Download INFECTIOUS AGENT Acute pharyngitis is one of the most common

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Extrachromosomal DNA wikipedia , lookup

Nucleic acid analogue wikipedia , lookup

DNA vaccination wikipedia , lookup

Pathogenomics wikipedia , lookup

Therapeutic gene modulation wikipedia , lookup

Point mutation wikipedia , lookup

History of genetic engineering wikipedia , lookup

Helitron (biology) wikipedia , lookup

Human microbiota wikipedia , lookup

Transcript
INFECTIOUS AGENT
Acute pharyngitis is one of the most common childhood illnesses to be diagnosed in an
outpatient setting (Bisno, 2001). Viruses and Streptococcus pyogenes are considered to be the
most frequent causes of this disease, but particular attention is usually given only to
streptococcal cases, as they may be followed by severe early and late complications and are
the only ones for which antibiotic treatment is definitely indicated (Bisno et al., 2002; Bisno,
2001).
Group A Streptococcus (GAS), also known as streptococcal pyogenes is the causative agent
in Group A streptococcal infections, including streptococcal pharyngitis ("strep throat").
GAS is spherical gram-positive bacteria that grows in long chains and is the cause of Group
A streptococcal infections. S. pyogenes displays streptococcal group A antigen on its cell
wall. S. pyogenes typically produces large zones of beta-hemolysis (the complete disruption
of erythrocytes and the release of hemoglobin) when cultured on blood agar plates and are
therefore also called Group A (beta-hemolytic) Streptococcus (abbreviated GAS) (Cooper RJ
et al 2001).
GROUP A STREPTOCOCCAL INFECTION
S. pyogenes is the cause of many important human diseases ranging from mild superficial
skin infections to life-threatening systemic diseases. Infections typically begin in the throat or
skin. Examples of mild S. pyogenes infections include pharyngitis ("strep throat") and
localized skin infection (“impetigo’’). Infections due to certain strains of S. pyogenes can be
associated with the release of bacterial toxins.
VIRULENCE FACTORS
S. pyogenes has several virulence factors that enable it to attach to host tissues, evade the
immune response, and penetrate the host tissue layers. Polysaccharide capsule composed of
hyaluronic acid surrounds the bacterium, protecting it from phagocytosis by neutrophils. The
Streptococcus pyogenes stand-alone Mga regulator has been shown to positively control
surface-expressed virulence factors like the antiphagocytic M protein during exponential
growth phase and thus, was implicated to contribute to the acute infection process (Tomas
Fiedler, 2010).
S. pyogenes releases a number of proteins, including several virulence factors, into its host:
Streptolysin O and S: These are toxins which are the basis of the organism's beta-hemolytic
property. Streptolysin O is cardiotoxic and also affects neutrophils, platelets, and sub-cellular
organelles.
Hyaluronidase: mainly degrades hyaluronan (hyaluronic acid), a linear, non-sulfated
polysaccharide composed of repeating disaccharide units [D-glucuronic acid (1-β-3) Nacetyl-D-glucosamine (1-β-4)]n (Nermeen S. El-Safory, 2010), an important component of
connective tissue.
Streptococcal pyogenic exotoxins (Spe) A and C: there are secreted by many strains of
S.pyogenes and are responsible for the rash of scarlet fever etc.
Streptokinase enzymatically activates plasminogen, a proteolytic enzyme, into plasmin
which in turn digests fibrin and other proteins.
Streptodornase has been shown to exhibit no activity against RNA and digests native DNA
more rapidly than single-stranded DNA (Ian C. L., and Brian G. C., 2004). Stretodornase
protect the bacteria from being trapped in neutrophil extracellular traps (NETs) by digesting
the NET's web of DNA, to which are bound neutrophil serine proteases that can kill the
bacteria.
Streptococcal chemokine protease is responsible for preventing the migration of neutrophils
to the spreading infection by degradation of the chemokine IL-8.
REFERENCES
Bisno, A. L., Acute pharyngitis. New England journal of medicine, 2001, 344: 205–11.
Bisno, A. L., Gerber, M. A., Gwaltney, J. M., Jr, Kaplan, E. L. & Schwartz, R. H. (2002).
Diagnosis and management of group A streptococcal pharyngitis: a practice guideline. Clin
Infect Dis 25, 574–583.
Cooper RJ et al. Principles of appropriate antibiotic use for acute pharyngitis in adults:
Background. Annals of internal medicine, 2001, 134:509–17.
Ian C. Locke and, Brian G. Carpenter. Functional characteristics of the streptococcal
deoxyribonuclease ‘streptodornase’, a protein with DNase activity present in the medicament
Varidase. Enzyme and Microbial Technology, Volume 35, Issue 1, 6 July 2004, Pages 67-73.
J. Boukadida, N. Hannechi, N. Boukadida, H. Ben Said, H. Elmherbech and S. Errai, bhaemolytic streptococci in acute pharyngitis, Volume 9, Nos 1/2 ,January 2003.
Nermeen S. El-Saforya, Ahmed E. Fazaryb, c and Cheng-Kang Lee. Hyaluronidases, a group
of glycosidases: Current and future perspectives. Carbohydrate Polymers Volume 81, Issue
2, 11 June 2010, Pages 165-181.
Tomas Fiedlera, Bernd Kreikemeyer, Venelina Sugarevaa, Sylvio Redanza, Regina Arlta,
Kerstin Standara and Andreas Podbielskia. Impact of the Streptococcus pyogenes Mga
regulator on human matrix protein binding and interaction with eukaryotic cells.
International Journal of Medical Microbiology, Volume 300, Issue 4, April 2010, Pages 248258.
Susanna Esposito, Francesco Blasi, Samantha Bosis, Roberta Droghetti, Nadia Faelli,
Annalisa Lastrico and Nicola Principi, Aetiology of acute pharyngitis: the role of atypical
Bacteria, Journal of Medical Microbiology, 2004, 53, 645–651