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Scarlet fever

Scarlet fever, also known as scarlatina, is an infectious disease caused by Streptococcus pyogenes, a Group A streptococcus (GAS).[3] It most commonly affects children between five and 15 years of age.[1] The signs and symptoms include a sore throat, fever, headache, swollen lymph nodes, and a characteristic rash.[1] The face is flushed and the rash is red and blanching.[5] It typically feels like sandpaper and the tongue may be red and bumpy.[1] The rash occurs as a result of capillary damage by exotoxins produced by S.pyogenes.[6] On darker-pigmented skin the rash may be hard to discern.[7]

For other uses, see Scarlet fever (disambiguation).

Scarlet fever

Scarlatina,[1] scarletina[2]

Infectious disease

Sore throat, fever, headaches, swollen lymph nodes in the neck, characteristic rash[1]

Kidney disease, rheumatic fever, arthritis[1]

5–15 years old[1]

Group A streptococcal infection[3]

Throat culture[1]

Handwashing, not sharing personal items, staying away from sick people[1]

Antibiotics[1]

Penicillin VK, cefalexin, amoxicillin, clindamycin, erythromycin[4]

Typically good[1]

Scarlet fever develops in a small number of people who have strep throat or streptococcal skin infections.[1] The bacteria are usually spread by people coughing or sneezing.[1] It can also be spread when a person touches an object that has the bacteria on it and then touches their mouth or nose.[1] The diagnosis is typically confirmed by culturing swabs of the throat.[1]


There is no vaccine for scarlet fever.[1] Prevention is by frequent handwashing, not sharing personal items, and staying away from other people when sick.[1] The disease is treatable with antibiotics, which reduce symptoms and spread, and prevent most complications.[1] Outcomes with scarlet fever are typically good if treated.[1] Long-term complications as a result of scarlet fever include kidney disease, rheumatic fever, and arthritis.[1]


In the early 20th century it was a leading cause of death in children, but even before the Second World War and the introduction of antibiotics, its severity was already declining, perhaps due to better living conditions, the introduction of better control measures, or a decline in the virulence of the bacteria.[8][9] In recent years, there have been signs of antibiotic resistance; there was an outbreak in Hong Kong in 2011 and in the UK in 2014, and occurrence of the disease rose by 68% in the UK between 2014 and 2018. Research published in October 2020 showed that infection of the bacterium by three viruses has led to more virulent strains of the bacterium.[10]

: This is a complication that results 2–6 weeks after a group A streptococcal infection of the upper respiratory tract.[21] It presents in developing countries, where antibiotic treatment of streptococcal infections is less common, as a febrile illness with several clinical manifestations, which are organized into what is called the Jones criteria. These criteria include arthritis, carditis, neurological issues, and skin findings. Diagnosis also depends on evidence of a prior group A streptococcal infection in the upper respiratory tract (as seen in streptococcal pharyngitis and scarlet fever). The carditis is the result of the immunologic response targeting the person's heart tissue, and it is the most serious sequelae that develops from acute rheumatic fever. When this involvement of the heart tissue occurs, it is called rheumatic heart disease. In most cases of rheumatic heart disease, the mitral valve is affected, ultimately leading to mitral stenosis.[22] The link to rheumatic fever and heart disease is a particular concern in Australia, because of the high prevalence of these diseases in Aboriginal and Torres Strait Islander communities.[10]

Acute rheumatic fever

: This is inflammation of the kidney, which presents 1–2 weeks after a group A streptococcal pharyngitis. It can also develop after an episode of Impetigo or any group A streptococcal infection in the skin (this differs from acute rheumatic fever which only follows group A streptococcal pharyngitis).[21][24] It is the result of the autoimmune response to the streptococcal infection affecting part of the kidney. Persons present with what is called acute nephritic syndrome, in which they have high blood pressure, swelling, and urinary abnormalities. Urinary abnormalities include blood and protein found in the urine, as well as less urine production overall.[21]

Poststreptococcal glomerulonephritis

Poststreptococcal reactive arthritis: The presentation of arthritis after a recent episode of group A streptococcal pharyngitis raises suspicion for acute rheumatic fever, since it is one of the for that separate complication. But, when the arthritis is an isolated symptom, it is referred to as poststreptococcal reactive arthritis. This arthritis can involve a variety of joints throughout the body, unlike the arthritis of acute rheumatic fever, which primarily affects larger joints such as the knee joints. It can present less than 10 days after the group A streptococcal pharyngitis.[21]

Jones criteria

Cause[edit]

Strep throat spreads by close contact among people, via respiratory droplets (for example, saliva or nasal discharge).[21] A person in close contact with another person infected with group A streptococcal pharyngitis has a 35% chance of becoming infected.[22] One in ten children who are infected with group A streptococcal pharyngitis will develop scarlet fever.[16]

Viral : Viral infections are often accompanied by a rash which can be described as morbilliform or maculopapular. This type of rash is accompanied by a prodromal period of cough and runny nose in addition to a fever, indicative of a viral process.[17]

exanthem

Allergic or : The erythematous appearance of the skin will be in a more localized distribution rather than the diffuse and generalized rash seen in scarlet fever.[16]

contact dermatitis

: These are potential side effects of taking certain drugs such as penicillin. The reddened maculopapular rash which results can be itchy and be accompanied by a fever.[35]

Drug eruption

Kawasaki disease: Children with this disease also present with a strawberry tongue and undergo a desquamative process on their palms and soles. However, these children tend to be younger than five years old, their fever lasts longer (at least five days), and they have additional clinical criteria (including signs such as conjunctival redness and cracked lips), which can help distinguish this from scarlet fever.

[36]

: Both streptococcal and staphylococcal bacteria can cause this syndrome. Clinical manifestations include diffuse rash and desquamation of the palms and soles. It can be distinguished from scarlet fever by low blood pressure, lack of sandpaper texture for the rash, and multi-organ system involvement.[37]

Toxic shock syndrome

: This is a disease that occurs primarily in young children due to a toxin-producing strain of the bacteria Staphylococcus aureus. The abrupt start of the fever and diffused sunburned appearance of the rash can resemble scarlet fever. However, this rash is associated with tenderness and large blister formation. These blisters easily pop, followed by causing the skin to peel.[38]

Staphylococcal scalded skin syndrome

Staphylococcal scarlet fever: The rash is identical to the streptococcal scarlet fever in distribution and texture, but the skin affected by the rash will be tender.

[5]

Prevention[edit]

One method is long-term use of antibiotics to prevent future group A streptococcal infections. This method is only indicated for people who have had complications like recurrent attacks of acute rheumatic fever or rheumatic heart disease. Antibiotics are limited in their ability to prevent these infections since there are a variety of subtypes of group A streptococci that can cause the infection.[21]


Although there are currently no vaccines available, the vaccine approach has a greater likelihood of effectively preventing group A streptococcal infections in the future because vaccine formulations can target multiple subtypes of the bacteria.[21] A vaccine developed by George and Gladys Dick in 1924 was discontinued due to poor efficacy and the introduction of antibiotics. Difficulties in vaccine development include the considerable strain variety of group A streptococci present in the environment and the amount of time and number of people needed for appropriate trials for safety and efficacy of any potential vaccine.[39] There have been several attempts to create a vaccine in the past few decades. These vaccines, which are still in the development phase, expose the person to proteins present on the surface of the group A streptococci to activate an immune response that will prepare the person to fight and prevent future infections.[40]


There used to be a diphtheria scarlet fever vaccine.[41] It was, however, found not to be effective.[42] This product was discontinued by the end of World War II.

Epidemiology[edit]

Scarlet fever occurs equally in both males and females.[16] Children are most commonly infected, typically between 5–15 years old. Although streptococcal infections can happen at any time of year, infection rates peak in the winter and spring months, typically in colder climates.[21]


The morbidity and mortality of scarlet fever has declined since the 18th and 19th centuries when there were epidemics of this disease.[46] Around 1900 the mortality rate in multiple places reached 25%.[47] The improvement in prognosis can be attributed to the use of penicillin in the treatment of this disease.[13] The frequency of scarlet fever cases has also been declining over the past century.


There have been several reported outbreaks of the disease in various countries in the past decade.[48] The reason for these increases remains unclear in the medical community. Between 2013 and 2016 population rates of scarlet fever in England increased from 8.2 to 33.2 per 100,000 and hospital admissions for scarlet fever increased by 97%.[49] Further increases in the reporting of scarlet fever cases have been noted in England during the 2021–2022 season (September to September) and so far also in the season 2022–2023.[50] The World Health Organization has reported an increase in scarlet fever (and iGAS – invasive GAS cases) in England, and other European countries during this time. Increases have been reported in France and Ireland.[51] In the US, cases of scarlet fever are not reported, but as of December 2022, the CDC was looking at a possible increase in the numbers of invasive GAS infections reported in children.[52] In late December 2022, the CDC's Health Alert Network issued an advisory on the reported increases in invasive GAS infections.[53]

Otto Kalischer wrote a doctoral thesis on scarlet fever in 1891.

Otto Kalischer wrote a doctoral thesis on scarlet fever in 1891.

A 1930s American poster attempting to curb the spread of such diseases as scarlet fever by regulating milk supply

A 1930s American poster attempting to curb the spread of such diseases as scarlet fever by regulating milk supply

Gladys Henry Dick (pictured) and George Frederick Dick developed an antitoxin and vaccine for scarlet fever in 1924 which were later eclipsed by penicillin in the 1940s.

Gladys Henry Dick (pictured) and George Frederick Dick developed an antitoxin and vaccine for scarlet fever in 1924 which were later eclipsed by penicillin in the 1940s.