Scarlet Fever

Name of the Student
Professor’s Name
Biology
4th December, 2015
Scarlet Fever
Introduction
Scarlet fever is an infectious disease caused by a bacterium Streptococcus pyrogens (which is also called Group A Streptococci). The disease is caused due to the liberation of toxic substances released by the bacterium. The disease primarily affects children, and also leads to glomerulonephritis or endocarditis if the infection is not managed. The disease is caused by the liberation of exotoxins that are not inherited within the bacterium but is injected into the bacterium through a virus. This bacteriophage ( the virus that affects bacterium), inserts the toxin gene into the bacterium. The toxin gene is present in the viral DNA and integrates with the bacterial genome during the lysogenic phase (Czarkowski, Kondej, & Staszewska 209-212).
The most common symptoms are sore throat and white rashes on the surface of the tongue. Sometimes it is confused with pharyngitis, where the causative pathogen is the same or might be different. In Scarlet fever, the nature of pharyngitis is exudative and is always caused by Group A Streptococci. On the other hand, pharyngitis is not associated with exudations and may be caused by other strains of bacteria including Staphylococci, Acinetobacter and others. The disease affects children between the ages of 5 years to 15 years when their immunity is low. However, by the age of 10 years, children who are once affected by Scarlet fever develop antibodies against the bacterial exotoxins (Czarkowski, Kondej, & Staszewska 209-212).

The exotoxins are pyrogenic in nature and are the cause of fever associated with the infection. The exotoxins are different types A, B and C. 80% of children develop secondary immunity by that period and hence further episodes of scarlet fever is prevented in them. The disease is contagious and is communicated through the air. Vaccinations are still not available, and the disease is presently managed with different antibiotics. The disease is also referred as Scarlatina due to the presence of bright red erythematic on the tongue (Czarkowski, Kondej, & Staszewska 209-212).
Mechanism of Transmission
The disease spreads through contact with the infected persons and also occurs due to droplet infections. Transmission takes place through sneezes, coughing and sinus drainage. The disease spreads through unhygienic and improper sanitization, involving the affected persons. The disease spreads in overcrowded areas (Krause 219-241).
Epidemiology of the Disease
Scarlet fever is prevalent in 10% of individuals who are infected with Group A Streptococcal bacteria. 10% of individuals in a population are affected by the streptococcal infection. During the past century, the prevalence of scarlet fever was high, however, due to the advancement with treatment regimes with antibiotics the incidences have decreased. The disease mainly spreads to close contact or overcrowding of affected individuals. On the other hand, immunity develops in carrier individuals (Krause 219-241).
Complications of scarlet fever like rheumatoid arthritis or glomerulonephritis is more common in immigrants to the United States. Scarlet fever is rare in children below the age of one year because of the presence antibodies against the exotoxins. Such antibodies are passed on to the child from a mother. The disease is associated with the development of various neuropsychiatric disorders like attention deficit hyperactivity disorder and major depressive disorder (Krause 219-241).
Males and females are equally prone to the infection and ethnicity, and racial dominance has still not been reported so far. The fever is predisposed in those individuals who had recent burns, wound infections or with upper respiratory tract infections. The disease predominantly originates from a tonsilar focus, but it is not often associated with strep throat. In fact, strep throat is presented in 10% of individuals who incurs Scarlet fever. The disease is prevalent during different times of a year, but the major outbreak occurs during the winter season and spring. School going children are most affected, compared to children who do not visit schools. The disease spreads as respiratory droplets and may be spread through contaminated foods. In fact a massive outbreak of Scarlet fever occurred due to food contamination in China (Yang et al 419-424).
Pathogenesis
Scarlet fever is caused by Group A beta-hemolytic strains of streptococci and is associated with an erythematous swelling that is associated with a febrile condition. The exotoxin is released by the bacterium and produces the typical rash. The release of exotoxins causes signaling of various inflammatory mediators and alteration in the titer of cytokine levels. The release of inflammatory mediators causes erythema and dilatation of blood vessels. The increased blood supply to the erythematous swelling is responsible for the “Scarlet” color associated with the disease (Krause 219-241).
This group of bacteria grows in a chain shaped colony and has the ability to hemolyze the red blood cells placed on a agar plate. The basis of hemolysis or pathogenicity is associated with the carbohydrate side chain in the cell wall of this bacterium. Streptococcus pyrogens occur in three forms based on the carbohydrate composition of their cell wall. These are alpha hemolytic, beta hemolytic and gamma hemolytic strains of streptococcus. The alpha hemolytic strain causes partial hemolysis of the RBCs placed in in-vitro settings, beta hemolytic strain causes complete hemolysis of the RBCs placed in in-vitro settings and gamma hemolytic strain causes no hemolysis of the RBCs placed in in-vitro settings. Scarlet fever is caused by the beta-hemolytic strain of streptococcus. The bacterial species is a normal inhabitant of the nasopharynx region and is also associated with pharyngitis and skin infections like cellulitis. The protein consists of a signal sequence of and is under the strong regulation of promoter and operator binding kinetics of RNA polymerase present in the bacterial nucleus. The exotoxin bears homology with staphylococcus enterotoxins (Weeks & Ferretti 144-150).
The disease is caused by the secretions of pyrogenic exotoxins released by the bacterium. Exotoxin A is the most widely studied exotoxin. The exotoxin is the product of the specific gene spe A. The genome is carried through the virus T12 bacteriophage as a process of specialized transduction. The bacteriophage infects the bacterium and injects its DNA into the bacterium. The viral DNA gets integrated into the bacterial DNA and while it gets inserted into the bacterial genome, it passes through a lysogenic phase. When the conditions are favorable they cause lysis of the bacterial cell and is emitted out of the bacterium (Weeks & Ferretti 144-150).
During such process the viral DNA also carries with it the bacterial DNA portions, specifically the spe A gene. The speA gene is actually a part of the viral DNA and is specific for the viral species related to Siphoviridae. This bacterial strain when infects the bacteria integrates its spe A genome in the bacterial genome. While the integrated viral DNA is within the bacterial genome, it leads to the expression of the spe A exotoxins and causes the Scarlet fever. As discussed the integrated genome may be transferred to another bacterium through lysis. The spe A gene have been cloned and consists of 753 base pairs and encodes for an exotoxin protein with a molecular weight of 29.24 kilo Dalton (Yu & Ferretti 161-168). The erythrogenic protein is responsible for the bacterial infection. The protein was first discovered by Dick and Dick in 1924 (Weeks & Ferretti 144-150).
Etiology & Symptoms of the Disease
With proper management, the fever is managed with 4-5 days and the skin eruptions subside within period over several weeks. When antibiotic therapy was not developed Scarlet fever accounted for mortality in 15-20% affected with the disease. The disease was an epidemic during the 1800s. Presently mortality due to scarlet fever is 1% in people affected with the disease. Presently, the complications of scarlet fever are the major cause of morbidity and mortality. The reduction in the episodes of scarlet fever is due to an increased immune status of the vulnerable children. The increased immune status has been due to the socio-economic status of such children all across the globe (Krause 219-241).
The major complication of Scarlet fever includes pharyngotosilittis, bronchopneumonia, abscess in the tonsils, other upper respiratory tract infections like sinusitis and meningitis. Due to the overactive immune status and the release of inflammatory mediators, immune complexes are formed and get deposited in various parts of the blood vessels. This results in the development of Rheumatic arthritis and endocarditis. If untreated, the disease may lead to septicemia. This is because the focal origin of the infection may be transferred to the blood, due to the increased vascularity in buccal and pharyngeal cavity. The bacterium spreads into the blood and is the cause of septicemia or infection of the blood. Further complications include vasculitis, hepatitis, glomerulonephritis, and rheumatic fever. Scarlet fever may occur due to various underlying infections. Such infections are osteomyelitic or may occur from cellulitis. The disease has an incubation period of 1-4 days (Yang et al 419-424).
Symptoms of Scarlet Fever
After the incubation period is over, the infection manifests itself with various systemic and localized symptoms. The major symptom is sudden onset of fever which is often associated with a sore throat. Headaches and chills are the initial symptoms, of contracting such disease. The typical rash appears after 12-48 hours of the onset of the fever and strep throat. The infection is often associated with malaise and myalgia. The rash manifests itself generally on the neck, and with the progression of the disease spreads to the trunk and the extremities.
When the fever is not managed with antipyretic or antibiotic, the fever can reach very high grades up to 103 to 104 degree centigrade. The fever is remitted after two days of antibiotic therapy, as the spread of infection gets prevented. Further, the patient with scarlet fever presents with tachycardia or increased heart rate beyond 100 beats /minute. The lymph glands often become swollen, due to the stimulation of the immune system. Cervical lymphadenopathy is very common in individuals affected with scarlet fever.
The symptoms of scarlet fever are widely manifested in the tongue. The mucous membranes appear bright red in color and consist of numerous petechiae and popular lesions. During the first and second day of incurring a beta hemolytic infection the soft plate including the tongue consists of edematous papillae, which is the basis of the classical “strawberry tongue”. During the 4th and the 5th day, after incurring the disease, the white membranes are sloughed, off and the red papillae are expressed. The tonsils also appear red and edematous (Elishkewitz et al 569-570).
The exanthema and the rashes usually develop after 12-48 hours after the onset of fever, and they appear as patches beneath the ear, chest and the axillary regions. The exanthema contains exudates which exhibit as an eruption. The eruption creates a dry and rough texture to the skin, which is very coarse in texture. Pruritus can develop on the skin, but it is not associated with pain. Progression to the trunk and other peripheries takes place much later. The erythematous patches become very prominent, in the pressure zones of the body. These include the buttocks or the knees. The capillaries become very fragile and break open. Areas of hyperpigmentation also develop in the axillary regions, and inguinal regions (Elishkewitz et al 569-570).
Such patches persist even after disappearance of the rashes (Elishkewitz et al 569-570). The summary of various symptoms include:
High fever in the range of 102 degree to 104 degree.
The skin rashes are red and coarse
The rashes blanches after pressure is applied
Red cheeks accompanied by pale areas around the mouth takes place
The rashes usually occur beneath the ear, chest and armpits initially and then spread to other areas.
Appearance at the Pastia’s Lines (skin folds).
Management of Scarlet Fever
The management of Scarlet fever is dependent on supportive and antibiotic therapy. Supportive therapy deals with administration of acetaminophen for the reduction of fever and inflammation. In certain instances, low dose systemic corticosteroids are also indicated. The remission of fever mainly depends on the eradication and control of the Streptococcus bacterium below pathogenic levels. Macrolide group of antibiotics and beta-lactam antibiotics are indicated for the treatment of group A beta-hemolytic infections. Macrolides like clindamycin have been associated with greater eradication of Streptococcus pyogenes, and has been associated with positive health care outcomes in individuals, who have incurred a streptococcal infection (Prevost et al 53-83).
Summary and Conclusion
Scarlet fever is caused due to an infective pathogen called streptococcus pyogenes. The beta haemolytic strain of the bacteria is responsible for the infection and the characteristic symptoms. The bacterial genome consists of a specific gene called speA, which is integrated to its genome through a T12 bacteriophage, during the lysogenic phase. The gene is put under the promoter/operator control of the bacterial genome and results in over expression of the speA gene. The speA gene encodes for an mRNA that produces the exotoxin. The exotoxin acts as an inflammatory mediator and activates various inflammatory pathways. The stimulation of various inflammatory pathways leads to the formation of rashes on the tongue, soft palate and the skin. The rashes develop after 1-4 days after incurring of the infection.
The disease often mimics the symptoms of pharyngitis or strep throat, but is not associated with pain. The disease mainly affects school going children in the age range of 5 to 10 years and is a contagious one. It is managed by both bactericidal and bacteriostatic antibiotics. However, the dilemma of treatment may be associated with resistance development against antibiotics. The beta lactam antibiotics may be destroyed by the beta-lactamase enzymes produced by the bacterium. There can be a possibility of mutation of porin channels which renders the entry of antibiotics difficult into the bacterial cell to exert its action. Therefore, management of Streptococcus should be planned with non beta-lactam antibiotics and antibiotics that have the potency to enter through all the porin channels. Finally, research should be carried with some form of vaccination targeted towards the expression of speA gene.
Works Cited
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