Group A streptococcal infection

Humans may also carry the GAS either on the skin or in the throat and show no symptoms.^[8] These carriers are less contagious than symptomatic carriers of the bacteria.^[8]

The non-invasive infections caused by GAS tend to be less severe and more common. They occur when the bacteria colonizes the throat area, where it recognizes

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

Most common:

• impetigo, cellulitis, and erysipelas – infections of the skin which can be complicated by necrotizing fasciitis – skin, fascia and muscle
• strep throat AKA strep pharyngitis – pharynx

• bacteremia
  can be associated with these infections, but is not typical.
• septic arthritis – joints
• osteomyelitis – bones
• vaginitis – vagina (more common in pre-pubescent girls)
• meningitis* – meninges
• sinuses
• pneumonia* – pulmonary alveolus

(*Note that meningitis, sinusitis and pneumonia can all be caused by Group A Strep, but are much more commonly associated with Streptococcus pneumoniae and should not be confused.)

Severe infections

Some strains of group A streptococci (GAS) cause severe infection. Severe infections are usually invasive, meaning that the

All severe GAS infections may lead to

Severe Group A streptococcal infections often occur sporadically but can be spread by person-to-person contact.[14] Close contacts of people affected by severe Group A streptococcal infections, defined as those having had prolonged household contact in the week before the onset of illness, may be at increased risk of infection. This increased risk may be due to a combination of shared genetic susceptibility within the family, close contact with carriers, and the virulence of the Group A streptococcal strain that is involved.^[15]

Public health policies internationally reflect differing views of how the close contacts of people affected by severe Group A streptococcal infections should be treated. Health Canada^[16] and the US CDC recommend close contacts see their doctor for full evaluation and may require antibiotics;^[17] current UK Health Protection Agency guidance is that, for a number of reasons, close contacts should not receive antibiotics unless they are symptomatic but that they should receive information and advice to seek immediate medical attention if they develop symptoms.^[15] However, guidance is clearer in the case of mother-baby pairs: both mother and baby should be treated if either develops an invasive GAS infection within the first 28 days following birth^[15] (though some evidence suggests that this guidance is not routinely followed in the UK^[18]).

Diagnosis

Diagnosis is by a swab of the affected area for laboratory testing. A

S. pyogenes infections are best prevented through effective hand hygiene.[20] No vaccines are currently available to protect against S. pyogenes infection, although research has been conducted into the development of one.^[21] Difficulties in developing a vaccine include the wide variety of strains of S. pyogenes present in the environment and the large amount of time and number of people that will be needed for appropriate trials for safety and efficacy of the vaccine.^[21][22]

Treatment

The treatment of choice is penicillin, and the duration of treatment is around 10 days.

Treatment with ampicillin/sulbactam, amoxicillin/clavulanic acid, or clindamycin is appropriate if deep oropharyngeal abscesses are present, in conjunction with aspiration or drainage.^[26] In cases of streptococcal toxic shock syndrome, treatment consists of penicillin and clindamycin, given with intravenous immunoglobulin.^[27]

For toxic shock syndrome and necrotizing fasciitis, high-dose penicillin and clindamycin are used. Additionally, for necrotizing fasciitis, surgery is often needed to remove damaged tissue and stop the spread of the infection.^[20]

No instance of penicillin resistance has been reported to date, although since 1985, many reports of penicillin tolerance have been made.

The 30-valent N-terminal M-protein-based vaccine as well as the M-protein vaccine (minimal epitope J8 vaccine) are two vaccines for GAS that are currently getting close or becoming clinical studies, however, other vaccines using conserved epitopes are progressing.[29]

Epidemiology

Cases of GAS are still present today, but were also evident before World War I. This was shown by a training camp located in Texas, where a harmful strain of pneumonia complicating measles was caused by a strain of Streptococcus.^[30] Existence of streptococci strains was additionally found in World War II. An epidemic of streptococcal infection in the United States Navy during this war indicated that this type of disease was able to exist and spread in formerly unexposed individuals by environments that serological types of group A streptococci preferred.^[30] In later years, a positive test result for the presence of group A streptococci was found in 32.1 percent of individuals after throat cultures were carried out in a 20 yearlong (1953/1954-1973/1974) study performed in Nashville, TN.^[30] Also, from 1972 to 1974, recurring GAS illness was observed with a prevalence of 19 percent in school-aged children as well as a prevalence rate of 25 percent in families.^[30] The severity of streptococcal infections has decreased over the years, and so has rheumatic fever (a sequelae of GAS) which is indicated by the change in numerous hospitals from containing wards allocated for the sole purpose of treating rheumatic fever to hardly seeing the disease at all.^[30] Environmental factors, such as less crowding and the increase of family living space, can account for the reduction in incidence and severity of group A streptococci.^[30] With more space for individuals to reside in, it provides the bacteria with less opportunities to spread from person to person. This is especially important considering an estimated 500,000 deaths worldwide all occurring after acute rheumatic fever, invasive infection, or subsequent heart disease can be accredited to GAS.^[31] This number is quite large, often leaving the health care system encumbered, since 91 percent of patients infected with invasive GAS need to be hospitalized with 8950–11,500 episodes and 1050-1850 deaths taking place each year.^[31] A later study that occurred from 2005 to 2012 found that there were 10,649-13,434 cases consequently resulting in 1136-1607 deaths per year.^[29]

Complications

• Post-streptococcal glomerulonephritis
• Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS)
• Rheumatic fever
• Scarlet fever
• Toxic shock syndrome

Acute rheumatic fever

Although common in developing countries, ARF is rare in the United States, possibly secondary to improved antibiotic treatment, with small isolated outbreaks reported only occasionally. It is most common among children between 5 and 15 years old and occurs 1–3 weeks after an untreated GAS pharyngitis, but caution is advised when interpreting the demographics of the contemporary picture of pediatric cases in the United States.^[32]

ARF is often clinically diagnosed based on

Further endocarditis can develop with aseptic vegetations along the valve closure lines, in particular the mitral valve. Chronic rheumatic heart disease mostly affects the mitral valve, which can become thickened with calcification of the leaflets, often causing fusion of the commissures and chordae tendineae.

Other findings of ARF include erythema marginatum (usually over the spine or other bony areas) and a red expanding rash on the trunk and extremities that recurs over weeks to months. Because of the different ways ARF presents itself, the disease may be difficult to diagnose.

A neurological disorder, Sydenham

It is important to distinguish ARF from

Obsessive–compulsive disorder and tic disorders are hypothesized to arise in a subset of children as a result of a post-streptococcal autoimmune process.^[34][35][36] Its potential effect was described in 1998 by the controversial hypothesis called PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections), a condition thought to be triggered by GABHS infections.^[37][38] The PANDAS hypothesis is unconfirmed and unsupported by data, and two new categories have been proposed: PANS (pediatric acute-onset neuropsychiatric syndrome) and CANS (childhood acute neuropsychiatric syndrome).^[35][36] The CANS/PANS hypotheses include different possible mechanisms underlying acute-onset neuropsychiatric conditions, but do not exclude GABHS infections as a cause in a subset of individuals.^[35][36] PANDAS, PANS and CANS are the focus of clinical and laboratory research but remain unproven.^[34][35][36]

References