{"content":{"sharePage":{"page":0,"digests":[{"id":"32557906","dateCreated":"1294785836","smartDate":"Jan 11, 2011","userCreated":{"username":"ronik1","url":"https:\/\/www.wikispaces.com\/user\/view\/ronik1","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"},"monitored":false,"locked":false,"links":{"self":"https:\/\/medicalmicrobiology-group2.wikispaces.com\/share\/view\/32557906"},"dateDigested":1532725946,"startDate":null,"sharedType":"discussion","title":"Therapies for pharyngitis","description":"Patients with GAS pharyngitis, empirical treatment should be done immediately to prevent suppurative and nonsuppurative complications, to reduce the infection and transmissibility, and to induce clinical improvement of symptoms. Patients with a higher level of suspicion of GAS pharyngitis but delayedculture results can also be given empirical antibiotics. Alternatively antibiotics can be withheld until the culture is positive for S pyogenes. Delaying the treatment for GAS doesn't have any effect on rheumatic heart disease or the strain of S pyogenes. The latter will reduce the inappropriate antibiotic usage and control the antibiotic resistance.
\n
\nSelecting antibiotic primarily depend on the way it is to be administered, its effect, cost and condition that is not limited the antibiotic. Penicillin V or amoxicillin is used for around ten days. Intramuscular penicillin G benzathine may be administreted in patients who are unable to complete the ten days period. Macrolides like erythromycin, azithromycin are alternatively used in penicillin allergic patients. Absence of penicillin-resistant GAS compels a cheaper alternative than latest antibiotics which are expensive. Penicillin is not able to prevent nasopharyngeal carriage in patients with frequent GAS pharyngitis .
\nAmoxicillin\/clavulanate or rifampin may be used in such patients. Antibiotics should not be used in patients with negative throat RADT\/cultures.
\n
\nPharyngitis caused by anaerobic bacteria may respond to penicillins or clindamycin.Yersinia pharyngitis is treated with latest cephalosporin. Mycoplasma pharyngitis is treated by doxycycline or macrolides. Symptomatic oropharyngeal in immunodeficient patients are treated by acyclovir ten days.
\nAmantadine or neuraminidase inhibitors are used to treat Influenza A pharyngitis if the patient is presented immediately after the start of symptoms. Antiretroviral therapy maybe used for HIV acute retroviral syndrome.
\nFluids, gargling with warm and salty water, nonsteroidal anti-inflammatory drugs and rest of voice are some symptomatic relief. Gargling with Chamomile, Blackberry, sage may also help.
\n
\nReferences :
\n
\nInformation from your family doctor. Sore throat. American Family Physician. 2006;74:1185.
\n
\nJonas WB, Jacobs J. Healing with Homeopathy: The Doctors' Guide. New York, NY: Warner Books; 1996: 208.
\n
\nSeller RH. Differential Diagnosis of Common Complaints. 5th ed. Philadelphia, Pa.: Saunders Elsevier; 2007","replyPages":[{"page":0,"digests":[],"more":0}]},{"id":"32432164","dateCreated":"1294521255","smartDate":"Jan 8, 2011","userCreated":{"username":"Sylvia.C.I","url":"https:\/\/www.wikispaces.com\/user\/view\/Sylvia.C.I","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"},"monitored":false,"locked":false,"links":{"self":"https:\/\/medicalmicrobiology-group2.wikispaces.com\/share\/view\/32432164"},"dateDigested":1532725946,"startDate":null,"sharedType":"discussion","title":"Your work","description":"Hi Amanda,
\n Got your message and I have seen your work. Thanks.
\n
\nSylvia","replyPages":[{"page":0,"digests":[],"more":0}]},{"id":"30598279","dateCreated":"1290414312","smartDate":"Nov 22, 2010","userCreated":{"username":"Sylvia.C.I","url":"https:\/\/www.wikispaces.com\/user\/view\/Sylvia.C.I","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"},"monitored":false,"locked":false,"links":{"self":"https:\/\/medicalmicrobiology-group2.wikispaces.com\/share\/view\/30598279"},"dateDigested":1532725946,"startDate":null,"sharedType":"discussion","title":"Articles","description":"I have some materials which I will post on the page section ASAP. Tnx!","replyPages":[{"page":0,"digests":[{"id":"30847475","body":"what is the article on? still expecting it.","dateCreated":"1291031349","smartDate":"Nov 29, 2010","userCreated":{"username":"clemmwealth","url":"https:\/\/www.wikispaces.com\/user\/view\/clemmwealth","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"}}],"more":0}]},{"id":"30559733","dateCreated":"1290293939","smartDate":"Nov 20, 2010","userCreated":{"username":"Sylvia.C.I","url":"https:\/\/www.wikispaces.com\/user\/view\/Sylvia.C.I","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"},"monitored":false,"locked":false,"links":{"self":"https:\/\/medicalmicrobiology-group2.wikispaces.com\/share\/view\/30559733"},"dateDigested":1532725946,"startDate":null,"sharedType":"discussion","title":"**Important points to note!**","description":"PLEASE NOTE THE FOLLOWING!<\/strong>
\nWe are presently working on part 3 of the case study which accounts for 80% out of a 100%.
\nThe marks will be distributed as follows:
\n
\nPresence at meetings: 10% (Individual)
\nIndividual topics: 40% (Individual)
\nPresentation: 10% (Group)
\nStructure: 10% (Group)
\nConclusion and References: 10% (Group)
\n
\nWith reference to the feedback from our lecturer on part 2 which was marked some days ago, the following points need to be acted upon as soon as possible by all members to ensure we get the maximum grade possible. We need to:
\n
\n- Create individual pages on the wiki and work on layout of page (presentation) to show improvement in IT skills.<\/li>
- Upload materials and drafts onto the page created.<\/li>
- Refer to peer reviewed papers when writing and reference throughout our work.<\/li>
- Contribute to discussions on the wiki.<\/li><\/ul><\/ul>
\nThanks all!","replyPages":[{"page":0,"digests":[],"more":0}]},{"id":"30423779","dateCreated":"1290076159","smartDate":"Nov 18, 2010","userCreated":{"username":"Sylvia.C.I","url":"https:\/\/www.wikispaces.com\/user\/view\/Sylvia.C.I","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"},"monitored":false,"locked":false,"links":{"self":"https:\/\/medicalmicrobiology-group2.wikispaces.com\/share\/view\/30423779"},"dateDigested":1532725946,"startDate":null,"sharedType":"discussion","title":"Adding materials to the wiki page","description":"Please, can all members of this group upload materials i.e. articles e.t.c. in relation to Acute Pharyngitis unto the page section of the wiki. For those who are having difficulties navigating the wiki, I will take you through the wiki at the next meeting.Thanks.","replyPages":[{"page":0,"digests":[],"more":0}]},{"id":"30272475","dateCreated":"1289904598","smartDate":"Nov 16, 2010","userCreated":{"username":"clemmwealth","url":"https:\/\/www.wikispaces.com\/user\/view\/clemmwealth","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"},"monitored":false,"locked":false,"links":{"self":"https:\/\/medicalmicrobiology-group2.wikispaces.com\/share\/view\/30272475"},"dateDigested":1532725946,"startDate":null,"sharedType":"discussion","title":"Pathogenesis of Acute Pharyngitis","description":"PATHOGENESIS
\nGroup A Streptococcus (GAS) is the most common cause of human acute bacterial pharyngitis (Hoe etal., 2002) and it can be disseminated through aerosols from person to person, or by consuming contaminated food. The virus enters the body through the ciliated epithelium that lines the nose, which results in edema and hyperemia of the nasal mucous membranes. This condition leads to increased secretory activity of the mucous glands; swelling of the mucous membranes of the nasal cavity, eustachian tubes, and pharynx; and narrowing of nasal passages, causing obstructive symptoms (Red Book, 2006). Bradykinin and lysyl-bradykinin are produced in the nasal passages of patients with rhinovirus colds, and these mediators stimulate pain nerve endings. S. pyogenes is a pathogen that possesses several virulence factors which enables it to invade tissue and escape host defences ( Ashbaugh etal., 2000) Some strains produce pyrogenic exotoxins, which cause serious systemic illness, such as toxic shock\u2013like syndrome, which is associated with a high morbidity and mortality. The principal virulence factors produced by S. pyogenes are listed in Table 1
\nVirulence Factor Activity and Importance
\nStrep pyrogenic
\nexotoxins (Spe A,B, C) Cause release of host cytokines (interleukin, tumor necrosis factor),
\nresulting in multisystem organ failure known as toxic shock-like
\nsyndrome
\nM protein Major virulence factor allowing bacteria to resist phagocytosis by host
\nCells Appears as hair-like projections on cell surface
\n>80 different serotypes Immunogenic (type-specific antibody is protective)
\nStreptolysin O Hemolyzes red blood cells Activity destroyed by oxygen
\nImmunogenic [antistreptolysin O (ASO) antibody formed during
\ninfection; can be used to diagnose recent infection]
\nHyaluronic acid capsule Protects bacteria from killing by phagocytosis
\nStreptokinase
\nDNases
\nHyaluronidase Hydrolytic enzymes allowing bacteria to spread in host tissues Immunogenic (antibodies can be used to diagnose recent infection)
\nHyaluronic acid capsule Protects bacteria from killing by phagocytosis
\nTable 1
\n
\n
\nModels for studying the pathogenesis of GAS pharyngitis
\nSaliva plays a central role in GAS transmission and is a key mediator of innate and acquired immunity in the human oropharynx (Amerongen and Veerman, 2002). To better study the behaviour of GAS in the human oropharynx, the interaction of GAS with human saliva ex vivo has been investigated (Shelburne et al., 2005a; Edwards et al., 2008). The finding that many genes key to GAS pharyngitis are upregulated in human saliva compared with standard laboratory medium led to the proposition that GAS\u2013saliva interaction is the initial stage in host\u2013pathogen interaction, thereby adding an additional step in GAS oropharyngeal pathogenesis. The relative technical ease of examining GAS behaviour in saliva ex vivo means that analysis of GAS\u2013saliva interaction is a powerful tool for generating new hypotheses and understanding regarding the role of particular gene\/gene products in GAS pharyngeal pathogenesis.
\nEpithelial cell adherence
\nAdherence of GAS to pharyngeal epithelial cells has been extensively investigated and much is known (Courtney et al., 2002). A key recent advance has been the discovery that GAS pili-like cell surface structures are central players in pharyngeal epithelial cell adherence and biofilm formation (Fig. 1B) (Table S1). GAS pili examined to date are encoded by genes located in the so-called FCT (fibronectin, collagen-binding, T-antigen) gene region and are composed of the main pilus subunit (spy0128 in the serotype M1 strain SF370) and two ancillary proteins (Mora et al., 2005). The main pilus subunit corresponds to the T antigen of the Lancefield T serotypes, one of the two major GAS classification schemes (Kang et al., 2007). Assembly of GAS pili is dependent on a sortase encoded by genes in the FCT region, and at least in M3 strains, on a signal peptidase encoded immediately upstream of the T antigen (Zahner and Scott, 2007).
\nOther GAS proteins have recently been demonstrated to contribute to epithelial cell adherence. For example, the worldwide emergence of a particular clone of serotype M3 GAS has been strongly linked to the acquisition of a bacteriophage-encoded phospholipase A2 (SlaA) that contributes to adherence to host pharyngeal epithelium. The mechanism of action of SlaA appears to involve entry into host cells. A \u0394slaA strain was significantly impaired in its ability to cause pharyngitis in the cynomolgus macaque, providing strong evidence of the key role of SlaA in GAS pharyngeal pathogenesis (Sitkiewicz et al., 2006). Similarly, serum opacity factor also has been demonstrated to participate in Fn-mediated host cell adherence (Table S1). In summary, despite decades of investigation, the molecular basis of GAS eukaryotic cell adherence remains a very active field of investigation with new insights accumulating rapidly.
\nIntracellular invasion
\nAlthough GAS is predominantly an extracellular pathogen, data over the past decade have shown that the organism may invade and persist within epithelial cells (Wang et al., 2006a). The exact role of this event in GAS pathogenesis is not clear. Many of the proteins involved in GAS epithelial cell invasion also participate in adherence, including FnBPs, M protein and streptocococcal collagen-like protein 1 (Table S1). The eukaryotic signalling pathways mediating GAS invasion begin with bacterial binding to eukaryotic cell surface integrins, eventually resulting in actin cytoskeletal rearrangement and GAS internalization (Purushothaman et al., 2003; Wang et al., 2006b,c; 2007). Interaction of GAS with integrin-bound Fn results in the upregulation of transforming growth factor \u03b21, which in turn upregulates cell surface expression of 5 integrin and Fn, making the cells better targets for streptococcal binding (Wang et al., 2006b). The ability of GAS to invade and persist intracellularly has been associated with penicillin treatment failure and recurrent tonsillitis, but a definitive link between GAS eukaryotic cell invasion and pharyngeal pathogenesis has yet to be made.
\nProliferation
\nDevelopment of GAS pharyngeal infection occurs following transmission of relatively small numbers of organisms from an infected or colonized host to a non-infected host. Following adhesion to the pharyngeal epithelium, GAS proliferation in the oropharynx triggers the signs and symptoms of pharyngitis. Detailed understanding of this process has been provided recently using a non-human primate model of GAS pharyngitis (Virtaneva et al., 2005). Correlation of organism density with pharyngeal evaluation demonstrated that GAS proliferation preceded the clinical development of pharyngitis, suggesting that the organism did not obtain nutrients needed for proliferation from eukaryotic cell lysis.
\n Infection with S. pyogenes may present in children as scarlet fever, which is fever and sore throat with a diffuse rash. The rash is caused by an erythrogenic exotoxin that has now been designated as one of the streptococcal pyrogenic exotoxins or Spe. The incidence of scarlet fever fell significantly in the 1950s largely because of the widespread use of penicillin. The two major sequellae of untreated S. pyogenes infection, rheumatic fever (RF) and acute glomerulonephritis (GN), occur weeks after the streptococcal infection (Shelburne etal., 2005). The organism can no longer be cultured from the throat or skin when the patient presentswith symptoms of RF or GN. RF occurs in <3% of people with strep pharyngitis. The patient presents with swelling and pain in more than one joint (migrating arthritis) and with a new heart murmur due to damage to the heart muscle and heart valves. The patient may also have a group of neurologic symptoms, including jerky or twitching movements (chorea). GN may occur 10 days or later after a skin infection with S. pyogenes. The patient has signs and symptoms of kidney dysfunction, such as swollen ankles and eyelids (edema), elevated bloodressure (hypertension), blood and protein in the urine, and decreased urine output. Deposition of antigen\u2013antibody\u2013complement complexes can be seen in a kidney biopsy using immunofluorescent stains (Zahner etal., 2007). The damage to the heart and kidney is not causedby toxic streptococcal products (streptolysin O, streptokinase, and Spe) or an autoimmune response by the host. When the streptococcal bacteria are lysed by the host cells, antigens are released that evoke an immune response. Antibodies produced to the antigenic components of the bacteria cross-react with the patient\u2019s cardiac proteins, allowing the antibodies to attack the heart tissue and cause valvular damage. Later in life these damaged heart valves are a prime site where bacteria lodge and cause an infection of the heart known as endocarditis (Ashbaugh etal., 2000). There is no antibiotic treatment for RF or GN; however, prophylactic penicillin is given to peoplewith a history of RF to prevent recurrent streptococcal infections. Tests needed in the diagnosis of RF or GN may include antibody tests, such as antistreptolysinOor anti-DNase B to detect a recent infection after the viable organisms have disappeared. An acute (immediate) and a convalescent serum (drawn 14 days later) may be submitted for antibody titers to prove that the patient had a recent GAS infection. A fourfold rise in titer between the acute and convalescent sera indicates a recent infection, for example, an acute titer of 1 : 8 increases to 1 : 64 in the convalescent serum. by systemic infection with the bacteria, but is theorized to be a result of direct damage.
\nReferences
\nAshbaugh, C. D., T. J. Moser, M. H. Shearer, G. L. White, R. C. Kennedy, and M. R. Wessel. 2000. Bacterial determinants of persistent throat colonization and the associated immune response in a primate model of human group A streptococcal pharyngeal infection. Cell. Microbiol. 2:283-292.
\nEdwards, A.M., Manetti, A.G., Falugi, F., Zingaretti, C., Capo, S., Buccato, S., et al. (2008) Scavenger receptor gp340 aggregates group A streptococci by binding pili. Mol Microbiol 68: 1378\u20131394
\nHoe, N. P., R. M. Ireland, F. R. DeLeo, B. B. Gowen, D. W. Dorward, J. M. Voyich, M. Liu, E. H. Burns, Jr., D. M. Culnan, A. Bretscher, and J. M. Musser. 2002. Insight into the molecular basis of pathogen abundance: group A Streptococcus inhibitor of complement inhibits bacterial adherence and internalization into human cells. Proc. Natl. Acad. Sci. USA 99:7646-7651
\nRed Book, Report of the Committee on Infectious Diseases of the American Academy of Pediatrics,27th ed., 2006, pp. 610\u2013620.
\nShelburne, S.A., Sumby, P., Sitkiewicz, I., Granville, C.N., DeLeo, F.R., and Musser, J.M. (2005a) Central role of a two-component gene regulatory system of previously unknown function in pathogen persistence in human saliva. Proc Natl Acad Sci USA 102: 16037\u201316042.
\nSumby, P., Tart, A.H., and Musser, J.M. (2008) A non-human primate model of acute group a Streptococcus pharyngitis. Methods Mol Biol 431: 255\u2013267.
\nVirtaneva, K., Porcella, S.F., Graham, M.R., Ireland, R.M., Johnson, C.A., Ricklefs, S.M., et al. (2005) Longitudinal analysis of the group A Streptococcus transcriptome in experimental pharyngitis in cynomolgus macaques. Proc Natl Acad Sci USA 102: 9014\u20139019.
\nZahner, D., and Scott, J.R. (2007) SipA is required for pilus formation in Streptococcus pyogenes serotype M3. J Bacteriol 190: 527\u2013535.","replyPages":[{"page":0,"digests":[{"id":"30423839","body":"Have seen your work. Will see you in the meeting. Thanks.","dateCreated":"1290076339","smartDate":"Nov 18, 2010","userCreated":{"username":"Sylvia.C.I","url":"https:\/\/www.wikispaces.com\/user\/view\/Sylvia.C.I","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"}}],"more":0}]},{"id":"30176367","dateCreated":"1289783499","smartDate":"Nov 14, 2010","userCreated":{"username":"Sylvia.C.I","url":"https:\/\/www.wikispaces.com\/user\/view\/Sylvia.C.I","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"},"monitored":false,"locked":false,"links":{"self":"https:\/\/medicalmicrobiology-group2.wikispaces.com\/share\/view\/30176367"},"dateDigested":1532725947,"startDate":null,"sharedType":"discussion","title":"Second meeting minutes","description":"Second meeting<\/u>
\nDate<\/strong>: 4th November, 2010
\nLocation<\/strong>: Room 007, Nelson Building, Medway campus.
\nTime<\/strong>: 1.00pm
\n
\nThose present<\/u>
\n\u2022 Miss Amanda Aryee
\n\u2022 Mr Nurudeen Kallon
\n\u2022 Mr Clement Utti
\n\u2022 Mr Rounik Mazumdar
\n\u2022 Ms Chibuzo Igboanugo
\n
\nApologies<\/strong>: None
\n
\nTopics for discussion<\/u>
\n\u2022 Choice of topics.
\n\u2022 Creation of Wiki on Wikispaces.
\n
\nContribution to discussion<\/u>
\nAll group members put forward their topic of preference to write on and all agreed on the following topic choices with the reference for each sub-heading in Harvard style included:
\n
\n\u2022 Introduction - To be written as a group
\n\u2022 Infectious agent - Miss Amanda Aryee
\n\u2022 Epidermiology - Mr Nurudeen Kallon
\n\u2022 Pathogenicity - Mr Clement Utti
\n\u2022 Clinical aspects - Ms Chibuzo Igboanugo
\n\u2022 Therapies - Mr Rounik Mazumdar
\n\u2022 Conclusion \u2013 To be written as a group (200 words)
\n
\nThe number of words to be written for each topic was agreed on to be 300-350 words. The writing of the introduction and conclusion were to be discussed in the next meeting when members had finished their write-ups on the topics chosen as agreed by all. Members who had not placed their emails on the blog gave them to the group leader so that they could have access to the group wiki.
\n
\nNext meeting<\/strong>: 18th November, 2010
\nLocation<\/strong>: Room 007, Nelson Building, Medway campus.
\nTime<\/strong>: 1.00pm","replyPages":[{"page":0,"digests":[{"id":"30271799","body":" Hi,
\n Just to let you know that l might be coming a bit late for the meeting cos l will be having project presentation with my supervisors and colleagues. But l shall be there as soon as it's over.
\n
\n Kind regards,
\n Clement","dateCreated":"1289902506","smartDate":"Nov 16, 2010","userCreated":{"username":"clemmwealth","url":"https:\/\/www.wikispaces.com\/user\/view\/clemmwealth","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"}},{"id":"30423457","body":"No problems. Thanks for the information.","dateCreated":"1290074202","smartDate":"Nov 18, 2010","userCreated":{"username":"Sylvia.C.I","url":"https:\/\/www.wikispaces.com\/user\/view\/Sylvia.C.I","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"}}],"more":0}]},{"id":"30176071","dateCreated":"1289783129","smartDate":"Nov 14, 2010","userCreated":{"username":"Sylvia.C.I","url":"https:\/\/www.wikispaces.com\/user\/view\/Sylvia.C.I","imageUrl":"https:\/\/ssl.wikicdn.com\/i\/user_none_lg.jpg"},"monitored":false,"locked":false,"links":{"self":"https:\/\/medicalmicrobiology-group2.wikispaces.com\/share\/view\/30176071"},"dateDigested":1532725947,"startDate":null,"sharedType":"discussion","title":"First meeting minutes","description":"Case study<\/u>
\nThe patient is a 6 years old male who had been in good health with no significant medical problems. In late September he presented to his paediatrician\u2019s office with a complaint of sore throat, fever, headache, and swollen glands in his neck for the past 36 h. On physical examination (PE), he had fever of 38\u00baC, a red posterior pharynx, yellowish exudate on his tonsils, and multiple, enlarged, tender cervical lymph nodes.
\n
\nFirst meeting<\/u>
\nDate<\/strong>: 25th October, 2010
\nLocation<\/strong>: Room 3, Drill hall library, Medway campus.
\nTime<\/strong>: 12 noon
\n
\nThose present<\/u>
\n\u2022 Miss Amanda Aryee
\n\u2022 Mr Nurudeen Kallon
\n\u2022 Mr Clement Utti
\n\u2022 Mr Rounik Mazumdar
\n\u2022 Ms Chibuzo Igboanugo
\n
\nApologies<\/strong>: None
\n
\nTopics for discussion<\/u>
\n\u2022 Review of the case study.
\n\u2022 Expectations from us on what to write on the sub-headings for the case study.
\n
\nContribution to discussion<\/u>
\nAll group members critically reviewed the case study by interpreting and discussing the results of the tests involved with the case study shown above. They also expressed their opinion on what was expected to be written on the sub-headings which are; Introduction, Infectious agent, Epidermiology, Pathogenicity, Clinical aspects, Therapies and Conclusion. It was agreed by all that topics will be chosen in the next meeting pending further review of the case study individually and searching for supporting journals. It was also agreed upon that the introduction and conclusion will be written by all group members after the other sub-headings have been written.
\n
\nNext meeting<\/strong>: 28th October, 2010
\nLocation<\/strong>: Room 3, Drill hall library, Medway campus.
\nTime<\/strong>: 12noon
\nMeeting date was later changed due to time being inconvenient for some group members to the 4th November, 2010 to take place in Room 007, Nelson Building, Medway campus at 1.00pm.","replyPages":[{"page":0,"digests":[],"more":0}]}],"more":false},"comments":[]},"http":{"code":200,"status":"OK"},"redirectUrl":null,"javascript":null,"notices":{"warning":[],"error":[],"info":[],"success":[]}}