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Scarlet fever pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology[edit | edit source]
It is usually spread by the aerosol route (inhalation) but may also be spread by skin contact or by fomites. Although not normally considered a food borne illness an outbreak due to chicken meat has been reported in China.[1]
Asymptomatic carriage may occur in 15–20% of school-age children.
The incubation period is 1–4 days.
This illness can be caught from contact with the sick person because this germ is carried in the mouth and nasal fluids. The disease can be spread through contact with droplets shed when an infected person coughs or sneezes. If you touch your mouth, nose, or eyes after touching something that has these fluids on them, you may become ill. Also, if you drink from the same glass or eat from the same plate as the sick person, you could also become ill. The best way to keep from getting sick is to wash your hands often and avoid sharing eating utensils. It is especially important for anyone with a sore throat to wash his or her hands often and not share eating or drinking utensils.
The disease itself is caused by secretion of pyrogenic exotoxins by the infecting Streptococcus.[2][3] Exotoxin A (speA) is probably the best studied of these toxins. It is carried by the bacteriophage T12 which integrates into the Streptococcal genome from where the toxin is transcribed. The phage itself integrates into a serine tRNA gene on the chromosome.[4]
The T12 virus itself has not been placed into a taxon by the International Committee on Taxonomy of Viruses. It has a double stranded DNA genome and on morphological grounds appears to be a member of the Siphoviridae.
The speA gene was cloned and sequenced in 1986.[5] It is 753 base pairs in length and encodes a 29.244 kiloDalton (kDa) protein. The protein contains a putative 30 amino acid signal peptide: removal of the signal sequence gives a predicted molecular weight of 25.787 (kDa) for the secreted protein. Both a promoter and a ribosome binding site (Shine-Dalgarno sequence) are present upstream of the gene. A transcriptional terminator is located 69 bases downstream from the translational termination codon. The carboxy terminal portion of the protein exhibits extensive homology with the carboxy terminus of Staphylococcus aureus enterotoxins B and C1.
Streptococcal phages other than T12 may also carry the speA gene.[6]
Resources[edit | edit source]
References[edit | edit source]
- ↑ Yang, S. G.; Dong, H. J.; Li, F. R.; Xie, S. Y.; Cao, H. C.; Xia, S. C.; Yu, Z.; Li, L. J. (2007). "Report and analysis of a scarlet fever outbreak among adults through food-borne transmission in China". J Infect. 55 (5): 419–424. doi:10.1016/j.jinf.2007.07.011.
- ↑ Zabriskie, J. B. (1964). "The role of temperate bacteriophage in the production of erythrogenic toxin by Group A Streptococci". J Exp Med. 119 (5): 761–780. doi:10.1084/jem.119.5.761. PMC 2137738. PMID 14157029.
- ↑ Krause, R. M. (2002). "A Half-century of Streptococcal Research: Then & Now". Indian J Med Res. 115: 215–241. PMID 12440194.
- ↑ McShan, W. M.; Ferretti, J. J. (1997). "Genetic diversity in temperate bacteriophages of Streptococcus pyogenes: identification of a second attachment site for phages carrying the erythrogenic toxin A gene". J Bacteriol. 179 (20): 6509–6511. PMC 179571. PMID 9335304.
- ↑ Weeks, C. R.; Ferretti, J. J. (1986). "Nucleotide sequence of the type A streptococcal exotoxin (erythrogenic toxin) gene from Streptococcus pyogenes bacteriophage T12". Infect Immun. 52 (1): 144–150. PMID 262210.
- ↑ Yu, C. E.; Ferretti, J. J. (1991). "Molecular characterization of new group A streptococcal bacteriophages containing the gene for streptococcal erythrogenic toxin A (speA)". Mol Gen Genet. 231 (1): 161–168. doi:10.1007/BF00293833. PMID 1753942.
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