Scarlet fever is a disease that can occur as a result of a streptococcal group infection (group A strep). The signs and symptoms include sore throat, fever, headache, swollen lymph nodes, and a distinctive rash. The rash is red and feels like sandpaper and the tongue may be red and wavy. Most common in children between five and 15 years.
Scarlet fever affects a small number of people who have a strep throat or streptococcal infection of the skin. Bacteria are usually spread by people who cough or sneeze. It can also spread when a person touches an object that has bacteria on it and then touches their mouth or nose. A typical rash is caused by an erythrogenic toxin, a substance produced by several types of bacteria. Diagnosis is usually confirmed by breeding the throat.
There is no vaccine. Prevention is to frequently wash hands, not share personal items, and stay away from others when sick. The disease can be treated with antibiotics, which prevents most of the complications. Results with dengue are usually good if treated. Long-term complications from dengue fever include kidney disease, rheumatic heart disease, and arthritis. It was the leading cause of death in children in the early 20th century.
Video Scarlet fever
Signs and symptoms
Rashes that have a distinctive appearance, dispersal pattern, and desquamating process "Strawberry Tongue"
- The tongue begins with having a white coating on it while the tongue papillae is swollen and flushed. Projection of red papillae through a white coating gives the tongue the appearance of "white strawberries".
- Then a few days later (after the desquamating process, or the tissue shedding that creates the white layer), the whiteness disappears while the red and enlarged papillae gives it a "red strawberry" appearance.
- Note that the involvement of the tongue is part of the rash that is characteristic of dengue fever.
Past Line
- Petechiae lines that appear as pink/red areas located in the arm and elbow holes
Vomiting and abdominal pain
Strep throat
Typical symptoms of streptococcal pharyngitis (also known as strep throat):
- Sore throat, painful swallowing
- Fever - usually more than 39Ã, Â ° C (102,2Ã, Â ° F)
- Fatigue
- Enlarged and reddened tonsils with exudates are yellow or white (usually this is exudative pharyngitis)
- Enlarged lymph nodes are usually located on the front of the neck
The following symptoms will usually be absent: cough, hoarseness, runny nose, diarrhea, and conjunctivitis. Their presence suggests it is more likely to be a viral infection.
Rash
The rash begins 1-2 days after the onset of symptoms caused by sore throat (sore throat, fever, fatigue). This typical rash has been epitomized as "scarlatiniform" and appears as a skin diffuse redness with small papules, or lumps, resembling acne goose. This lump is what gives a typical sandpaper texture to the rash. The reddened skin will blush when you press it. It is possible for the skin to become itchy but it will not be painful. It usually first appears in the trunk and then gradually spreads to the arms and legs. The palms, palms and faces are usually left uninvolved by the rash. The face, however, is usually flushed, most prominent in the cheeks, with a pale circle around the mouth. After the rash is spread, it becomes more pronounced in the creases in the skin, such as the skin folds in the inguinal and axillary regions of the body. Also in those areas there may be Paste Line which petechiae is arranged in a linear pattern. Within 1 week the onset of the rash begins to fade followed by a longer process of desquamation, or shedding of the outer layer of skin, which lasts several weeks. The desquamation process usually begins on the face and continues downward on the body. After deskuamasi skin will be left with a sunburned appearance.
Mouth
The streptococcal pharyngitis which is an ordinary presentation of scarlet fever in combination with a characteristic rash usually involves the tonsils. The tonsils will appear swollen and flushed. The ceiling and uvula are also often infected. Involvement of the soft palate can be seen as small red and round spots known as Forscheimer spots.
Presentation of variables
The characteristics of dengue can vary depending on the person's age and race. Children younger than 5 years may have atypical presentations. Children younger than 3 years may present with stuffy nose and low grade fever. Babies can only present with increased irritability and decreased appetite.
Children who have darker skin can have different presentations because the redness of the skin involved in rashes and pale circles around the mouth can be less obvious. Suspicions based on accompanying symptoms and important diagnostic studies in this case.
Course
After exposure to streptococcus, it takes 12 hours to 7 days for the onset of symptoms. This may include fever, fatigue, and sore throat. A typical scarlatiniform rash then appears 12-48 hours later. During the first few days of rapid rash and generalization developments, Pastoral lines and strawberry tongues will also be present. The rash begins to fade within 3-4 days followed by a rash desquamation that will last several weeks to a month. If the case of dengue fever is not complicated, recovery from fever and clinical symptoms other than desquamation process occurs within 5-10 days.
Complications
Complications that can arise from dengue when not treated or treated inadequately can be divided into two categories: suppurative and nonsuppurative.
Suppurative complications: This is a rare complication arising from direct spread to structures close to the site of major infection, which in most cases Scarlet Fever is a pharynx. Possible problems with this spread method include peritonsillar or retropharyngeal abscesses, cellulitis, mastoiditis or sinusitis. It is also possible for streptococcal infection to spread through the lymphatic system or blood to the body area farther from the pharynx. Some examples of the many complications that can arise from this spread method include endocarditis, pneumonia, or meningitis.
Nonsuppurative Complications: These complications arise from certain subtypes of group A streptococci that cause an autoimmune response in the body through what is called molecular mimicry. Antibodies developed by a person's immune system to attack group A streptococci in this case can also invade the person's own tissue. The result of the following complications depends on which tissue in the body of a person is targeted by the antibody
- Acute rheumatic fever This is a complication that occurs 2-6 weeks after group A streptococcal infection in the upper respiratory tract. It is present in developing countries, where antibiotic treatment of streptococcal infection is less common, as a febrile illness with some clinical manifestations that are set into what Jones calls the criteria. These criteria include arthritis, carditis, neurological problems and skin findings. There should also be evidence of previous group A streptococcal infections in the upper respiratory tract (as seen in streptococcal and dengue pharyngitis). Carditis is the result of an immunological response that targets a person's heart tissue and is the most serious sequel to developing from acute rheumatic fever. When this cardiac tissue involvement occurs it is called rheumatic heart disease. In most cases rheumatic heart disease, mitral valve is affected, which ultimately leads to mitral stenosis.
- Post-Streptococcal glomerulonephritis: This is a renal inflammation occurring 1-2 weeks after group A streptococcal pharyngitis. It may also develop after an Impetigo episode or group A streptococcal infection in the skin (this differs from acute rheumatic fever that follows only group A streptococcal pharyngitis). This is the result of an autoimmune response to a streptococcal infection that affects the kidneys. Present the patient with what is called acute nephritic syndrome in which they have high blood pressure, swelling and urinary abnormalities. Urinary disorders include blood and protein found in the urine and less urine production overall.
- Reactive post-reptid arthritis: Presentation of arthritis after the latest episode of group streptococcal pharyngitis raises suspicion for acute rheumatic fever as it is one of Jones's criteria for separate complications. However, when arthritis is an isolated symptom then it is referred to as poststreptococcal reactive arthritis. This arthritis can involve various joints throughout the body, unlike arthritis of acute rheumatic fever which mainly affects larger joints such as knee joints. May be present less than 10 days after group A streptococcal pharyngitis.
Maps Scarlet fever
Cause
The spread of sore throat occurs by close contact, via respiratory droplets (eg, saliva or nasal secretions). A person in close contact with another person infected with group A streptococcal pharyngitis may be 35% infected. One in ten children infected with group A streptococcal pharyngitis will have dengue fever.
Pathophysiology
Dengue fever, which distinguishes this disease from isolated Group A strep pharyngitis (or sore throat), is caused by a specific strain of Group A Streptococcus that produces a pyogenic exotoxin. This toxin-producing strain causes dengue fever in people who do not yet have antitoxin antibodies. Pyogenic exotoxins of streptococcus A, B, and C (speA, speB, and speC) have been identified. Pyogenic exotoxins are also called erythrogenic toxins and cause a dengue rash. The Streptococcus Group A strain that causes dengue requires certain bacteriophages to produce pyogenic exotoxin production. Specifically, T12 bacteriophage is responsible for the production of speA. Pyotoic Streptococcal Exotoxin A, speA, is one of the most commonly associated with cases of dengue fever compounded by acute immune-mediated rheumatic fever and post-infective glomerulonephritis.
These toxins are also known as "superantigens" because they are capable of causing a broad immune response in the body through activation of some of the major cells responsible for the person's immune system. The body responds to these toxins by making antibodies to their specific ones. poison. However, these antibodies do not fully protect people from future Group A Streptococcal infections because there are 12 different pyogenic exotoxins.
Microbiology
This disease is caused by the secretion of pyogenic exotoxins by bacteria that infect Streptococcus . The pyogenic exogenesis of streptococcus A ( speA ) may be best learned from these toxins. This is carried by the T12 bacteriophage that integrates with the streptococcal genome from where the toxin is transcribed. The fag itself integrates into the serine tRNA gene on the chromosome.
The T12 virus itself has not been placed into taxon by the International Committee on Virus Taxonomy. It has a double-stranded DNA genome and on morphology appears to be a member of Siphoviridae.
The gene speA was cloned and sequenced in 1986. It is 753 long base pairs and encodes a 29,244 kiloDalton (kDa) protein. Protein contains 30-second suspected amino acid signal peptides; the removal of the signal circuit gives a 25787 kDa molecular weight prediction for the secreted protein. Both the promoter and the ribosome binding site (the Shine-Dalgarno sequence) are present in the upstream of the gene. The transcription terminator lies 69 downstream bases of translational termination codon. The carbok terminal portion of the protein shows extensive homology with the carbox ends of Staphylococcus aureus enterotoxins B and C1.
Freak streptococci besides T12 can also carry the gene speA .
Diagnosis
Although the presentation of dengue fever can be diagnosed clinically, further testing may be needed to differentiate it from other diseases. Also, a history of recent exposure to someone with strep throat may be helpful. There are two methods used to confirm suspicion of fast antigen detection test of fever and throat culture.
Rapid antigen detection test is a very specific but not very sensitive test. This means that if the results are positive (indicating that Group A Stigen Oigen is detected and therefore confirm that the patient has Group A Strep Pharyngitis) then it is appropriate to treat them with antibiotics. However, if the Fast Antigen Detection Test is negative (indicating that they do not have Group A Strep Pharyngitis), then a throat culture is needed to confirm because it could be a false negative result. The culture of the throat is the current gold standard for diagnosis.
Serological examinations look for antibodies produced by the body against streptococcal infections including antistreptolysin-O and antideoxyribonuclease B. It takes the body 2-3 weeks to make these antibodies so that this type of test is not useful for diagnosing current infections. However, this is useful when assessing patients who may have had one of the complications of a previous streptococcal infection.
Throat cultures performed after antibiotic therapy can tell you if the infection has been removed. However, this throat swab is not indicated because up to 25% of properly treated individuals can continue to carry asymptomatic streptococcal infection.
Differential diagnosis
- Exanthemic virus: Viral infection is often accompanied by a rash that can be described as morbilliform or makulopapular. This type of rash is accompanied by prodromal periods of cough and runny nose besides fever, indicating viral process.
- Allergic or contact dermatitis: The erythematous appearance of the skin will be in a more localized distribution than the common and spreading rash seen on Scarlet Fever.
- Drug eruption: This is a potential side effect of using certain drugs such as Penicillin. Maculopapular rash is flushed which results can be itchy and accompanied by fever.
- Kawasaki's Disease Children with this disease also come with strawberry tongues and undergo a desquamative process in their palms and soles. However, these children tend to be younger than 5 years, their fever lasts longer (at least five days) and they have additional clinical criteria (including signs like conjunctival redness and chapped lips) that can help distinguish this from Scarlet Fever.
- Toxic shock syndrome: Streptococcal and Staphylococcal bacteria can cause this syndrome. Clinical manifestations include rash and diffuse desquamation of the palms and soles of the feet. Can be differentiated from Scarlet Fever with low blood pressure, rashes will lack of sandpaper texture, and multi-organ system involvement.
- Staphylococcal scalded skin syndrome: This is a disease that occurs primarily in young children because of the toxins that produce the strains of Staphylococcus aureus bacteria. The sudden onset of fever and scorching sunburn appear to resemble Scarlet Fever. However, this rash is associated with tenderness and the formation of large blisters. These blisters easily erupt and then cause the skin to peel.
- Staphylococcal Scarlet Fever: This rash is synonymous with scarlet streptococcus fever in distribution and texture but the affected skin will become soft rash.
Prevention
One method is the long-term use of antibiotics to prevent future group A streptococcal infections. This method is only indicated for people who experience complications such as recurrent attacks of acute rheumatic fever or rheumatic heart disease. Antibiotics are limited in their ability to prevent this infection because there are various subtypes of group A streptococci that can cause infection.
Vaccine approaches are more likely to effectively prevent group A streptococcal infection because vaccine formulations can target multiple subtypes of bacteria. The vaccine developed by George and Gladys Dick in 1924 was discontinued due to poor efficacy and introduction of antibiotics. Difficulties in vaccine development include the wide variety of strains of group A streptococcus in the environment and the amount of time and quantity of people needed for proper testing for the safety and efficacy of potential vaccines. There have been several attempts to make vaccines in recent decades. These vaccines, which are still in the development stage, expose to people for proteins present on the surface of the A streptococcus group to activate an immune response that will prepare people to fight and prevent future infections.
There used to be diphtheria dengue fever vaccine. However, it was not effective. This product was discontinued at the end of World War II.
Treatment
Antibiotics for fighting streptococcal infections are a mainstay of treatment for dengue fever. Immediate administration of appropriate antibiotics reduces the duration of the disease. Peeling the outer layer of the skin however occurs despite treatment. One of the main aims of treatment is to prevent children from developing one of the suppurative or nonsuppurative complications, especially acute rheumatic fever. As long as antibiotics begin within 9 days, it is highly unlikely for a child to develop acute rheumatic fever. Antibiotic therapy has not been proven to prevent the development of post-streptococcal glomerulonephritis. Another important reason for rapid treatment with antibiotics is the ability to prevent transmission of infection among children. An infected person is most likely to transmit the infection to another person during the first 2 weeks. A child is no longer infectious (can transmit the infection to another child) after 24 hours of antibiotics.
The antibiotic of choice is penicillin V taken in pill form. Children who can not take the pills can be given amoxicillin that comes in liquid form and is just as effective. The duration of treatment is 10 days. Benzathine Penicillin G may be given as a one-time intramuscular injection as an alternative if swallowing pills is not possible. If patients are allergic to a good antibiotic family penicillin and amoxicillin are part of (beta-lactam antibiotics), first-generation cephalosporins are used. However, cephalosporin antibiotics can still cause adverse reactions in patients whose allergic reaction to penicillin is a Type 1 Hypersensitivity reaction. In those cases it is appropriate to choose clindamycin or erythromycin.
Tonsillectomy, although once a reasonable treatment for recurrent streptococcal pharyngitis, is not indicated. This is due to the fact that a person can still be infected with group A streptococci without his tonsils.
Antibiotic resistance
Drug-resistant dengue fever, resistant to macrolide antibiotics such as erythromycin, but retains the drug's sensitivity to beta-lactam antibiotics such as penicillin, emerged in Hong Kong in 2011, which caused at least two deaths in the city - first as in more than one decades. About 60% of the circulating strains of the Streptococcus group that cause dengue in Hong Kong are resistant to macrolide antibiotics, says Professor Kwok-yung Yuen, head of the University of Hong Kong's microbiology department. Previously, the observed resistance level was 10-30%; an increased likelihood of results from excessive use of macrolide antibiotics in recent years.
Epidemiology
Scarlet fever occurs equally in men and women. Children are most often infected, usually between 5-15 years old. Although streptococcal infections can occur at any time of the year, infection rates peak in winter and spring, usually in colder climates.
Morbidity and mortality of dengue have declined since the 18th and 19th centuries when there was an epidemic caused by this disease. Around 1900 death rates in many places accounted for 25%. An increased prognosis can be attributed to the use of penicillin in the treatment of this disease. The frequency of dengue fever cases has also declined over the last century. However, there have been several outbreaks of disease reported in various countries in the last decade. The reasons for the recent increase are still unclear in the medical community. Between 2013 and 2016 the level of dengue populations in the UK rose from 8.2 to 33.2 per 100,000 and hospital admissions for dengue increased by 97%.
History
It is not clear when the description of the disease was first noted. Hippocrates, writing about 400 BC, describes the condition of the patient with reddened skin and fever.
The first description of the disease in medical literature appears in the book 1553 De Tumoribus praeter Naturam by the anatomist and physician Sicilia Giovanni Filippo Ingrassia, where he referred to it as
In 1675 a term that has been commonly used to refer to dengue fever, "scarlatina", was written by Thomas Sydenham, a British physician.
In 1827, Richard Bright was the first to recognize the involvement of the kidney system in dengue fever.
The relationship between streptococcus and disease was first described in 1874 by Theodor Billroth, discussing patients with skin infections. Billroth also created the name of the genus Streptococcus . In 1884 Friedrich Julius Rosenbach edited his name to the present name, Streptococcus pyogenes, after looking further into the bacteria in the skin lesions. The organism was first cultured in 1883 by German surgeon Friedrich Fehleisen. It cultivates it from an erysipelas lesion.
Also in 1884, German physician Friedrich Loeffler was the first to show the presence of streptococci in the patient's throat with dengue fever. Since not all patients with pharyngeal streptococcus develop into dengue, these findings remain controversial for some time. The relationship between streptococcus and dengue was confirmed by Alphonse Dochez and George and Gladys Dick in the early 1900s.
Nil Filatow (1895) and Clement Dukes (in 1894) described the exanthematous disease which they thought was a form of rubella, but in 1900 Dukes described it as a separate disease later known as Dukes disease, Filatov disease, or fourth disease. However, in 1979, Keith Powell identified him as the same disease with dengue fever caused by staphylococcal exotoxins and is known as Staphylococcal dyed skin syndrome.
Dengue fever from horse is used in the treatment of children starting in 1900 and the mortality rate is significantly reduced.
In 1906, Austrian pediatrician Clemens von Pirquet postulated that the immune complex that causes the disease is responsible for nephritis that follows dengue fever.
Bacteriophages were discovered in 1915 by Frederick Twort. His work was ignored and bacteriophage was rediscovered by Felix d'Herelle in 1917. The specific relationship of dengue fever with group A streptococcus had to wait for the development of the Lancefield streptococcal grouping scheme in the 1920s. George and Gladys Dick suggest that cell-free filtrate can induce the characteristic dengue fever erythematous reaction, proving that this reaction is caused by toxins. Karelitz and Stempien found that extracts from human serum globulin and placental globulin could be used as a brightening agent for dengue and this was used later as a basis for the Dick test. The association of dengue fever and bacteriophage was described in 1926 by Cantucuzene and Boncieu.
Antitoxin for dengue was developed in 1924.
The first toxin that caused the disease was cloned and sequenced in 1986 by Weeks and Ferretti. The discovery of penicillin and its widespread use has significantly reduced the death of this once dreaded disease. Reports of Scarlet fever cases in recent years have increased. Countries including England, Wales, South Korea, Vietnam, China and Hong Kong. Researchers are not sure what causes a spike in the case of the disease.
Tes Dick
Dick tests were discovered in 1924 and were used to identify those prone to dengue fever. The Dick test consists of injecting an aqueous strain of streptococcus that is known to cause dengue fever to a person's skin. Local reactions in the skin at the injection site appear in people susceptible to dengue fever. This reaction is most prominent about 24 hours after injection but can be seen as early as 4-6 hours. If no reaction is seen on the skin, then the person is considered to have developed immunity to the disease and not risk developing it.
References
![Quarantine: Scarlet Fever [ca. 1910]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_v89NI81lOVhrykKO8LUchde-Kug--AZG_xd3Lr08V7TiJQT_lEwznwn5ZBboWStN3IxF162OtWD4dziXNnmVTE6c3TLPIyYJEyMgfBS5dsP6zFOZa4J-z8Y0oXveyyitmmqGk9EuTuew=s0-d "Quarantine: Scarlet Fever [ca. 1910]")
External links
- Scarlet Fever dari PubMed Kesehatan
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Rolleston JD (November 1928). "Sejarah demam berdarah". Jurnal Medis Inggris . 2 (3542): 926-9. doi: 10.1136/bmj.2.3542.926. PMCÂ 2456687 . PMIDÂ 20774279 Â
Source of the article : Wikipedia
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