what causes group a strep infection

Explore

Group C Streptococci. Group C streptococci have been identified as part of the normal human microbiota of the nasopharynx, skin, and genital tract; the organism has also been isolated from up to two thirds of umbilical specimens in neonates without signs of infection and from routine puerperal vaginal cultures.

What is a group C strep infection?

• The Lancefield classification system for bacteria
• Features of streptococcus cells
• Group A streptococcus (or GAS) facts
• Five diseases caused by GAS
• Group B streptococcus (or GBS) facts
• Adult and infant problems caused by GBS

What group does Streptococcus belong to?

Method 2 Method 2 of 4: Self-Care Download Article

1. Stay home to rest your body. Your body needs lots of rest to recover from strep throat, especially if you’re trying to treat it naturally.
2. Drink a lot of fluids to help soothe your throat and stay hydrated. Keep a drink beside you at all times so you can sip throughout the day.
3. Eat warm, soothing foods that aren’t too spicy. ...

More items...

How to cure a strep throat naturally at home?

The doctor or medical professional takes a throat swab, called a rapid strep test, or a throat culture. If the test comes back positive for the bacteria, then the doctor will usually prescribe an antibiotic. But strep throat is a self-limited disease that will go away on its own, says Shulman.

Will strep throat go away by itself?

How do you get Streptococcus Group A?

These bacteria are spread by direct contact with discharges from the nose and throat of infected people or by contact with infected wounds or sores on the skin. The risk of spreading the infection is highest when a person is ill, such as when people have "strep throat" or an infected wound.

What bacteria causes group A strep?

Bacteria called group A Streptococcus (group A strep) can cause many different infections. The best way to protect yourself from group A strep infection is to practice good hygiene, like washing your hands often. Some of these are common, relatively minor infections, like strep throat.

Is Group strep A STD?

The bacteria that cause group B strep disease normally live in the intestine, vagina, or rectal areas. Group B strep colonization is not a sexually transmitted disease (STD).. One of every four or five pregnant women carries GBS in the rectum or vagina.

What are 2 illnesses that group A streptococcus can cause?

Diseases Caused by Group A StrepStrep Throat. Cellulitis.Scarlet Fever. Streptococcal Toxic Shock Syndrome.Impetigo. Rheumatic Fever.Necrotizing Fasciitis. Post-Streptococcal Glomerulonephritis.

How common is group A strep?

How common are group A strep infections? The U.S. Centers for Disease Control and Prevention (CDC) estimates that each year in the United States, there are several million cases of mild group A strep infections, and 11,000 to 13,000 cases of severe group A strep infections with 1,100 to 1,600 deaths.

Can Group A Streptococcus be cured?

Group A streptococcus bacteria can be treated with common, inexpensive antibiotics. Penicillin is the drug of choice for both mild and severe disease. For penicillin-allergic patients with mild illness, erythromycin can be used, although occasional resistance has been seen.

Is strep throat a chlamydia?

The main difference is that they are caused by a different bacterium. Chlamydia is caused by the bacteria called chlamydia trachomatis and strep throat is caused by bacteria streptococcus pyogenes.

What happens if you test positive for group A strep?

Your doctor can do a quick strep test to see if group A strep bacteria are causing your sore throat. If the test is positive, your doctor can prescribe antibiotics. Antibiotics help you feel better sooner, prevent serious health problems, and help prevent spreading the bacteria to others.

Where is strep A found?

General Information. Group A Streptococcus (GAS) or Streptococcus pyogenes is a bacterium commonly found in the throat and on the skin. Many people can carry this bacterium without any symptoms of disease.

Who is the most common victim of Streptococcus?

Strep throat and scarlet fever are most common in children between the ages of 5 and 15 years.

How long does strep A last?

A. Strep throat typically resolves in three to five days if untreated. Despite the short duration, antibiotic treatment is recommended to reduce the risk of complications. Symptoms typically resolve within one to three days following the start of antibiotics.

How long does group A strep live on surfaces?

SURVIVAL OUTSIDE HOST: The bacterium can survive on a dry surface for 3 days to 6.5 months (22).

What is strep group A antigen?

Group A Streptococcus (GAS) (Streptococcus pyogenes) is an important human pathogen associated with significant global morbidity and mortality for which there is no safe and efficacious vaccine. The T antigen, a protein that polymerizes to form the backbone of the GAS pilus structure, is a potential vaccine candidate.

Is strep caused by a virus or bacteria?

Strep throat is an infection in the throat and tonsils caused by group A Streptococcus bacteria (called “group A strep”). However, viruses — not bacteria — cause most sore throats. Group A strep bacteria spread through contact with droplets from an infected person when they talk, cough, or sneeze.

Why Is the Study of Group A Streptococcal Infections a Priority for NIAID?

Health experts estimate that more than 10 million mild infections (throat and skin) occur every year.

What is the most common form of strep throat?

Most people are familiar with strep throat, which along with minor skin infections, is the most common form of the disease. Health experts estimate that more than 10 million mild infections (throat and skin) occur every year.

What is a GAS infection?

Group A streptococcal (GAS) infections can range from a mild skin infection or a sore throat to severe, life-threatening conditions. Most people are familiar with strep throat, which along with minor skin infections, is the most common form of the disease.

What causes a sore throat?

Many things can cause that unpleasant, scratchy, and sometimes painful condition known as a sore throat. Viruses, bacteria, allergens, environmental irritants (such as cigarette smoke), chronic postnasal drip, and fungi can all cause a sore throat.

What is impetigo in children?

Impetigo is an infection of the top layers of the skin and is most common among children ages 2 to 6 years. It usually starts when bacteria get into a cut, scratch, or insect bite.

How many strains of streptococci are there?

Biology & Genetics. Through research, health experts have learned that there are more than 120 different strains of group A streptococci bacteria, each producing its own unique proteins. Some of these proteins are responsible for specific GAS diseases.

What is post streptococcal reactive arthritis?

Poststreptococcal reactive arthritis, a condition that causes inflammation of the joints. A possible relationship has been suggested between strep infection and a rare condition called pediatric autoimmune neuropsychiatric disorder associated with group A streptococci (PANDAS).

What are the symptoms of strep throat?

This photo of strep throat shows inflammation and red spots, caused by the infection. Signs and symptoms of strep throat can include: Red and swollen tonsils, sometimes with white patches or streaks of pus.

How long does a sore throat last?

A sore throat that lasts longer than 48 hours. A fever. A sore throat accompanied by a rash. Problems breathing or swallowing.

What is the CDC website for strep throat?

Strep throat: All you need to know. Centers for Disease Control and Prevention. https://www.cdc.gov/groupastrep/diseases-public/strep-throat. html?CD. Accessed Dec. 2, 2020.

What does it mean when your tonsils are red?

Tiny red spots on the area at the back of the roof of the mouth (soft or hard palate) It's possible for you or your child to have many of these signs and symptoms but not have strep throat.

What is scarlet fever?

Scarlet fever, a streptococcal infection characterized by a prominent rash. Inflammation of the kidney (poststreptococcal glomerulonephritis) Rheumatic fever, a serious inflammatory condition that can affect the heart, joints, nervous system and skin.

How do you get streptococcal?

Streptococcal bacteria are contagious. They can spread through droplets when someone with the infection coughs or sneezes, or through shared food or drinks. You can also pick up the bacteria from a doorknob or other surface and transfer them to your nose, mouth or eyes.

What is the AOG opinion 797?

Committee opinion No. 797: Prevention of group B streptococcal early-onset disease in newborns. Obstetrics and Gynecology. 2020; doi: 10.1097/AOG.0000000000003668.

What are the complications of group B strep?

If you're an older adult or you have a chronic health condition, group B strep bacteria can cause complications such as: Skin infection. Infection of the bloodstream. Urinary tract infection. Pneumonia. Bone and joint infections. Infection of the heart valves (endocarditis)

What to do if your baby has group B strep?

If you notice your infant has signs or symptoms of group B strep disease, contact your baby's doctor immediately.

How long does it take for a baby to get strep?

In infants, illness caused by group B strep can be within six hours of birth (early onset) — or weeks or months after birth (late onset). Signs and symptoms might include: Fever. Difficulty feeding.

Why can't you take antibiotics before labor?

Taking oral antibiotics ahead of time won't help because the bacteria can return before labor begins.

What antibiotics can you give to a baby during labor?

To prevent group B bacteria from spreading to your baby during labor, your doctor can give you an IV antibiotic — usually penicillin or a related drug — when labor begins. If you're allergic to penicillin and related drugs, you might receive cefazolin or clindamycin as an alternative.

What is the term for inflammation of the membranes and fluid surrounding the brain and spinal cord?

Inflammation of the membranes and fluid surrounding the brain and spinal cord (meningitis)

How is group A strep spread?

Group A strep bacteria live in your nose and throat, so they are spread through droplets that become airborne from coughing or sneezing or by direct contact with the mucus. You might breathe droplets in if you’re close enough when an infected person coughs or sneezes.

What is the treatment for group A strep?

Sepsis caused by group A strep should be treated urgently with both antibiotics and IV fluids. For people with necrotizing fasciitis, surgery may likely be needed to remove the affected tissue.

How do you know if you have a group A strep infection?

Group A strep infection symptoms depend on where the infection is. The common symptoms include pain in the affected area, redness, and swelling. If the infection progresses or is a systemic infection, such as scarlet fever or toxic shock syndrome, you would develop fever, muscle aches, and flu-like symptoms.

How does sepsis affect the body?

Sepsis kills and disables millions and requires early suspicion and treatment for survival. Sepsis and septic shock can result from an infection anywhere in the body, such as pneumonia, influenza, or urinary tract infections. Worldwide, one-third of people who develop sepsis die.

What happens if you have cellulitis?

If the skin is infected, as with cellulitis or impetigo, the bacteria must come in contact with a spot of skin that had an open area, such as a cut, scrape, or bite. The opening may be so tiny that you didn’t notice anything beforehand. Impetigo is common among young children as they share toys and play together.

How many people die from sepsis?

Worldwide, one-third of people who develop sepsis die. Many who do survive are left with life-changing effects, such as post-traumatic stress disorder (PTSD), chronic pain and fatigue, organ dysfunction (organs don’t work properly), and/or amputations.

What is the name of the bacterium that causes sepsis?

Group A Streptococcus, also called group A strep, is a bacterium that can cause many different infections. These may cause sepsis. Sometimes incorrectly called blood poisoning, sepsis is the body’s often deadly response to infection. Sepsis kills and disables millions and requires early suspicion and treatment for survival.

What are the symptoms of a streptococcal infection?

The first phase of StrepTSS begins with an influenza-like prodrome that is characterized by fever, chills, myalgias, nausea, vomiting, and diarrhea that precedes hypotension by 24–48 hours ( Stevens, et al., 1989 ). Confusion and/or combativeness is present in 55% of patients. Where there is a defined portal of entry, early cutaneous evidence of streptococcal infection may be present. In contrast, in patients without a portal of entry (~50% of cases) and who subsequently develop necrotizing infection, increasingly severe pain is the most common symptom. Such pain is so severe as to prompt patients to seek medical care and, interestingly, often precedes cutaneous evidence of localized infection by 12-24 hours ( Stevens, et al., 1989 ). In both children ( Kiska, et al., 1997) and adults ( Stevens, et al., 1989 ), the soft tissues are the most common primary site of infection. In the remaining cases, pneumonia, meningitis, endophthalmitis, peritonitis, myocarditis, joint infection, and intrauterine infection have been described.

What is the role of antecedent soft tissue injury?

A critical role for antecedent soft-tissue injury has been well established for some bacterial infections, such as clostridial myonecrosis, where a deep, penetrating injury interrupts the blood supply and directly introduces organisms (or spores) into devitalized tissues. Though the rate at which S. pyogenes myonecrosis progresses is comparable to that of clostridial gangrene (inches per hour), the types of predisposing injuries are distinctly different. With S. pyogenes infection, a minor muscle strain, sprain, or bruise is often the rule ( Adams, et al., 1985; Stevens, et al., 1989 ). For instance, in our initial report of 20 cases of invasive streptococcal infection, one had a superficial bruise to the hand, and the portal of entry was entirely unknown in the other 7 patients ( Stevens, et al., 1989 ). Thus, 8 of 20 patients (40%) had no known portal of entry, and overall mortality was 30% ( Stevens, et al., 1989 ). Similarly, Adams et al. documented 21 cases of life-threatening S. pyogenes infection, 19 of which lacked an obvious portal of entry and 18 (85.7%) died ( Adams, et al., 1985 ). Finally, a recent case-controlled study found that non-penetrating trauma was significantly associated with S. pyogenes necrotizing fasciitis ( Nuwayhid, Aronoff, & Mulla, 2007 ). In these “no portal” cryptic infections, the correct diagnosis is often delayed until after shock and organ failure manifest ( Bisno & Stevens, 1996 ), which often causes mortality to exceed 70% ( Adams, et al., 1985 ). Survivors undergo emergent amputation or extensive surgical debridement and prolonged hospitalization ( Bisno & Stevens, 1996; Stevens, et al., 1989; Schurr, Engelhardt, & Helgerson, 1998 ). Such findings have prompted several authors to conclude that non-penetrating muscle injury may be a prerequisite for S. pyogenes necrotizing fasciitis or myonecrosis ( Adams, et al., 1985; Nuwayhid, Aronoff, & Mulla, 2007 ).

What is a streptss?

StrepTSS is more fully defined in Table 1 ( The Working Group on Severe Streptococcal Infections, 1993 ), but, simply stated, is any streptococcal infection that is associated with the sudden onset of shock and organ failure. Definite cases are those in which S. pyogenes is isolated from a normally sterile body site. Such cases were first described in the United States and Europe during the mid- to late 1980s ( Martin & Høiby, 1990; Stevens, et al., 1989; Francis & Warren, 1988 ). Since then, reports of StrepTSS in adults and children have emerged worldwide. Most cases have occurred sporadically, though some clusters have been reported. The highest incidence of invasive streptococcal disease occurred in a small Minnesota community, where 26 cases/100,000 population were recorded ( Cockerill, et al., 1997 ). In addition, outbreaks have occurred in closed environments, such as nursing homes ( Thigpen, et al., 2007; Hohenboken, Anderson, & Kaplan, 1994; Jordan, Richards, Burton, Thigpen, & Van Beneden, 2007; Harkness, Bentley, Mottley, & Lee, 1992; Ruben, Norden, Heisler, & Korica, 1984) and hospitals ( DiPersio, et al., 1996 ). Secondary cases of StrepTSS are unusual, but transmission to family members ( DiPersio, et al., 1996; Gamba, et al., 1997) or health care workers ( DiPersio, et al., 1996; Valenzuela, Hooton, Kaplan, & Schlievert, 1991) has been well documented by demonstrating identical pulsed-field gel electrophoresis patterns from cross-infecting strains. Although many of the initial reports described StrepTSS in adults, children are also affected ( Cockerill, et al., 1997; Wheeler, Roe, Kaplan, Schlievert, & Todd, 1991; Kiska, et al., 1997; Givner, Abramson, & Wasilauskas, 1991; Brogan, Nizet, Waldhausen, Rubens, & Clarke, 1995; Stockmann, et al., 2012 ). In 2010, the incidence of invasive infection in children in Utah reached 14 cases/100,000 population ( Stockmann, et al., 2012 ). Thus, persons of all ages can be afflicted and, although some have underlying medical conditions such as diabetes and alcoholism ( Francis & Warren, 1988; Wheeler, Roe, Kaplan, Schlievert, & Todd, 1991; Schwartz, Facklam, & Breiman, 1990; Barnham, 1989; Braunstein, 1991; Holm, Norrby, Bergholm, & Norgren, 1992 ), many have no predisposing medical condition and are not immunocompromised. This contrasts sharply with reviews of S. pyogenes bacteremia from several decades ago ( Francis & Warren, 1988; Barnham, 1989; Braunstein, 1991 ), which found that the disease occurred primarily among the very young, the very old, or patients with predisposing conditions, such as cancer, renal failure, leukemia, severe burns, or iatrogenic immunosuppression.

How does S. pyogenes enter the bloodstream?

The entry of S. pyogenes into the bloodstream and deeper tissues may occur as a result of a breach of an epithelial barrier , or the organism itself may penetrate intact membranes, such as the pharyngeal mucosa. Although bacteremia rarely follows streptococcal pharyngitis, transient bacteremia likely occurs in ~50% of patients who develop invasive infections without a portal of entry. The organism adeptly avoids destruction by the host’s immune system largely because of the anti-phagocytic properties of the M protein ( Lancefield, 1933 ). Adherence of S. pyogenes to pharyngeal mucosal cells is a prerequisite to colonization or infection, and has been related to surface structures, such as lipoteichoic acid and fibronectin-binding proteins. Penetration or translocation of the organism through respiratory epithelial cells has been demonstrated for M-type 1 S. pyogenes. Some have suggested that M-1 strains possessing an invasin ( inv +) gene penetrate more efficiently ( LaPenta, Rubens, Chi, & Cleary, 1994 ). If penetration of mucosal barriers occurs readily with these strains, it generally does not result in clinically detectable bacteremia in the vast majority of cases, since the incidence of invasive infection remains generally very low (~3.5 cases/100,000 population) ( O'Brien, et al., 2002 ). Thus, the clearance of S. pyogenes by the human immune system must be highly efficient.

What is necrotizing fasciitis?

Necrotizing fasciitis (NF) is an infection of the deeper subcutaneous tissues and fascia that is characterized by extensive and rapidly spreading necrosis (gangrene) of the skin and underlying structures. While necrotizing soft-tissue infections may be caused by multiple aerobic and anaerobic microorganisms and may vary in their clinical manifestations, the present discussion is limited to necrotizing fasciitis caused by S. pyogenes ( Bisno & Stevens, 1996 ), and as described by Meleney in 1924 as hemolytic streptococcal gangrene ( Meleney, 1924 ). Characteristically, streptococcal gangrene begins at a site of trivial or even unapparent trauma or in an operative incision. The initial lesion may appear only as an area of mild erythema, but undergoes a rapid evolution over the next 24–72 hours. The inflammation becomes more pronounced and extensive, the skin becomes dusky and then purplish, and bullae containing yellow or hemorrhagic fluid appear. Bacteremia is frequently present, and metastatic abscesses may occur. By the fourth to fifth day, frank gangrenous changes are evident in the affected skin, followed by extensive sloughing. The process may march inexorably over large body areas unless measures are taken to contain it. The patient with streptococcal gangrene appears perilously ill, with high fever and extreme prostration. Mortality rates are high, even with appropriate treatment ( Stevens, 1992 ).

What is a life threatening infection caused by Streptococcus pyogenes?

Life-threatening infections caused by Streptococcus pyogenes (group A streptococcus) include scarlet fever, bacteremia, pneumonia, necrotizing fasciitis, myonecrosis and Streptococcal Toxic Shock Syndrome (StrepTSS). This chapter focuses on the clinical and epidemiological features of these infections, as well as treatment options and bacterial pathogenesis. In brief, such invasive infections can simply be defined as any infection in which S. pyogenes is isolated from a normally sterile body site. Patients with invasive S. pyogenes infections have a relatively low mortality rate, unless they meet the established criteria for StrepTSS.

How long does it take for a pyogenes to appear?

pyogenes necrotizing fasciitis appears to be much more fulminant than that described by Meleney. Specifically, ecchymoses and bullae may appear within 2-3 days and deep muscle involvement is more common. In addition, the mortality rate in 1924 was only 20%, despite the lack of antibiotics, IV fluids, ventilators, and dialysis. In contrast, mortality rates of as high as 70–80% have been reported in the current era (reviewed in ( Wong & Stevens, 2013 )). Given the destruction of multiple layers of soft tissue (epidermis, dermis, subcutaneous tissue, fascia, muscle) in today’s infections, this author believes that “necrotizing soft-tissue infection” is a more accurate term to describe the modern disease.

What are the virulence factors of streptococci?

These virulence factors are the extracellular pyrogenic exotoxins A, B, and C as well as newly discovered exotoxins and superantigens such as exotoxin F (mitogenic factor) and streptococcal superantigen (SSA) (366, 394, 395). In addition, several new superantigens with strong mitogenic activity have recently been reported as SpeG, SpeH, SpeJ, SmeZ, and SmeZ-2 (274, 434). Details about the mitogenic toxins are described in a separate section under virulence factors. These new data point to the fact that there are a large number of superantigens which may play a role in toxic streptococcal syndrome. All of these toxins act as superantigens which interact with major histocompatibility complex (MHC) class II molecules and a limited number of Vβ regions of the T-lymphocyte receptor to activate massive numbers of T cells nonspecifically. The activation liberates large amounts of interleukins as well as other inflammatory cytokines such as tumor necrosis factor and gamma interferon (171, 221, 395). The pyrogenic exotoxins are potentially responsible for at least some of the manifestations of toxic streptococcal syndrome. Kotb and colleagues demonstrated evidence for selective depletion of T cells expressing Vβ1, Vβ5.1, and Vβ12 in patients with streptococcal toxic shock syndrome, further supporting the hypothesis that the streptococcal superantigens play an important role in disease pathogenesis (544). Further evidence also suggests that streptococcal isolates from toxic streptococcal syndrome induce a Th1 rather than a Th2 cytokine response, which is characteristic of superantigens (393).

What is the serological diagnosis of streptococcal infection?

Serological diagnosis of group A streptococcal infections is based on immune responses against the extracellular products streptolysin O, DNase B, hyaluronidase, NADase, and streptokinase, which induce strong immune responses in the infected host (507). Anti-streptolysin O (ASO) is the antibody response most often examined in serological tests to confirm antecedent streptococcal infection. Todd developed the assay for ASO antibodies by 1932 (520). An increase in the ASO titer of ≥166 Todd units is generally accepted as evidence of a group A streptococcal infection. In previous studies it has been shown that infants are born with maternal levels of antistreptococcal antibodies and that infants develop streptococcal infections after the first year of life. ASO antibodies may not demonstrate a detectable rise in 1- to 3-year-olds, who have had few previous group A streptococcal infections (349). At <2 years of age, >50% of the patients had ASO titers of <50 Todd units, and none of the patients had titers above 166 (349). In the same study, older school-age children developed higher ASO titers. All five of the extracellular streptococcal enzymes may become significantly elevated over normal levels during a streptococcal infection. Although the ASO titer is the standard serological assay for confirmation of a group A streptococcal infection, assay of several of the enzymes enhances the chance for a positive test if the patient did not produce high levels of antibody against one or more of the extracellular enzymes. In general, the titers of antibodies against the extracellular products parallel each other; however, exceptions may be seen in infections with pyoderma or nephritogenic strains, when the anti-DNase B titers have been found to be a reliable indicator of streptococcal infection (507). Infection of the skin does not always elicit a strong ASO response.

What is the role of pyrogenic exotoxin B in fibronectin?

Pyrogenic exotoxin B is an extracellular cysteine protease which has been shown to cleave fibronec tin and vitronectin (288), extracellular matrix proteins, and human interleukin-1β into the active form of the molecule (287). Therefore, the protease may be important in inflammation, shock, and tissue destruction. Humans with a diverse range of invasive disease (erysipelas, cellulitis, pneumonia, bacteremia, septic arthritis, toxic shock syndrome, and necrotizing fasciitis) all produced elevated levels of antibodies against streptococcal pyrogenic exotoxin B following infection (214).

What is the name of the group of streptococci that causes impetigo?

The skin infections and nephritis are seasonal, usually occurring during the summer months and in temperate climates. The infection is limited to the epidermis, usually on the face or extremities, and is highly contagious (65). Streptococcal strains which cause pyoderma do not cause rheumatic fever. Staphylococci may be mixed with streptococci in impetigo, and thus the treatment of choice is not penicillin for penicillinase-producing staphylococci (65). Group A streptococcal strains may enter the skin through abrasions and other types of lesions to penetrate the epidermis and produce erysipelas or cellulitis. Erysipelas is a distinctive form of cellulitis with characteristically raised and erythematous superficial layers of the skin, while cellulitis affects subcutaneous tissues (65). Cellulitis may occur from infected burns or wounds. Both erysipelas and cellulitis can be caused by streptococcal groups A, B, C, and G.

What is the most common cause of pharyngitis?

Group A streptococci are the most common bacterial cause of pharyngitis and primarily affect school-age children 5 to 15 years of age (62). All ages are susceptible to spread of the organism under crowded conditions, such as those at schools and military facilities. Pharyngitis and its association with rheumatic fever are seasonal, occurring in the fall and winter (62, 506, 507). This is in contrast to pyoderma or skin infection, which occurs in the summer and can be associated with the production of acute glomerulonephritis (61). Organisms which colonize the skin can also colonize the throat, but streptococcal strains which commonly produce skin infections do not lead to rheumatic fever. Groups C and G can also cause pharyngitis and must be distinguished from group A organisms after throat culture (58, 62). Although they are not considered normal flora, pharyngeal carriage of group A streptococci can occur without clinical symptoms of disease.

Why does scarlet fever occur?

Although usually associated with streptococcal throat infection, scarlet fever may occur due to infections at other sites (62). The group A streptococcal strain producing scarlet fever does so because it carries the genes for one or more of the streptococcal pyrogenic exotoxins A, B, and C. The genes for exotoxins A and C are encoded on a lysogenic temperate bacteriophage (66, 546), while exotoxin B is chromosomal. The pyrogenic exotoxins, currently known as streptococcal superantigens, are responsible for the rash, strawberry tongue, and desquamation of the skin seen in scarlet fever.

What is a streptococci?

Group A streptococci are model extracellular gram-positive pathogens responsible for pharyngitis, impetigo, rheumatic fever, and acute glomerulonephritis. A resurgence of invasive streptococcal diseases and rheumatic fever has appeared in outbreaks over the past 10 years, with a predominant M1 serotype as well as others identified with the outbreaks. emm (M protein) gene sequencing has changed serotyping, and new virulence genes and new virulence regulatory networks have been defined. The emm gene superfamily has expanded to include antiphagocytic molecules and immunoglobulin-binding proteins with common structural features. At least nine superantigens have been characterized, all of which may contribute to toxic streptococcal syndrome. An emerging theme is the dichotomy between skin and throat strains in their epidemiology and genetic makeup. Eleven adhesins have been reported, and surface plasmin-binding proteins have been defined. The strong resistance of the group A streptococcus to phagocytosis is related to factor H and fibrinogen binding by M protein and to disarming complement component C5a by the C5a peptidase. Molecular mimicry appears to play a role in autoimmune mechanisms involved in rheumatic fever, while nephritis strain-associated proteins may lead to immune-mediated acute glomerulonephritis. Vaccine strategies have focused on recombinant M protein and C5a peptidase vaccines, and mucosal vaccine delivery systems are under investigation.

What is group A streptococcal infection?

Group A streptococcus, also known by the abbreviation GAS, is a type of bacteria often found in the throat and on the skin. Group A streptococcal infections commonly cause sore throats, also known as strep throat. This type of bacteria can be the cause of a rash sometimes known as scarlet fever and skin infections such as impetigo and cellulitis.

When should I see my doctor?

Visit your doctor if you have a sore throat or skin sores or a wound that seems to spread or is not getting better. If you think you or someone you care for has a group A streptococcal infection , it is important to see a doctor as soon as possible. The infection can spread through the body and can become serious if not promptly treated with antibiotics.

What is the most severe form of igas?

Two of the most severe forms of iGAS are necrotising fasciitis (sometimes called ‘flesh-eating bacteria’) and streptococcal toxic shock syndrome.

What is the name of the bacteria that causes strep throat?

Group A streptococcal bacteria can cause strep throat, scarlet fever, impetigo, cellulitis and other rarer but severe health conditions.

How do you get streptococcus?

However, people who carry group A streptococcus can also spread the infection by coughing and sneezing droplets that contain the bacteria, or by direct skin contact. For example, if you are in close contact with someone with group A streptococcal bacteria, you may become infected if you:

What tests are needed for strep throat?

Serious group A streptococcal disease (iGAS), including necrotising fasciitis and toxic shock syndrome will require blood tests and swabs of the infected areas.

What are the symptoms of strep throat?

Strep throat symptoms may include a sore throat and tonsils, pain when swallowing, fever, muscle aches and pains, and tiredness.

What is a group A streptococcal infection?

Group A streptococcal infection. A group A streptococcal infection is an infection with group A streptococcus (GAS). Streptococcus pyogenes comprises the vast majority of the Lancefield group A streptococci, and is often used as a synonym for GAS. However, S. dysgalactiae can also be group A. S.

How long does it take for a PSGN to develop?

It is classified as a type III hypersensitivity reaction. Symptoms of PSGN develop within 10 days following a strep throat or 3 weeks following a GAS skin infection. PSGN involves inflammation of the kidney. Symptoms include pale skin, lethargy, loss of appetite, headache, and dull back pain.

What are the different types of streptococci?

There are many other types of streptococci (species of Streptococcus ), including group B streptococcus ( Streptococcus agalactiae) and Streptococcus pneumoniae, which cause other types of infections and should not be confused with group A strep. Several virulence factors contribute to the pathogenesis of GAS, such as M protein, hemolysins, ...

What is the name of the group of bacteria that causes infections of the throat and skin?

Types of infection. Group A β-hemolytic streptococcus can cause infections of the throat and skin. These may vary from very mild conditions to severe, life-threatening diseases. Although it is not completely clear what causes different people to develop different diseases as a result of infection with the same pathogenic bacteria, ...

What is a severe infection?

Severe infections. Some strains of group A streptococci (GAS) cause severe infection. Severe infections are usually invasive, meaning that the bacteria has entered parts of the body where bacteria are not usually found, such as the blood, lungs, deep muscle or fat tissue.

How to diagnose S. pyogenes?

Diagnosis is by a swab of the affected area for laboratory testing. A Gram stain is performed to show Gram-positive cocci in chains. Then, the organism is cultured on blood agar with an added bacitracin antibiotic disk to show beta-hemolytic colonies and sensitivity (zone of inhibition around the disk) for the antibiotic. Culture on agar not containing blood, and then performing the catalase test should show a negative reaction for all streptococci. S. pyogenes is CAMP and hippurate tests negative. Serological identification of the organism involves testing for the presence of group-A-specific polysaccharide in the bacterium's cell wall using the Phadebact test.

What are the complications of GAS?

In addition, infection of GAS may lead to further complications and health conditions, namely acute rheumatic fever and poststreptococcal glomerulonephritis .

Epidemiology

• Health experts estimate that more than 10 million mild infections (throat and skin) occur every year.

See more on my.clevelandclinic.org

Genetics

Research

Classification

Cause

Overview