Each organism has a particular structure. Both Streptococcus pyogenes and Staphylococcus aureus are Gram-positive cocci and non-spore forming organism. These are surrounded by sticky capsule that can be polysaccharide and/or polypeptide in structure. This capsule is a gelatinous layer synthesized inside of cell. Under microscope Streptococci look as chains of varying length, on the other hand staphylococci appear as grape-like structure (Lee, Bishop, 2010). Group A Streptococci has fimbriae on outside of cells, which is long, thin, flexible, hair-like appendages composed of pilin protein (Paul, Janet, 2011, p. 244). Apart from this
staphylococci has no fimbriae. This fimbriae actually contains on Gram-negative bacterial cell wall. On the cell surface of streptococci, there is a branched polymers which contain protein called M protein, while it is absent in staphylococci.. Streptococcus pyogenes have adhesin molecule named as protein F on their surface, that is also absent in Staphylococcus aureus. As like as other bacteria they have cell wall containing thick layer of peptidoglycan and other complex polysaccharides called teichoic acid is adherent to this thick layer (Lee, Bishop, 2010). These structures provide various characteristics to both of pathogen.
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Each bacteria tries to maintain characteristics in various condition. S. pyogenes is facultative anaerobes unlike to that S. aureus survive only in aerobic condition (Gillespie & Bamford, 2012, p. 34). S. pyogenes is able to form chains of bacteria by dividing in a single plane, particularly in liquid cultures. On the basis of acid-extractable polysaccharide of streptococci, Lancefield developed a classification, from group A to O. By the development of rapid latex agglutination schemes, this typing is has been done. Growth of group A streptococcus (GAS) is enhanced by 10% carbon dioxide (Dennis, 2006, p. 356). S. pyogenes require rich blood-containing media as it creates a characteristics change in appearance of agar around the colony by producing haemolysins toxin (Wilson, 2006). It breaks red blood cells in blood agar. For partial breakdown it results green zone around colony (by alpha-hemolytic bacteria) and clear zone after full breakdown (by beta-hemolytic bacteria) (Paul, Janet, 2011, p. 247).
While S. aureus can not release haemolysins toxin. It grows in selective laboratory medium containing high concentration of salt (high osmotic pressure) and low moisture because of their tolerance of this condition and it can easily colonizes skin. Thatââ‚¬â„¢s why staphylococci are commonly presents on axillae, groins and perineum. It also sometimes found on preserved foods or meats (Lee, Bishop, 2010). There is a extracellular protein fibronectin (Fn) that belong to the MSCRAMM (microbial surface components recognizing adhesive matrix molecules) family of adhesions, helps in formation of molecular bridge between host cell integrins and bacterial cell surface. For example, the Sfbl protein of S. pyogenes provide internalization by endothelial and epithelial cells. In contrast, FnBPA (Fn-binding protein) provide host-pathogen interaction for S. aureus (Ulrich, Magnus, & Jennifer, 2006). Bacteria produce various exoenzymes and toxins for causing disease. S. pyogenes release coagulase enzymes but S. aureus produce both coagulase and kinase (fibrinolysins). This streptokinase is used as a drug for coronary thrombosis patients. Hyaluronidase is produced by both of them. However, proteases and collagenases are produced by S. pyogenes, but lipase enzymes released by S. aureus. Streptococci produce erythrogenic toxin, pyrogenic exotoxins. On the other hand enterotoxins, exfoliative toxin are released by staphylococci. Lecucodins are secreted by both of them. Toxic shock syndrome toxin (TSST) is released by both of them but mainly by staphylococci (Paul, Janet, 2011, p. 247-248). Most of these characteristics are act as a virulence factor for occurring disease.
In Gram-positive bacteria there is cysteine transpeptidases enzyme sortase that cause covalent attachment cell wall to substrate proteins. The sortase Spy0129 from S. pyogenes and Srt from S. aureus are involved in forming the covalent linkages between the substrate pilin proteins in the pili to their cell wall and anchor the pili expressed by them. These proteins are involved in virulence, infection and colonization. (Kang, Coulibaly, Proft, Baker, 2011). By activating T cells superantigens are capable to produce serious diseade as these are the protein toxins. They cause massive T-cell eaxpansion. Inflammatory cytokines, such as tumor necrosis factor (TNF), interleukin-2 are released by them and cause food poisoning, toxic shock syndrome.
For disease production each bacteria has some factors for their virulence. Streptococcus pyogenes has ability to protest itself from leucocyte phagocytosis by its particular extracellular M protein (eMP) antigen and is an important virulence factor. For protective immune response, it acts as a target and in order to evade the immune response, amino acid portion in this protein would allow this pathogen. This protein is found to bind to the
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human plasma proteins, fibrinogen, IgG, and albumin. There are multiple structures of M protein such as M1 and M3 are involved in necrotizing fascitis, a soft tissue infection characterized by tissue necrosis (Gillespie & Bamford, 2012, p. 32-37). The antibodies generated against M protein may cross react with cardiac myofiber protein myosin, heart muscle glycogen and smooth muscle cells of arteries, causing cytokine release and tissue destruction e.g. rheumatic fever, acute glomerulonephritis (AGN) (Fae KC, Da Silva DD, Oshiro SE, 2006). The capsular hyaluronic acid (HA) causes a variety of infections by confers invasiveness in vivo, by inhibiting with the binding of antibodies and thus it resist phagocytosis. There are more invasive and severe infections are occurred by this highly expressed HA. With the help of fibronectin receptor they adhere themselves (Gillespie & Bamford, 2012, p. 32-37). The Spy0129 is involved for adherence of pili to human tonsil epithelia, skin, keratinocytes and pharyngeal cells for their pathogenesis. Streptococcal Pyrogenic Exotoxins (SPE) such as SpeA, SpeB and SpeC are known as erythrogenic toxin causes scarlet fever. Due to superantigenic activity SpeA and SpeB stimulate human T cells, specifically MHC-II (major histocompatibility complex) and release cytokines mediators. Due to cystein protease activity of SpeB, it can activate caspase cascade for apoptosis mechanism in macrophages and epithelial cells (Ikebe, Watanabe, 2005). Streptococcal shock is caused by pyrogenic toxin-producing strain, some degrading enzymes such as immunoglobin proteases, collagenases. Hyaluronic acid of tissue is degraded by hyluronidase. It can degrade fibrin and fibrinogen by activating plasminogen by streptokinase enzymes and blood coagulation process is hampered. In order to prevent from eradication by penicillin it has ability to invade and survive intracellularly. About 40% of healthy people are the habitant of Staphylococcus aureus in the nose, skin, perineum or axilla.
There are many pathogenic determinants of this bacteria such as coagulase, which provide protective barrier by catalyzing the conversion of fibrinogen to fibrin. Adhesion molecules assist themselves by binding fibronectin and collagen. Enterotoxins are one of the important member of suparantigen family. Lipase is a lytic enzyme that breaks down host tissue. This organism also causes shock and toxicity by toxic shock syndrome toxin (TSST) which is a protein toxin. Another protein toxin is panton-valentine leucocidin (PVL) toxin, responsible for tissue damage (Gillespie & Bamford, 2012, p. 32-37).
Transmissibility is one of the vital factor for spreading disease. Both of bacteria spread by mucocutaneous contamination. One of the community acquired infectious pathogen is methicillin-resistant Staphylococcus aureus (MRSA) is increasing in population as a pathogen as well as commensal (Davidson, Benjamin, 2006). The main reservoir of staphylococcus is skin and nasal mucosa, patient may acquire it both by endogenous source or exogenous source. Damaged skin sites of burn patients or wound or cannulae insertion sites are vulnerable to staphylococci infection. Itââ‚¬â„¢s commonly presents in axillae, groin and perineum. The carriage rate higher in hospital patients and staff, after colonization they may act as a reservoir for transmission and then spread by contact (Wilson, 2006). During handling of tracheal tube, staphylococci can enter through respiratory tract as the wound associated with tracheotomy may be colonized by this pathogen. It can enters through GIT (gastro-intestinal tract) by producing enterotoxin before ingestion (Lee, Bishop, 2010).
On the other hand group A streptococci was isolated from 5-15% of throat healthy people and sometimes from nose in the bacteriological studies in 1930. It spreads by airborne droplet from healthcare workers and direct contact by contaminated skin scales (Graham, Mary, 2003). Precautions are needed to prevent these transmission.
In order to keep safe ourselves preventive measures is essential in our life. Close contact of patient with streptococcal pharyngitis or skin infection should be avoided at least 24 hours after beginning of treatment, and until become afebrile. Risk of recurrence can be reduced by secondary prophylaxis in case of rheumatic heart disease and endocarditis patients. Careful washing and drying hand is most important way to prevent cross-infection of staphylococci. It should be routine work before and after every patient contact (Peter, Lepow, McCracken, Phillips, 1991). Personal protective equipment (PPE) such as disposable or reusable gowns, plastic aprons, gloves, masks, goggles, are used in hospital to protect hospital personnel from contamination of their hands, eyes or clothing. Aseptic technique should be used to handle invasive device such as urinary catheter, intravascular cannulae, and endotracheal and drainage tubes.
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Handling and disposal of sharp objects and other contaminated and infectious waste should be done properly (Lee, Bishop, 2010). For controlling MRSA spreading, there is a need of prudent use of antimicrobial therapy. Active screening of high risk patients in hospital and single room isolation is recommended for patients with MRSA colonization (Wilson, 2006).
A number of various methods are used in laboratory for diagnosis purpose. Proper collection of appropriate specimen is needed for accurate diagnosis. Microscopic test on glass slide can reveal information about structure, shape and arrangement. Streptococci form into chains but staphylococci arrange into clumps. Both of them are Gram-positive so they appear as blue colour (Wilson, 2006). One important test for streptococci is culture of throat swab in sheep blood agar medium. This specimen can be collected from posterior pharynx (nasopharyngeal suction) and tonsils. In contrast to staphylococci, for detection of carriers, nasal swab is needed. This organism can be isolated by culture of blood, tissue, pleural fluid, bones, vomitus, stool or skin lesions. To differentiate GAS from other beta hemolytic streptococci, bacitracin-sensitivity disks on culture plate or latex, agglutination or precipitation techniques can be used. Antigen can be detected by direct extraction of group A carbohydrate antigen from throat swab.
For diagnosis of nonsuppurative complications of streptococcal infection antibody can be detected, such as antistreptolysin O (ASO) and antideoxyribonuclease B (anti-DNase B). In case of streptococci, catalase test is negative but staphylococci is positive. For differentiation of Staphylococcus aureus (coagulase test positive) from coagulase-negative staphylococci, coagulase test or mannitol fermentation test can be done. One molecular technique known as hybridisation with nucleic acid probes is used for detection of antibiotic resistance genes in staphylococci e.g. mecA gene for methicillin resistance (Peter, Lepow, McCracken, Phillips, 1991).