Strep is short for Streptococcus, a type of bacteria. There are two types: group A and group B.

Group A strep causes

• Strep throat - a sore, red throat. Your tonsils may be swollen and have white spots on them.
• Scarlet fever - an illness that follows strep throat. It causes a red rash on the body.
• Impetigo - a skin infection
• Toxic shock syndrome
• Cellulitis and necrotizing fasciitis (flesh-eating disease)

Group B strep can cause blood infections, pneumonia and meningitis in newborns. A screening test during pregnancy can tell if you have it. If you do, I.V. antibiotics during labor can save your baby's life. Adults can also get group B strep infections, especially if they are elderly or already have health problems. Strep B can cause urinary tract infections, blood infections, skin infections and pneumonia in adults.

Antibiotics are used to treat strep infections.

What You Need to Know

• CDC is investigating a possible increase in intracranial (within the head) infections in children.
• A preliminary analysis of hospitalizations from a wide range of children’s hospitals across the United States has not found an increase in intracranial infections in children. Additional analyses are ongoing and results may change, but the preliminary data are reassuring.
• Seek medical care immediately if your child has symptoms of a head infection.

Types of infections

The types of head infections CDC is investigating include

• Brain abscess — a collection of pus from an infection in the brain that puts harmful pressure on brain tissue
• Subdural empyema — a collection of pus from an infection in the subdural space, which is between the outer and middle layers of membrane around the brain
• Epidural empyema — a collection of pus from an infection in the epidural space, which is the area between the skull and the thick membrane that covers the brain

In children, head infections are rare.

In healthy children, these infections are most often caused by Streptococcus bacteria commonly found in the nose and throat, such as S. intermedius and S. pneumoniae. Most children will not have any illness from these bacteria when they are found in the nose and throat. However, in rare cases the germs may enter parts of the body that are normally free from germs. When this happens, it is called invasive disease and is usually very severe.

What parents can do

If you have any questions about your child’s health, call your child’s healthcare provider. Other things you can do:

Seek medical care immediately if your child has symptoms of a head infection.

Symptoms of a head infection include:

• Severe headache
• Changes in personality or behavior (e.g., confusion, irritability)
• Seizures
• Changes in speech (e.g., slurred speech)
• Weakness on one side of the body
• Changes in vision, such as blurring or double vision
• Stiff neck or back

Children with head infections may also have a fever and vomit.

Keep children up to date on all their vaccinations. Help your child take everyday actions to help prevent disease.

• All children should get vaccinated against pneumococcal disease, which helps prevent S. pneumoniae infections.
• There’s no vaccine to prevent S. intermedius infections.
• All children should be up to date with recommended vaccinations, including flu and COVID-19.

Help your child take everyday actions to help prevent disease, like

• Washing hands often
• Avoiding people who are sick
• Covering coughs and sneezes
• Not touching their eyes, nose, or mouth

About Streptococcus bacteria causing head infections

Infections of the brain are rare because the body has several defenses to protect it. One of these is the blood-brain barrier, a thick membrane that keeps germs from getting into the brain. However, in some cases, germs can get through these defenses and infect the brain.

S. intermedius is a type of bacteria that rarely causes illness. But when they do, the bacteria can cause abscesses—collections of pus. These bacteria most commonly cause abscesses in the liver and brain. They can also cause an infection in the heart, known as endocarditis. S. intermedius can affect people of all ages and cause severe illness in otherwise healthy people.

S. pneumoniae can cause many types of infections, which are collectively known as pneumococcal disease. These infections range from ear and sinus infections to infections of the lung, blood, or lining of the brain and spinal cord. Most pneumococcal infections are mild, but some can be severe. Anyone can get pneumococcal disease, but being younger than 2 years old or 65 years or older or having certain medical conditions can increase risk.

Spread

Germs that can cause head infections, such as S. intermedius, are commonly found in the nose, mouth, and throat. These bacteria can enter the body and spread to the brain or the layers around the brain

• Through the bloodstream from an infection in other parts of the body, such as ears, eyes, sinuses, or teeth
• By entering the brain directly through an open wound in the head

However, we do know that pediatric intracranial infections can rarely follow viral and bacterial respiratory infections, like sinusitis.

Diagnosis

Doctors diagnose head infections by first conducting a physical exam and obtaining a complete medical history of the patient. To confirm the diagnosis, doctors may use diagnostic tests, such as

• Magnetic resonance imaging (MRI)
• Computed tomography (CT) scan
• Blood tests
• Lumbar puncture (spinal tap)

Doctors may also collect a sample of pus to determine which germ is causing the infection.

Treatment

Head infections can be difficult to treat. Antibiotics are used to kill the bacteria causing the infections, and surgery is often needed to drain the pus. Getting treatment quickly is important.

Complications

Even with treatment, head infections can sometimes lead to long-term neurological (nervous system) problems, such as weakness or trouble moving. These infections can also lead to the body having an extreme response to the infection, which is known as sepsis. With treatment, these infections rarely result in death.

Streptococcus are gram-positive cocci with a microscopic morphology that resembles chains of bacteria. Colonies are typically small (1–2 mm in diameter), translucent, entire edge, with a slightly raised elevation that can be either nonhemolytic, alpha-hemolytic, or beta-hemolytic when grown on blood agar. Additionally, they are facultative anaerobes that are catalase-negative.

The genus Streptococcus includes important pathogens that are categorized in serological Lancefield groups based on the distinguishing characteristics of their surface carbohydrates. The most clinically important streptococcal species in humans is S. pyogenes, also known as group A streptococcus (GAS). S. pyogenes produces a variety of extracellular enzymes, including streptolysins O and S, hyaluronidase, and streptokinase. These enzymes can aid in transmission and contribute to the inflammatory response. S. pyogenes also produces a capsule and M protein, a streptococcal cell wall protein. These virulence factors help the bacteria to avoid phagocytosis while provoking a substantial immune response that contributes to symptoms associated with streptococcal infections.

S. pyogenes causes a wide variety of diseases not only in the skin, but in other organ systems as well. Examples of diseases elsewhere in the body include pharyngitis and scarlet fever, which will be covered in later chapters.

Cellulitis, Erysipelas, and Erythema Nosodum

Common streptococcal conditions of the skin include cellulitis, erysipelas, and erythema nodosum. An infection that develops in the dermis or hypodermis can cause cellulitis, which presents as a reddened area of the skin that is warm to the touch and painful. The causative agent is often S. pyogenes, which may breach the epidermis through a cut or abrasion, although cellulitis may also be caused by staphylococci. S. pyogenes can also cause erysipelas, a condition that presents as a large, intensely inflamed patch of skin involving the dermis (often on the legs or face). These infections can be suppurative, which results in a bullous form of erysipelas. Streptococcal and other pathogens may also cause a condition called erythema nodosum, characterized by inflammation in the subcutaneous fat cells of the hypodermis. It sometimes results from a streptococcal infection, though other pathogens can also cause the condition. It is not suppurative, but leads to red nodules on the skin, most frequently on the shins.

In general, streptococcal infections are best treated through identification of the specific pathogen followed by treatment based upon that particular pathogen’s susceptibility to different antibiotics. Many immunological tests, including agglutination reactionsand ELISAs, can be used to detect streptococci. Penicillin is commonly prescribed for treatment of cellulitis and erysipelas because resistance is not widespread in streptococci at this time. In most patients, erythema nodosum is self-limiting and is not treated with antimicrobial drugs. Recommended treatments may include nonsteroidal anti-inflammatory drugs (NSAIDs), cool wet compresses, elevation, and bed rest.

Necrotizing Fasciitis

Streptococcal infections that start in the skin can sometimes spread elsewhere, resulting in a rare but potentially life-threatening condition called necrotizing fasciitis, sometimes referred to as flesh-eating bacterial syndrome. S. pyogenes is one of several species that can cause this rare but potentially-fatal condition; others include Klebsiella, Clostridium, Escherichia coli, S.aureus, and Aeromonas hydrophila.

Necrotizing fasciitis occurs when the fascia, a thin layer of connective tissue between the skin and muscle, becomes infected. Severe invasive necrotizing fasciitis due to Streptococcus pyogenes occurs when virulence factors that are responsible for adhesion and invasion overcome host defenses. S. pyogenes invasins allow bacterial cells to adhere to tissues and establish infection. Bacterial proteases unique to S. pyogenes aggressively infiltrate and destroy host tissues, inactivate complement, and prevent neutrophil migration to the site of infection. The infection and resulting tissue death can spread very rapidly, as large areas of skin become detached and die. Treatment generally requires debridement (surgical removal of dead or infected tissue) or amputation of infected limbs to stop the spread of the infection; surgical treatment is supplemented with intravenous antibiotics and other therapies.

Necrotizing fasciitis does not always originate from a skin infection; in some cases there is no known portal of entry. Some studies have suggested that experiencing a blunt force trauma can increase the risk of developing streptococcal necrotizing fasciitis.

A common upper respiratory infection, streptococcal pharyngitis (strep throat) is caused by Streptococcus pyogenes. This gram-positive bacterium appears as chains of cocci, as seen below. Rebecca Lancefield serologically classified streptococci in the 1930s using carbohydrate antigens from the bacterial cell walls. S. pyogenes is the sole member of the Lancefield group A streptococci and is often referred to as GAS, or group A strep.

Similar to streptococcal infections of the skin, the mucosal membranes of the pharynx are damaged by the release of a variety of exoenzymes and exotoxins by this extracellular pathogen. Many strains of S. pyogenes can degrade connective tissues by using hyaluronidase, collagenase and streptokinase. Streptokinase activates plasmin, which leads to degradation of fibrin and, in turn, dissolution of blood clots, which assists in the spread of the pathogen. Released toxins include streptolysins that can destroy red and white blood cells. The classic signs of streptococcal pharyngitis are a fever higher than 38 °C (100.4 °F); intense pharyngeal pain; erythema associated with pharyngeal inflammation; and swollen, dark-red palatine tonsils, often dotted with patches of pus; and petechiae (microcapillary hemorrhages) on the soft or hard palate (roof of the mouth) (Figure). The submandibular lymph nodes beneath the angle of the jaw are also often swollen during strep throat.

Some strains of group A streptococci produce erythrogenic toxin. This exotoxin is encoded by a temperate bacteriophage (bacterial virus) and is an example of phage conversion. The toxin attacks the plasma membranes of capillary endothelial cells and leads to scarlet fever (or scarlatina), a disseminated fine red rash on the skin, and strawberry tongue, a red rash on the tongue (Figure). Severe cases may even lead to streptococcal toxic shock syndrome (STSS), which results from massive superantigen production that leads to septic shock and death.

S. pyogenes can be easily spread by direct contact or droplet transmission through coughing and sneezing. The disease can be diagnosed quickly using a rapid enzyme immunoassay for the group A antigen. However, due to a significant rate of false-negative results (up to 30%), culture identification is still the gold standard to confirm pharyngitis due to S. pyogenes. S. pyogenes can be identified as a catalase-negative, beta hemolytic bacterium that is susceptible to 0.04 units of bacitracin. Antibiotic resistance is limited for this bacterium, so most β-lactams remain effective; oral amoxicillin and intramuscular penicillin G are those most commonly prescribed.

Sequelae of S. pyogenes Infections

One reason strep throat infections are aggressively treated with antibiotics is because they can lead to serious sequelae, later clinical consequences of a primary infection. It is estimated that 1%–3% of untreated S. pyogenes infections can be followed by nonsuppurative (without the production of pus) sequelae that develop 1–3 weeks after the acute infection has resolved. Two such sequelae are acute rheumatic fever and acute glomerulonephritis.

Acute rheumatic fever can follow pharyngitis caused by specific rheumatogenic strains of S. pyogenes (strains 1, 3, 5, 6, and 18). Although the exact mechanism responsible for this sequela remains unclear, molecular mimicry between the M protein of rheumatogenic strains of S. pyogenes and heart tissue is thought to initiate the autoimmune attack. The most serious and lethal clinical manifestation of rheumatic fever is damage to and inflammation of the heart (carditis). Acute glomerulonephritis also results from an immune response to streptococcal antigens following pharyngitis and cutaneous infections. Acute glomerulonephritis develops within 6–10 days after pharyngitis, but can take up to 21 days after a cutaneous infection. Similar to acute rheumatic fever, there are strong associations between specific nephritogenic strains of S. pyogenes and acute glomerulonephritis, and evidence suggests a role for antigen mimicry and autoimmunity. However, the primary mechanism of acute glomerulonephritis appears to be the formation of immune complexes between S. pyogenes antigens and antibodies, and their deposition between endothelial cells of the glomeruli of kidney. Inflammatory response against the immune complexes leads to damage and inflammation of the glomeruli (glomerulonephritis).