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Streptococcal throat infections are very common in the winter season. These infections are caused by a Gram +ve bacteria namely Streptococcus pyogenes. Streptococcus pyogenes is a beta-hemolytic bacterium that belongs to Lancefield serogroup A. This is a capsulated bacterium. These bacteria often colonize in the upper respiratory tract of humans. They can overcome the host defiance mechanisms. The bacteria cause mainly skin and respiratory tract disorders. Pyogenes are complex and chemically diverse. The antigenic components of the cell are the virulence factors. The extracellular components responsible for the disease include invasins and exotoxins. The outermost capsule is composed of hyaluronic acid, which has a chemical structure resembling host connective tissue, allowing the bacterium to escape recognition by the host as an offending agent. The carbohydrate capsules protect the bacteria from the phagocytic effect of the body. The bacteria get in to the host body through the air, which is taken both by nose and mouth.
Review of literature:
Group A bacteria are the parasites in human and are known to have 90 serotypes. It is estimated that 5-15% of normal individual contains streptococcus in their throats and the respiratory tract without signs of disease (asymptomatic). When it successfully defeats the host's immune system it multiplies and causes acute infections. Acute streptococcal infections may occur as pharyngitis or strep throat. Patient may also develop post streptococcal disease such as acute rheumatic fever and glomerulonephritis with is more like an auto immune disease or antibody interaction of the body. Streptococcus pyogenes produces a wide array of virulent factors and a range of diseases. Virulence of Group A streptococcus includes M protein: virulent protein and lipolithic acids for adherence, Hyaluronic acid capsules: as an immune disguise and protecting it from Phagocytosis of the body, Invacins: such as streptokinase, streptodornase, hyalurinodase and Streptolysin, which causes cytolysis in host cell, Endotoxins: such as pyrogenin toxin which causes rashes of scarlet fever and systemic toxic shock syndrome. Streptococcus pyogenes owes its major success as a pathogen to its ability to colonize and rapidly multiply, spread in its host while evading phagocytosis and confusing the immune system. Small self replicating double standard DNA (plasmid) is the genetic material of streptococcus pyogenes. Streptococcal disease is most often a respiratory infection (pharyngitis or tonsillitis) or a skin infection (pyoderma). S.pyogenes is the leading cause of uncomplicated bacterial pharyngitis and tonsillitis commonly referred to a strep throat. S.pyogenes infections can also result in sinusitis, otitis, mastoiditis, pneumonia, joint or bone infections, necrotizing fasciitis and myositis, meningitis or endocarditis. S. pyogenes also infects the skin . Signs of a Strep Throat are fever above 101° F or 38 °C, chills, throat pain, trouble swallowing, neck swelling, trouble breathing, body aches, loss of appetite, nausea or vomiting, abdominal pain. Pharyngitis is also accompanied by other symptoms such as red throat, runny or stuffy nose, dry cough, hoarseness, redness of eyes, joint pain and muscle ache, skin rashes and swollen lymph node in the neck. Children may have diarrhea, sometimes lower WBC and lymphocytic shift, less tonsillar exudates (an exudate is any fluid that filters from the circulatory system into lesions or areas of inflammation) . The bacterium uses the TGFβ1 gene of human host for repeated multiplication. TGF-β1 is also a positive regulator of the integrin signal pathway by up-regulating integrin-linked kinase, phosphoinositide 3-kinase (PI3K), paxillin, and focal adhesion kinase (FAK). Actually TGFβ1 is the gene which encodes for 390 amino acids, signal peptides, and 29 receptors.
Figure.1 the mechanism of streptococcus action inside body.RGD is the bacterial motif.
The mechanism of streptococcal infections is as follows:
1ST the microbe enters body through the air we are taking by breathing. The microorganism then enters into the tonsil cells by phagocytosis, which is a cell eating process. It contains M protein or Fn binding protein which is the virulent factor of pyogene. The fibronectin binding protein then binds with the integrin of host with the help of RGD motif of bacteria. The integrins are the group of proteins which forms the extracellular matrix of cell (Fibronectin, collagens, laminin etc) . When the bacteria get integrated with the proteins the tonsils get infected. The infected tonsil are the main source of TGFβ1 (transforming growth factor) genes which are activated. When the gene is activated it encodes for a receptor that is α5β1 receptor in the cell . The receptor actively binds with the M protein of the bacteria in a lock and key fashion. This binding helps the bacteria to multiply and increase in size. After multiplying millions of bacteria are formed and they produce toxins called HEMOLYSINS which are labile, cause lysis of WBCs, platelets, tissue cells. This toxin is the factor which causes apoptosis of the host cell. Due to the accumulation of cell debris and broken WBCs, it leads to swelling in host tissues. HYALURONIDASE (spreading factor): Lysis of hyaluronic acid- spreads infection in surrounding part of the infected cells. Mef (A) gene codes for a group of protein which gives the bacteria resistance to a series of microlides (antibiotics). This gene stimulates the expression of Fn protein and M1 protein of the bacteria which gives it pathogenic nature .
Conclusion: From the above studies it is proved that the bacteria Streptococcus pyogenes is a very pathogenic bacterium. It is resistant to a group of antibiotics. The capsulated bacteria take the help of host cell mechanism for the multiplication. It causes strep throat, rheumatic fever, many upper respiratory infections such as Sinusitis, Epiglottitis, and Laryngitis in human host. The disease are many time fetal. It is actually an aerobic bacteria therefore it infects and colonizes only in that area where they get sufficient 0xigen. Throat and skin are therefore the main sites of infection.
3. 10/2005. Developed through a partnership of The Ohio State University Medical Center, Mount Carmel Health and OhioHealth, Columbus, Ohio.North Dakota Department of Health, Rev, September2005.
4. John J. Mekalanos Beinan Wang, Shaoying Li, Peter J. Southern, and Cleary P. December 21, 2005. Streptococcal modulation of cellular invasion via TGF-β1 signaling.vol. 103, pp.2380-2385.
Harvard Medical School.
Corona virus infections:
9 oct 2010
Corona viruses are the group of viruses that have a crown like appearance when viewed under the electronic microscope. They belong to the Coronaviridiae family. Corona virus causes the Severe Acute Respiratory Syndrome (SARS). They are commonly known to cause respiratory disease mainly in human beings. Sometimes they also cause gastrointestinal disease in different farm animals. They contain +ve single standed enveloped RNA as their genetic material. The genome of corona virus is the largest genome among the viruses (27-32 in length). Large, roughly spherical, enveloped particles with nuleocapsids and large petal like spikes 20nm long, protruding from the membrane appear as the crown. These viruses are very host or tissue specific based on the receptor specificity of their spike or S protein. It is an enveloped viruses, envelope is made up of glycoproteins.
REVIEW OF LITERATURE:
The microscopic particle is inactive outside because they are incapable of replicating on their own. They take the help of cellular mechanism for their own benefits. Human corona viruses of OC43 generally occur in the respiratory tract of the human beings. The virus envelope is made up of S: Spike protein, receptor binding, cell fusion, major antigen, and major antigen, E: small envelope associated protein, M: membrane protein helps in budding and envelope formations, HE: Haemagglutinin-esterase and genome is associated with phosphoprotein N. The virus primarily infects the upper respiratory tract. Significant range of common cold is caused by this virus. Unlike rhinovirus, the corona virus is difficult to grow in laboratory. Infection with corona virus causes alteration in the transcription and translation patterns in the cell cycle. They interfere with cytoskeleton, apoptosis, coagulation and inflammation and stress responses.
Fig 1: The structure of corona virus.
INFECTION CYCLE OF CORONA VIRUSE: (MECHANISM)
The host and pathogen interaction causes the disease. When once it enters into the host body, it follows replication and assembly phase. 1ST in the cytoplasm the virus particle is uncoated and the RNA genome is liberated in to the host cytoplasm. The corona viral RNA contains a 5'methylated cap and a 3'polyadenylated-A tail to make it look much like the host RNA. This helps the RNA to attach to the ribosome for translation. Infection cycle of CoronaVirus (CoV) starts by the binding to the receptor ACE2. Human ACE2 (is a carboxy monopeptide) that functions as an efficient receptor for the 2002-2003 SARS-Co. ACE is widely found in the Central Nervous System. It is expressed with highest level in the lung, kidney, heart and gastrointestinal system. The entry of corona virus is mainly driven by the S glycoprotein which is a fusion protein of class1. The receptor binding domain in SARS-COV, S protein has been mapped to residues 318-510. It is determined that in different groups of corona virus, the receptor domain occurs in different regions of the S1 subunits .The ectodomain of the S2 subunit contains two heptad repeat (HR) regions. A sequenced motif of the coil and a fusion peptide is predicted to be located immediately upstream of the 1st HR region. The binding of the S1 subunits to the receptor can trigger a series of conformational changes of that may result in the formation of an antiparallel heterotrimeric six helix bundles by the two HR regions . The structural changes of the S1 domain generate energy that drives the fusion of viral and cellular lipid membranes. In this process body cholesterol appears to be an essential factor. The component essential for SARS-CoV infection is the angiotensin-converting enzyme 2(ACE2). SARS-CoV does not contain hemagglutinin-esterase-like attachment factor. It was found that the presence of L-SIGN allows very efficient entry of the virus. Some virus takes the path of endosome and some at the plasma membrane. The infection mediated by this virus could be inhibited by specific inhibitor of the pH-sensitive endosomal protease cathepsin L. Angiotensin I converting enzyme 2 is an exopeptidase that catalyses the conversion of angiotensin 1 to the nonpeptide angiotensin. The protein cleaved angiotensinI to angiotensin1-9, angiotensinII to angiotensin 1-7. It is believed to regulate the rennin-angiotensin system by counter balancing ACE activities. Replication of the virus starts with the entry to the cell. Corona virus has a protein replicase in its genome that allows the RNA viral genome to be transcribed into new RNA copies using the host cells machinery. 1st the replicase protein is made when the gene encoding the replicase is translated. Then the translation is stopped by a stop codon. Corona virus transcription is involving a discontinuous RNA synthesis [1, 2]. There is base pairing during transcription. N proteins of virus help RNA synthesis. It has RNA chaperone activity that may be involved in template switch. Corona virus initiates the translation by cap-dependent mechanism.