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Before antibiotics in the 1940s (Ventola, 2015),

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Before antibiotics in the 1940s (Ventola, 2015), bacterial infections were treated with surgical drainage, antiseptics, silver compounds, arsenicals or “tincture of time”,  (Zinner, 2007). According to Zinner (2007), diseases caused by bacteria infection which includes pneumonia or meningitis were practically seen as death sentence. Antibiotics has fundamentally changed medicine in various respects, countless lives have been saved since the golden era (Aminov, 2010, Davies and Davies, 2010). Benefits of antibiotics include the successful prevention and treatment of infections that can arise in patients who are undergoing chemotherapy treatments and have chronic disease such as renal disease, rheumatoid arthritis or who have had complex surgery such as joint replacement or cardiac surgery (Centers for Disease Control and Prevention, 2013, Gould and Bal, 2013, Rossolini et al., 2014, Ventola, 2015, Wright, 2014). Some antibiotics work by inhibiting the transpeptidase that cross- links cell wall peptidoglycan during the cell cycle so it cannot reproduce (Giesbrecht et al., 1998)which leads to the cell stress response that result in cell lysis (Fair and Tor, 2014, Tomasz, 1979), while some inhibit elongation of translation, activating the premature disassociation of ribosomal peptidyl tRNA  (Tenson et al., 2003). Other antibiotics attack the DNA copying machinery  (Giesbrecht et al., 1998). The sulphonamides are synthetic antimetabolites which inhibit dihydropteroate synthase (Fair and Tor, 2014)- an important intermediate in folate synthesis that is found in bacteria (Hevener et al., 2010). Inhibition of this enzyme suppress the DNA replication and bacteriostatic activity of aerobic gram positive and gram-negative bacteria (Fair and Tor, 2014). Another group of antibodies called tetracycline are bacteriostatic agents which binds to the 30S ribosomal subunit blocking the aminoacyl tRNA access to the ribosome preventing protein synthesis (Chopra and Roberts, 2001, Fair and Tor, 2014, Li et al., 2017). This type of antibiotics attacks aerobic gram positive and gram-negative bacteria (Fair and Tor, 2014). The rest of the antibiotics out there either inhibit the elongation step in translation (Fair and Tor, 2014) by binding to the peptidyl transferase centre of the 50S ribosomal subunit (Bostan et al., 2009, Ma et al., 2014) or rifamcyins which exude antibacterial activity by binding to the ?- subunit of RNA polymerase inhibiting transcription (Fair and Tor, 2014, Campbell et al., 2001, Hartmann et al., 1967). Unfortunately, due to the misuse and inappropriate use of antibiotics, rapid emergence of resistant bacteria is occurring worldwide, endangering the efficacy of antibiotics, (Ventola, 2015, Rani et al., 2017, Llor and Bjerrum, 2014). From the microbiological point of view, bacterial resistance can be defined as the intransigence mechanism in a strain that reduces its susceptibility compared to wild type strains within that species against antibiotics (Cantón et al., 2013). Therefore, the effectiveness of antibiotics is slowly diminishing as more bacteria are evolving to be resistant, hence the need for alternative antimicrobial strategies such as the use of natural products which includes turmeric, ginger and honey (Rani et al., 2017). For example, curcumin in turmeric have been found to suppress the cytokinesis of B. subtilis through the induction of filamentation. According to Moghadamtousi et al. (2014) , the study on B. subtilis and E. coli demonstrated that curcumin inhibitory effect against FtsZ polymerization could suppress the FtsZ assembly leading to disruption of prokaryotic cell division. FtsZ is the building block in prokaryote that builds up the microtubule cytoskeleton which self-assembles into a membrane-associated ring structure early in the division process (Margolin, 2005). Honey is a viscous golden sugar concentrated solution that is derived from nectar of flowers gathered and modified by the honeybee, Apis mellifera (Yaghoobi et al., 2013, Mandal and Mandal, 2011). The components of honey are mainly monosaccharide and oligosaccharides carbohydrates (Vallianou et al., 2014), making up 82.4% of the solution of honey (Almasaudi et al., 2016) while other components include amino acids, phenolic compounds, and other substances (Allen et al., 1991, Carter et al., 2016).Honey is hygroscopic (Simon et al., 2009) which means it draws moisture from the environment causing the microbes to dehydrate unlike antibiotics that either attack the cell wall of the bacteria killing it (bactericidal) or stopping the growth of microbes (bacteriostatic) by inhibiting metabolic pathways (Kohanski et al., 2010). The functionality or properties of honey was described by (Albietz and Schmid, 2017, Simon et al., 2009, Molan, 1999) to reduce oedema and promote epithelisation.  Carter et al. (2016) established that asides the hygroscopic feature of honey, its high concentration of sugar and low pH level causes growth inhibition of microbes. Still, the sugar content of honey alone is not the only explanation for the antimicrobial properties of honey but the synergism of various factors which includes low water content, high sugar content, low acidity, production of hydrogen peroxide by the enzyme glucose oxidase and phytochemicals (Bang et al., 2003, Henriques et al., 2010). Research shows that in some flowering plants (Leptospermum species), non- peroxide antimicrobial activity is not destroyed by catalase present in body fluids and is unaffected by gamma irradiation than other plants in which their antimicrobial activity is associated with the levels of hydrogen peroxide produced (Allen et al., 1991, Irish et al., 2011). The mechanism of honey is unknown (Simon et al., 2009); however, one way honey is believed to work is through stimulating an inflammatory response in leukocytes (Tonks et al., 2001, Tonks et al., 2003) as cascade of cellular events, propagate the production of growth factors which controls proliferation of fibroblasts, epithelial cells and angiogenesis are triggered by inflammation (Tonks et al., 2001, Tonks et al., 2003, Majtan et al., 2010). In addition, a component in Manuka honey was discovered by Tonks et al. (2007) and it was proposed that this 5.8kDA component stimulates the production of TNF-? in monocytes through toll-like receptor 4 (Tonks et al., 2007, Majtan et al., 2010). A study conducted by Majtan et al. (2010) demonstrated that honey has the ability to express certain cytokines, like TNF-?, IL-1?  and TGF-?  and MMP-9  mRNA in human keratinocytes which supports the claim of honey can speed up wound healing. 

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