intimate interplay between streptococcal virulence factors and the susceptible host. That T cells play an integral role was demonstrated by obtaining T-cell clones from valvular tissue of patients with rheumatic fever and then showing that these clones were responsive to specific epitopes of type 5 M-protein That B-lymphocytes play an important role is suggested by the demonstration that antibodies raised against particular M-protein digests cross react with cardiac tissue including myosin and endothelium Interestingly anti-myosin antibodies also react strongly to cardiac endothelium Thus, as antibody against M-protein develops in a patient with antecedent Group A streptococcal pharyngitis, antibody could fix complement, thereby damaging and activating the endothelium yielding cytokines and chemokines which attract and activate T-lymphocytes.

Thus, molecular mimicry between specific epitopes on M-protein and cardiac tissue results in damage to endothelium on the heart valve mediated by specific B and T-lymphocytes.

P ost Streptococcal Glomerulonephritis: It is clear that only certain strains of streptococci are capable of causing post-streptococcal glomerulonephritis. The best hypothesis at the present time is that proteins with unique antigenic determinants produced only by Anephritogenic strains, intercalate into the lipid bilayer of the glomerular basement membrane during the course of pharyngitis or impetigo.

Recent studies suggest that streptokinase, which has certain lipophilic regions may be the streptococcal virulence factor responsible. Once streptokinase is membrane bound, complement is activated directly. Further glomerulus-bound streptokinase interacts with circulating anti-streptococcal antibodies, resulting in further complement fixation and glomerular damage Single Drug Susceptibility.

Susceptibilities for commonly used antibiotics in the treatment of GAS are presented in Table 1. Comb ination Drug Susceptibility. No in vitro susceptibility testing has been undertaken to investigate whether combinations of antibiotic may exert an additive, synergistic or antagonistic effect against GAS.

G eneral. Despite possible changes in virulence, group A streptococci have universally remained susceptible to penicillin since its introduction.

Penicillin is still considered first-line therapy in the treatment of most GAS infections despite a recognized increase in microbiologic failure rates. Thus, antibiotic treatment of GAS infections in general will likely become much more complex.

Special Infections. Treatment of GAS pharyngitis is primarily aimed at preventing non-suppurative in particular, rheumatic fever and suppurative complications. However, a study conducted by Gerber et al. Treatment with penicillin should be continued for 10 days since shorter courses of penicillin have shown decreased efficacy. A clinical response is generally obtained within 24 h of beginning therapy, and most children have a negative throat culture by 48 h and can return to school at that time.

Persistence of symptoms beyond this period suggests development of a suppurative complication of GAS, a lack of compliance, or the presence of another underlying disease. A single injection of 1. It can provide bactericidal levels against GAS for as long as 28 days. Children who weigh less than pounds 64 kg should receive an intramuscular injection composed of , units of benzathine penicillin G and , units of procaine penicillin G.

P enicillin's efficacy in preventing rheumatic fever is well established, and is related to the eradication of the organism from the pharynx. This efficacy, however, is dependent upon prolonged, rather than high-dose, therapy. Penicillin has been shown effective when therapy is started within 9 days of onset of symptoms of GAS pharyngitis Other desirable features of penicillin include lower cost, lower side effects, and a narrow antimicrobial spectrum. There has been no documentation of resistance in GAS to penicillin; the minimal bactericidal concentration of penicillin G for GAS has remained 0.

Erythromycin remains the first alternate choice in patients who are allergic to penicillin. However, documented reports of erythromycin-resistant GAS have occurred in Finland, Japan, and, most recently, in the United States 57 , 58 , 75 , Use of macrolides since then has declined, and a marked decrease in rates of erythromycin resistance has followed T he newest macrolides, azithromycin and clarithromycin , have been shown highly effective in the treatment of GAS pharyngitis.

They provide easier dosing schedules and thus improve patient compliance. Azithromycin has been shown to be efficacious in the treatment of GAS pharyngitis when given for only 3 - 5 days. However, azithromycin-resistant GAS have been reported in the United States 19 , and treatment failure of azithromycin was documented in the United States recently among children harboring GAS with high level azithromycin resistance The ability of macrolides to prevent episodes of rheumatic fever has not been studied.

Amoxicillin has been shown to be effective in eradicating GAS, is more palatable, and provides easier dosing than penicillin. Oral cephalosporins have been extensively studied in the treatment of GAS pharyngitis and are highly effective. Cefaclor has been associated with a higher incidence of serum sickness than most other antibiotics. In addition, cephalosporins as a class are more expensive than penicillin, are associated with greater side effects in general, and have a broader spectrum of activity.

I n many areas, tetracycline resistance occurs in a high percentage of strains of GAS and thus, this drug is not recommended for treatment of pharyngitis. Sulfonamides , including trimethoprim-sulfamethoxazole , are ineffective in the treatment of GAS pharyngitis, though sulfadiazine has proven useful for prophylaxis in acute rheumatic fever 8 , Treatment failures in GAS pharyngitis are of major concern in the prevention of rheumatic fever.

In fact, studies have shown that delaying therapy for 3 to 5 days resulted in an increase in anti-streptolysin O antibodies but did not affect development of type-specific antibodies Antibodies such as anti-streptolysin O, unlike type-specific antibodies, do not confer immunity on the host.

At present, it is unclear if delaying therapy for 2 to 3 days in patients with GAS pharyngitis results in a significantly greater antibody rise. Since adequate antimicrobial therapy prevents development of suppurative and non-suppurative complications of GAS, most authors do not recommend delaying therapy. Some bacteriologic and clinical failures may also represent infection with a tolerant strain or acquisition of a new strain of GAS.

In addition, GAS carriers with an intercurrent viral pharyngitis may be mistakenly diagnosed as patients with acute GAS pharyngitis and thus considered treatment failures, since penicillin is ineffective in eradication of the GAS carrier state Clindamycin has been extremely effective in the treatment of GAS. I n patients with recurring episodes of GAS pharyngitis or persistent, culture-positive, clinical GAS pharyngitis, it is often necessary to change antibiotic therapy.

S carlet Fever: Scarlet fever is characterized by high fever, circumoral pallor and a diffuse erythematous rash over the neck, trunk, face and limbs. There is a sandpaper consistency to the rash which blanches with pressure. A white coating over the tongue resolves quickly leaving a strawberry appearance to the tongue owing to the swollen papillae. The treatment of scarlet fever is the same as that for GAS pharyngitis as the disease usually results from infection of the pharynx with a streptococcal strain that elaborates one of the streptococcal pyrogenic exotoxin 8.

Scarlet fever can also result from GAS infections at other sites, such as the skin 8. Patients in modern times resolve the illness in days and by days there may be impressive desquamation of the skin particularly over the hands and feet. Recent reports have documented increased frequency and severity of invasive group A streptococcal infections of the skin and soft tissues, associated with group A streptococcal serotypes M-1 and M-3 7. This is of considerable interest because these serotypes are more often associated with episodes of pharyngitis.

Strains of group A streptococci that cause skin infections normally differ from those that cause pharyngitis and can be identified by their M serotypes. The most common streptococcal M serotypes that cause pharyngitis types 1, 3, 5, 6, 12, 18, 19, 24 and others , including M-1 and M-3, have rarely been identified in skin lesions 8. In contrast, "skin strains" have been found to colonize the pharynx but are rarely associated with acute episodes of pharyngitis 8.

G AS Pyoderma Streptococcal Impetigo, Impetigo Contagiosum, Ecthyma : Pyoderma is a term for a localized purulent infection of the skin and is used synonymously with streptococcal impetigo and impetigo contagiosa. Pyoderma is most common in children aged 2 to 5 years and occurs most commonly among economically disadvantaged children in tropical or subtropical climates but can occur in northern climates during the summer months. It normally results from direct inoculation of the skin surface with GAS following minor trauma, abrasions, or insect bites.

Often S. Penicillin was effective treatment in the past but is now often associated with treatment failures. First line therapy includes dicloxacillin , cephalexin , or cefadroxil. Erythromycin is an alternative for penicillin-allergic patients but must be used with caution in regions where erythromycin-resistant strains of S. Therapy is continued for 10 days. Mupirocin ointment applied to skin lesions 3 times daily for 10 days has achieved cure rates comparable to those with enteral therapy but is more expensive.

While rheumatic fever is not an associated complication of pyoderma, skin infections caused by nephritogenic strains of group A streptococci are the major antecedent of post-streptococcal glomerulonephritis reviewed in 7. E rysipelas: Erysipelas is an acute inflammation of the skin with involvement of cutaneous lymphatic vessels.

It is most commonly found in infants and adults over 30 years of age. Historically, erysipelas most commonly involved the face.

It is often preceded by a sore throat and commonly occurs at the site of a wound or surgical incision, especially when involving the trunk or extremities. The lesions are associated with fever and toxicity and are noted to spread outward. The rash itself is a scarlet-red or salmon color with well-defined borders. Facial erysipelas may spontaneously resolve in 4 to 10 days 7. The mainstay of treatment remains penicillin 7. Superficial infections may be treated orally for 10 days, while more aggressive infections require parenteral therapy.

Typical antimicrobial regimens include clindamycin , nafcillin , or a third generation cephalosporin. C ellulitis : Streptococcal cellulitis is an acute inflammation of the skin and subcutaneous tissues resulting from infection of burns, wounds, or surgical sites or following minor trauma. Symptoms include fever and toxicity and may be associated with lymphangitis or bacteremia. Cellulitis can be differentiated from erysipelas by noting that the skin lesion of cellulitis is not raised and the demarcation between involved and uninvolved skin is indistinct.

Therapy should consist of a semisynthetic, penicillinase-resistant penicillin, since it is often difficult to differentiate streptococcal from staphylococcal cellulitis 7. In patients who are penicillin allergic, a first generation cephalosporin may be used. Therapy can be given orally, unless there is evidence of lymphangitic spread. If lymphangitis is noted, parenterally administered antimicrobials should be used until there is marked clinical improvement. Oral antimicrobials can then be used to complete 10 days of therapy.

N ecrotizing Fasciitis Streptococcal Gangrene : GAS necrotizing fasciitis is a rapidly progressing infection of the deep subcutaneous tissues and fascia with extensive and rapidly spreading necrosis. Necrotizing fasciitis is often associated with severe systemic involvement and an associated high mortality rate 7 , 80 , As in other invasive streptococcal and staphylococcal skin infections, the site of inoculation is usually at area of minor trauma or the skin lesions of varicella.

Like streptococcal bacteremia, there is a clear association between varicella and necrotizing fasciitis. Varicella is characterized by full-thickness dermal lesions that may induce selective immunosuppression to GAS, though this has not been substantiated 7.

Necrotizing fasciitis caused by mixed infections, involving both aerobic and anaerobic Gram negative bacteria, is more likely to occur in the abdominal wall, following abdominal surgery or in diabetic patients. E arly and aggressive surgical debridement of the site of infection as well as appropriate antimicrobial therapy is required.

Due to the "inoculum effect," penicillin may be less effective in the treatment of necrotizing fasciitis Appropriate antibiotics include nafcillin and clindamycin 7 , Infections of the muscles are rarely caused by group A streptococcus but can occur. Infections occur following mild trauma, in toxic shock, and spontaneously. It is often difficult to differentiate streptococcal myonecrosis from necrotizing fasciitis, as the clinical features overlap, and the two entities often occur together.

Therapy includes extensive debridement of the infected muscle and parenterally administered antimicrobials. Penicillin has poor efficacy in the treatment of GAS myonecrosis, and aggressive surgical debridement remains the most important factor in treatment The failure of penicillin is attributed to decreased expression of penicillin-binding proteins during the stationary growth phase and the slow growth of group A streptococcus.

This is known as the Eagle effect and has been described elsewhere Clindamycin , erythromycin , and ceftriaxone have been more effective than penicillin in experimental models L ymphangitis : Lymphangitis may occur in association with cellulitis or after a clinically minor skin infection.

When group A streptococcus is implicated as the etiologic agent, therapy consists of parenterally administered penicillin. When the cause of the infection is in doubt, nafcillin can be used to provide coverage for S. Patients allergic to penicillin can be treated with a first generation cephalosporin, clindamycin , or vancomycin 8. P uerperal Sepsis: Puerperal sepsis occurs during pregnancy or during an abortion, when group A streptococcus colonizing the patient invades the endometrium and surrounding structures as well as the lymphatics and bloodstream.

Endometritis and septicemia result and can be complicated by pelvic cellulitis, thrombophlebitis, peritonitis, or pelvic abscess. Patients allergic to penicillin can be treated with a first generation cephalosporin, clindamycin, or vancomycin 8.

V ulvovaginitis : Group A streptococcus is a common cause of vulvovaginitis in the prepubertal female. Symptoms include a serous vaginal discharge, erythema of the vulvar area, and intense pruritus.

Therapy consists of orally administered penicillin for 10 days. Patients allergic to penicillin can be treated with erythromycin. P roctitis : Perianal cellulitis proctitis or asymptomatic anal infection has been associated with several reported outbreaks of hospital-acquired streptococcal infection.

Because it is difficult to differentiate streptococcal cellulitis from staphylococcal cellulitis, it is advisable to use a first generation cephalosporin, such cephalexin , for therapy. Therapy should be given enterally for 10 days. F unisitis and Omphalitis: Omphalitis is an infection of the umbilical cord and surrounding tissues.

Etiologic agents include group A streptococcus, S. Combination therapy is normally provided while culture results are pending and consists of a semisynthetic penicillin , such as oxacillin and gentamicin. Patients allergic to penicillin can be treated with a first generation cephalosporin. StrepTSS usually occurs secondary to soft tissue infections, particularly as a secondary infection of varicella lesions or as a complication of necrotizing fasciitis, myositis, pneumonia, or post-partum infection.

M-type l GAS has been the predominant serotype associated with StrepTSS, but types 3, 12, and 28 have been implicated as well 7 , 80 , Recent interest in the pathophysiology of this disorder has focused on the role of streptococcal pyrogenic exotoxins SPEs , extracellular products of group A streptococci that mediate not only scarlatiniform-like rashes but also multi-organ damage and shock. SPEA is the most common exotoxin found in the United States and has been shown to be both a superantigen and a potent inducer of tumor necrosis factor 7.

Recently, nicotine adenine glycohydrolase NADase has been linked with the resurgence of severe invasive group A streptococcal infections T he patient with StrepTSS requires intensive management of hemodynamic abnormalities and vital functions. Patients with a soft tissue focus of infection may require surgical intervention.

Broad spectrum antibiotic coverage should be instituted until the presence of group A streptococcus has been confirmed. Therapy may then consist of parenterally administered clindamycin. In StrepTSS, tissue destruction continues despite high concentrations of penicillin. Penicillin is known to be relatively ineffective in the treatment of soft tissue infections with a high concentration of organisms the Eagle effect 83 , This is thought to be due to the slow rate of replication of group A streptococci, decreased expression of penicillin-binding proteins, and the fact that penicillin acts by interfering with cell wall synthesis 83 , Clindamycin inhibits protein synthesis, decreases the production of M proteins and toxins, and is unaffected by slow growing toxin-producing streptococci 83 , A study by Brook et al.

A mouse model of a soft tissue infection with GAS showed clindamycin to be more effective than penicillin Erythromycin and ceftriaxone may also be more effective than penicillin in such cases. B acteremia. Accompanying the increase in number and severity of invasive group A streptococcal infections is an increase in the incidence of group A streptococcal bacteremia. There have been a number of cases associated with intravenous drug abuse as well as nosocomial outbreaks in nursing homes.

Intravenous drug use has become the leading cause of GAS bacteremia in individuals between the ages of 14 and 40 years Bacteremia usually follows a cutaneous focus of infection but may follow an upper respiratory infection.

In addition, the number of children with varicella who develop GAS bacteremia has increased Doctor et al. GAS bacteremia in varicella is thought to occur secondary to a superinfected cutaneous lesion. Serotypes M1, M3, and M18 are more invasive and are associated with higher morbidity and mortality rates than M4 and M12, which are generally considered less virulent.

M type 1 strains produce pyrogenic exotoxins A and B, and the latter toxin also has associated proteinase activity 7. Therapy for GAS bacteremia consists of parenterally administered penicillin.

Patients allergic to penicillin can be treated with clindamycin , vancomycin , or a first generation cephalosporin. P neumonia. Pneumonia secondary to group A streptococcus is frequently associated with preceding or concurrent viral infections such as measles, varicella, or influenza. Since the mid s, the number of reports describing this association has increased. Other complications include mediastinitis, pericarditis, pneumothorax, and bronchiectasis. Therapy consists of surgical drainage of an empyema and parenteral penicillin.

Adequate drainage of pleural infection may be difficult and frequently requires prolonged chest tube drainage, thoracoscopy or pleural surgery. In addition, there are certain types of GAS that are more likely to cause severe disease than others. Few people who come in contact with GAS will develop invasive GAS disease; most will have a mild throat or skin infection and some may have no symptoms whatsoever. Although healthy people can get invasive GAS disease, people with chronic illnesses like cancer or diabetes, those on kidney dialysis, and those who use medications such as steroids are at higher risk.

In addition, breaks in the skin like cuts, wounds, or chickenpox may provide an opportunity for the bacteria to enter the body. GAS infections can be treated with many different antibiotics. Early treatment may reduce the risk of death, although it unfortunately may not prevent death in every case.

The spread of GAS infection may be reduced by good handwashing, especially after coughing and sneezing, before preparing foods, and before eating. Persons with sore throats should be seen by a doctor who can perform tests to find out whether it is strep throat. Persons with strep throat should stay home from work, school, or day care until 24 hours or more after taking an antibiotic. All wounds should be kept clean and watched for possible signs of infection including increasing redness, swelling, drainage, and pain at the wound site.

A person with signs of an infected wound, especially if fever develops, should seek medical care.