My pathogen is Shigella species My topic is how can phyto-medicine (medicinal plants) become the best treatment against shigellosis. Shigella species is a big attribute to shigellosis & over the

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My pathogen is Shigella species

My topic is how can phyto-medicine (medicinal plants) become the best treatment against shigellosis. Shigella species is a big attribute  to shigellosis & over the century these species has increased there resistance to antibiotic.

I will be providing 5 peer review articles & 4 primary sources. I have went through all peer reviews and

highlighted all important info for the background information within the peer reviews.

I can only upload for four sources. These 4 will be my primary.

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If any questions message me. I‘ll respond quickly.

This paper must be at least 7 pages, but must not exceed 9 pages in length, excluding the Literature Cited section. (Aim for 8 pages, excluding the Literature Cited section.) The first page must include the Title and Author, plus a Summary of your paper (approximately 300 words). This leaves about 7 pages for the main body of your paper (see below). The paper must be typed in 12-point font, double-spaced, with margins set at 1 inch on all sides of the pages. Please carefully check your word processing program to be sure that additional space is not inserted below each line. All pages must be numbered at the bottom of the page.

About one-third (1-1/2 to 2-1/2 pages) of the main body of your paper (the part after the title page plus summary; approx.7 pages in length) must be devoted to general background information on the pathogen, its properties and transmission, the diseases it causes in humans, major signs and symptoms of these diseases; major virulence factors of the pathogen; treatment of and prevention of these diseases; and whether or not a vaccine is available. If you found a review article on the specific focus of your own writing, you may discuss that article briefly in the initial 2-1/2 pages of your paper to “transition” to your discussion of the specific primary sources you chose. The remaining two-thirds (4-1/2 to 5-1/2 pages) of the main body of the paper must be devoted to your primary sources. Examples of more specific aspects of your topic might include: antibiotic resistance in the particular pathogen; properties/research on a particular virulence factor of the pathogen; progress in development of a vaccine for prevention of diseases due to the pathogen; progress in developing better treatments for a specific disease(s) caused by the pathogen; or recent outbreaks of disease due to the pathogen. There are, of course, many other possibilities.

Papers may not include any direct quotations or any figures or tables from the references. A paper may also not repeat substantial amounts of data from the primary sources. A paper that is constructed from direct quotations does not convey an understanding of the material. No plagiarism.

My pathogen is Shigella species My topic is how can phyto-medicine (medicinal plants) become the best treatment against shigellosis. Shigella species is a big attribute to shigellosis & over the
Journal of Infection and Public Health 11 (2018) 451–454 Contents lists available at ScienceDirect Journal of Infection and Public Health journa l h om epa ge: http://www.elsevier.com/lo cate/jiph Emergence of antibiotic resistant Shigella species: A matter of concern Minakshi Puzari, Mohan Sharma, Pankaj Chetia ∗ Department of Life Sciences, Dibrugarh University, Dibrugarh, Assam 786004, India a r t i c l e i n f o Article history: Received 15 June 2017 Received in revised form 10 September 2017 Accepted 30 September 2017 Keywords: Shigellosis Antibiotic resistance Multidrug resistance Bacteria a b s t r a c t A major threat to the world is the emergence of antibiotic resistant bacteria, which has rendered previously susceptible drugs useless and increased the rate of therapeutic failures. Shigella species, which are the causative organism of Shigellosis, were earlier susceptible to ampicillin, chlorampheni- col, co-trimoxazole and nalidixic acid but now they have developed resistance against fluoroquinolones, cephalosporins and azithromycin. Many shigellosis outbreaks have been reported by resistant strains of Shigella species. This review attempts to provide a brief overview about the scenario of shigellosis and the emergence as well as ubiquitous nature of multidrug resistant (MDR) Shigella species. © 2017 The Authors. Published by Elsevier Limited on behalf of King Saud Bin Abdulaziz University for Health Sciences. This is an open access article under the CC BY-NC-ND license (http:// creativecommons.org/licenses/by-nc-nd/4.0/ ). Contents Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 451 Antibiotic resistance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 451 Classification and distribution . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 452 Transmission and diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 452 Symptoms and complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 452 Scenario of antibiotic resistance in Shigella spp. and molecular epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 452 Prevention and control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 453 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 453 Funding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 453 Competing interests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 453 Ethical approval . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 454 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 454 Introduction Antibiotic resistance The development of antibiotic resistance in bacteria, as a part of evolutionary process in them has now been declared as a mat- ter of global crisis by the World Health Organization [1] . It has resulted in increased failure rates of treatment of infectious dis- eases caused by bacteria, as drugs to which they were previously susceptible no longer works. Bacteria can be intrinsically resistant owning to its inherent properties or achieve this resistance capacity ∗ Corresponding author. E-mail addresses: [email protected]com (M. Puzari), [email protected] (M. Sharma), [email protected] (P. Chetia). by mutations and gene transfer. Various mechanisms of antibiotic resistance include poor penetration of drug into the cell, efflux of antibiotics by efflux pumps, target modification by mutation and hydrolysis of antibiotics [2] . Antibiotic resistance has been reported in both Gram positive bacteria as well as Gram negative bacteria [2,3] . One such case is the emergence of MDR Shigella species [4] . Shigella species are the causative organism of Shigellosis, which is an acute gastroenteritis infection [5] . Shigellosis is a global human health problem and major cause of diarrhoea causing about 700,000 deaths per year worldwide [6] . Most of the deaths involve children in the age group of below 5 years. Exposure to a certain serotype, leads to the development of serotype-specific protective immunity [7] . The first drugs used to treat Shigella infections were sulphonamides, which was followed by tetracycline and then by chloramphenicol. Shigella developed resistance to all of these and so accordingly treatment shifted to https://doi.org/10.1016/j.jiph.2017.09.0251876-0341/© 2017 The Authors. Published by Elsevier Limited on behalf of King Saud Bin Abdulaziz University for Health Sciences. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/ ). 452 M. Puzari et al. / Journal of Infection and Public Health 11 (2018) 451–454 Table 1 Conversion of Shigella flexneri serotypes by bacteriophages. Phage Conversion SfI Serotype Y to 1a SfII Serotype Y to 2a Sf6 Serotype Y to 3b SfIV Serotype Y to 4a SfV Serotype Y to 5a SfX Serotype Y to X ampicillin and co-trimoxazole. However, treatment recommen- dations were again changed to nalidixic acid because Shigella developed resistance to the former drugs. Later resistance capac- ity to nalidixic acid developed and soon after that fluoroquinolones were introduced. But now fluoroquinolones resistant strains have been isolated from various sources. WHO recommends ceftriax- one, pivmecillinam and azithromycin for treatment of infection by fluoroquinolones resistant Shigella species [8] . However, cef- triaxone resistant and azithromycin resistant isolates have also been reported [9] in some places. This has now become a threat to mankind and a matter of huge concern. Classification and distribution The genus Shigella is a part of Enterobacteriaceae family and includes four species: Shigella dysenteriae, Shigella flexneri, Shigella sonnei and Shigella boydii [10,11] . Each species has unique epi- demiological characteristics, despite having similar pathogenic properties and have diverse distribution pattern across different geographical regions. They can be further classified into serotypes based on O antigen of the cell envelope lipopolysaccharide- S. boydii has 20 serotypes [8] , S. flexneri has 6 serotypes and 14 subserotypes [12] , S. dysenteriae has 15 serotypes [7] with 2 provisional serotypes [12] and S. sonnei has only one serotype [7,8] . S. sonnei can be divided into five biotypes (a, b, e, f and g) based on biochemical properties [7] . S. flexneri has been reported to undergo serotype conversion mediated by temperate bacteriophages, in order to escape from immune responses of the host [7] . Six serotype con- verting phages have been reported for conversion of serotype Y ( Table 1). There have been reports of conversion of serotype X, 4a and Y to Xv, 4av and Yu due to modification of the O-antigen by plasmid-encoded phosphoethanolamine [7] . S. dysenteriae occurs in epidemic form, S. flexneri and S. sonnei are endemic to developing and developed nations while S. boydii is found in India and neighbouring nations. In India, there is het- erogeneous distribution of Shigella species and its serotypes [8] . A study in South India between 2001 and 2003 found S. flexneri to be most common (45%) followed by S. dysenteriae (29.4%), S. boydii (14.7%) and S. sonnei (10.2%). Again a drastic change was observed in another study conducted between 2003 and 2006, where S. flexneri remained as the most prevalent (45%) followed by S. sonnei (31%), S. boydii (15%) and S. dysenteriae (8%). In Andaman and Nicobar Islands, S. flexneri 2a serotype was found to be predominant [7] . Transmission and diagnosis Shigella species are primarily transmitted via faeco-oral route. Musca domestica, the common housefly act as a vector for trans- mission of the pathogen. They are easily transmitted via personal contact with the infected person or consumption of contaminated food or water. Bacterial count as low as 10–100 are potential of causing infection. Transmission is influenced by variations in envi- ronmental factors such as temperature and rainfall. Increase in infection rate has been observed during summer months. They are highly contagious and mostly occur in areas of poor sanitary conditions [11,13] . A study in Tanzania revealed that in children below 5 years of age, the pathogen mainly responsible for diarrhoea was Shigella spp. and many asymptomatic children were found to act as carriers, enabling the sustenance and dissemination of the enteropathogen [7] . In north India, asymptomatic food handlers acted as a source of infection at a tertiary care centre [8] . For diagnosis of shigellosis, culture isolation of Shigella is done from faecal specimens. In case of moderate to extreme infection, antibiotics are recommended for treatment. However, it is impor- tant to keep in mind the developing resistance in Shigella towards antibiotics. In patients with acute febrile gastroenteritis, blood cul- tures should be obtained to detect shigellemia [14] . Shigellosis is more likely to develop in case of travellers [10] ; however there have been reports of increasing shigellosis episodes among men with no travel history but record of having sex with unprotected men [15] . Symptoms and complications Symptoms of shigellosis include bloody diarrhoea accom- panied with abdominal cramps. The pathogen invades colonic mucosa, multiply causing epithelial cell death and spread laterally leading to mucosal ulcer, bleeding and inflammation [10] . Infec- tion is usually restricted to the gastro-intestinal tract; however, there are incidences of extra-intestinal infections such as infec- tion of bloodstream with fatality rate of 46% [7] . There might be other complications associated with Shigella infection, which includes haemolytic-uremic syndrome [8] , hypoxia [16] , hepatic dysfunction [17] , reactive arthritis, neurological complications, etc. Hyponatremia and pneumonia are unusual yet potential complica- tions associated with shigellosis [7] . Scenario of antibiotic resistance in Shigella spp. and molecular epidemiology Every year there are about 164.7 million Shigella episodes throughout the world. In Shiraz, Iran 719 stool samples of diarrhoea patients were analyzed, which revealed resistance to co- trimoxazole in 90.24% of Shigella isolates [11] . In United States, first national surveillance to determine of antimicrobial resistance among isolates of Shigella was carried out in 1999. It was a part of National Antibiotic Resistance Monitoring System (NARMS) for enteric bacteria. Annually about 450,000 people in the United States get infected by Shigella spp. leading to over 6000 hospitalizations [18] . There have been reports of diarrhoea outbreak caused by S. sonnei in child day care centers in Texas [19] . An investigation car- ried out in Ethiopia on the antibiotic susceptibility pattern revealed widespread resistance of the isolates to tetracycline, ampicillin and cotrimoxazole; leading to recommendations on gentamicin and ciprofloxacin usage only for severe cases [13] . Shigellosis usually occurs in epidemic forms [7] . It has been reported from many Asian countries such as Bhutan, Sri Lanka, Maldives, Myanmar, Bangladesh, Nepal etc. [7] . A nationwide sur- vey was carried out in Korea from 1991 to 2002, which showed that 20 out of 5911 isolates of Shigella were extended-spectrum – lactamase (ESBL) positive [20] . The predominant -lactamases in Gram-negative bacteria are TEM-, OXA-, SHV- and CTX-M [7] . In S. flexneri, ampicillin resistance is mainly due to bla- oxa gene while in S. sonnei it is mainly due to the presence of bla- TEM gene [21] . Analysis of 88 isolates from Bay of Bengal islands, India revealed the association of MDR with drug-resistant genes. Ampicillin resis- tance was found associated with TEM -lactamase genes in all the isolates, while in 22% of the isolates aac2 gene was found associated to gentamicin resistance [8] . Resistance of Shigella spp. to chloram- phenicol, streptomycin and tetracycline has mainly been attributed to the presence of catA1, strA and tetB genes. Resistance to trimetho- prim is associated with dhfrIa or dhfrIIIc genes [21] while SulI, SulII M. Puzari et al. / Journal of Infection and Public Health 11 (2018) 451–454 453 and SulIII are responsible for sulphonamide resistance [7] . A study conducted in Korea showed that two S. flexneri strains- S. flexneri 021787 and S. flexneri 021895 were resistant to fluoroquinolones; which was found to be result of target site mutation as well as overexpression of genes encoding efflux pumps [22] . A study conducted in Bangladesh revealed a rise in resistant strains of Shigella towards ciprofloxacin from 0% in 2004 to 44% in 2010. The predominant one was found to be S. flexneri [23] ; which was also found to be the most prevalent in Nepal [24] , China, Pakistan, Indonesia and Vietnam [25] . Most of the isolates were found to be resistant to amoxicillin and cotrimoxazole, while some isolates from China, Vietnam and Pakistan were reported as ciprofloxacin resistant [25] . On the other hand, S. sonnei was found to be more dominant in Thailand than the other species [25,26] . A molecular study in Faisalabad region of Pakistan also found S. flexneri as the most prevalent and resistant [4] . In China, clinical isolates of S. flexneri collected from rural hospitals when stud- ied, led to the conclusion that multiple antibiotic resistance (Mar) phenotypes were result of overexpression of acrA gene [27] . The role of efflux pump in the acquisition of resistance was proved as ciprofloxacin accumulation increased in the presence of carbonyl cyanidem-chlorophenylhydrazone (CCCP). Efflux pump inhibitor Phe-Arg- -naphthylamide (PA N) decreased MIC of ciprofloxacin against the isolates [27] . Mutation in acrA and tolC genes has been found to play a crucial role in antibiotic resistance in Shigella species isolated from stool samples of dysentery patients in Henan, China [28] . The genes mdfA [29] and acrB have also been found responsi- ble for efflux-modulated resistance [7] . Another study conducted in Taiwan using 103 S. sonnei isolates from outbreaks and 32 isolates from sporadic infections revealed that the spread of mul- tiple resistance genes in S. sonnei was promoted by the location of resistance genes in plasmids and horizontal plasmid transfer [30] . During a bacillary dysentery outbreak in Taiwan, CMY-2-type AmpC -lactamase, enoded by plasmids has also been reported in ceftriazone resistant S. sonnei isolates [31] . In India, Shigellosis has been reported from several locations such as Chandigarh, Vellore, Southern India, Eastern India and Andaman and Nicobar Islands. It has been a major cause of mor- bidity and mortality in case of children [8] . S. flexneri is of more common occurrence in the Indian subcontinent [32] . However, S. dysenteriae serotype 1 has also been of major concern [33] A study conducted between January 2001 and August 2004, on 193 strains of Shigella isolated from hospitalized children suffering from acute diarrhoea, showed S. flexneri to be most prevalent (60%). It was fol- lowed by S. sonnei (23.8%), S. dysenteriae (9.8%) and S. boydii (5.7%). An increase in resistance to fluoroquinolones year after another has been observed in case of S. dysenteriae type I and S. flexneri [34] . Mutation in the DNA gyrase and topoisomerase IV is the most prominent mechanism of quinolone resistance [7] . Another mech- anism is the presence of plasmid-mediated quinolone resistance genes, which has been reported from Japan, China, USA and India [8] . In 1984, shigellosis outbreak occurred in Tripura and West Ben- gal affecting 350,000 people and causing 3500 deaths. In 2002, there was a 25.6% attack rate in an outbreak that occurred in West Bengal and tea gardens of Siliguri. S. dysenteriae was responsible for these outbreaks and reported to have emerged again as mul- tidrug resistant in 2002 [33] . Studies on S. dysenteriae had shown involvement of a proton driven efflux pump in the development of antibiotic resistance [35] . High level resistance to fluoroquinolones is attributed to the overexpression of RND pump AcrAB [36] rather than that of MFS pump MdfA [29] . Outbreaks have been reported due to by S. flexneri and S. sonnei in West Bengal (2007), Kerela (2009) and then in Maharashtra (2010). Cephalosporins are used to treat fluoroquinolone resistant strains of Shigella spp. However, in 2001 first ceftriaxone resistant S. flexneri was reported and the number of resistant isolates has increased since then [8] . A study conducted from 2001 to 2009 in Chandigarh reported high level of ESBL and AmpC mediated cephalosporin resistance in Shigella spp. [37] . Mutations broaden the spectrum of ESBLs such as TEM-1, TEM-2 and SHV-1, which in turn are responsible for resistance to third-generation cephalosporins [8] . From 2002 to 2007, a study was carried out in a hospital at Bangalore, which showed more than 70% of Shigella isolates to be drug resistant; S. flexneri being the pre-dominant one. It was suggested that ciprofloxacin should not be used as first choice of drugs to treat shigellosis [5] . Another study conducted using stool samples from patients suffering with diarrhoea and dysentery in Dibrugarh, Assam also showed S. flexneri to be most common. It has been found that they show high resis- tance against nalidixic acid; while ciprofloxacin resistant strains were found to be emerging [38] . Prevention and control Awareness should be spread regarding the threat of antibiotic resistance in bacteria. Considering the clinical and epidemiological implications of Shigella, proper care should be taken to prevent the spread of the pathogen. Sanitation and personal hygiene should be maintained. Effective control measures should be formulated. Judicious utilization of antibiotics is necessary to control infections [39] . One such problem regarding antibiotic utilization is the use of antibiotics in disease whose condition can not be improved by its use. Again, the lack of access to appropriate antibiotics can result in death [40] . For appropriate use of antibiotics, proper regulations and good surveillance are needed [41] . In India there is an absence of a good surveillance system. Moreover, pharmacies are run by unqualified pharmacist which is a huge problem [40] . Reporting of antibiotic susceptibility after analysis from time to time is essential to serve as guidance for antibiotic treatment [5] . Safe, cheap and effective vaccine against Shigella is yet to be developed [10,42] ; which is of urgent need [26] as it would be sustainable strategy against shigellosis. The only licensed vaccine available is a S. flexneri 2a-S. sonnei bivalent vaccine, which is used in China [8] . Due to the heterogeneous distribution of the species, multivalent vaccines formulations are required to prevent shigel- losis [25] . Conclusion The food borne pathogen Shigella has huge public health impor- tance and the emergence of antibiotic resistance in them demands the development of new and better antimicrobial drugs. However, there is possibility that they might evolve and become resistant to those newly formulated drugs. It is therefore mandatory to under- stand the mechanism of resistance and build strategies to overcome it. Studies on the aspect of efflux pump activity as resistance mech- anism and their inhibition have been carried out. However no inhibitor has been approved clinically till date. Thus, treatment of shigellosis has become a therapeutic challenge. Or in a much broader sense, we can say that dealing with MDR bacteria has become the ultimate quest. Funding No funding sources. Competing interests None declared. 454 M. Puzari et al. / Journal of Infection and Public Health 11 (2018) 451–454 Ethical approval Not required. References [1] WHO. Antimicrobial resistance: global report on surveillance. 20 Avenue Appia, 1211 Geneva 27, Switzerland: WHO Press, World Health Organization; 2014. [2] Blair JMA, Webber MA, Baylay AJ, Ogbolu DO, Piddock LJV. Molecular mecha- nisms of antibiotic resistance. Nat Rev Microbiol 2015;13:42–51. [3] Fernández L, Hancock Robert EW. Adaptive and mutational resistance: role of porins and efflux pumps in drug resistance. Clin Microbiol Rev 2012;25:661–81. [4] Tariq A, Haque A, Ali A, Bashir S, Habeeb MA, Salman M, et al. Molecular profil- ing of antimicrobial resistance and integron association of multidrug-resistant clinical isolates of Shigella species from Faisalabad. Pakistan Can J Microbiol 2012;58:1047–54. [5] Srinivasa H, Baijayanti M, Raksha Y. 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