resistant bacteria had a 9-fold (OR 9.83%) risk for
resistance to at least 4 β-lactam and non-β-lactam
antibiotics (erythromycin, tetracycline,
chloramphenicol, gentamicin, ofloxacin, or
trimethoprim-sulfamethoxazole). (Cadilla, 2013)
Fusidic acid has a unique and very different
chemical structure. The carbon chains in the chemical
structure of fusidic acid are similar to steroids than
antibiotics so rarely cause cross-resistance
10
. The in
vitro efficacy of antibiotics is more significant if
proven to be in vivo. In vitro sensitivity is not entirely
predictable for in vivo effect. In addition, in vitro
resistance is common, but not necessarily related to
treatment failure
(McNeil,2014)
5 CONCLUSION
The results of this study showed that there has been
in vitro resistance of S. aureus and S. pyogenes to
mupirocin. In addition, S. aureus and S. pyogenes are
more susceptible to fusidic acid than mupirocin. In
vitro effectivity of fusidic acid was better than
mupirocin. The emergence of resistance in this study
is influenced by various factors, especially the use of
antibiotics that causes cross resistance between
bacterial carrier resistant genes.
ACKNOWLEDGEMENTS
The authors would like to thank Dr. dr. M.
Zulkarnain, ScPKK and dr. Lisa Dewi, M. KEs who
assist in the effort of this research. The authors also
would like to Department of Dermatology and
Venereology, and Faculty of Medicine of Sriwijaya
University.
REFERENCES
Antonov NK, Garzon MC, Morel KD, Whittier S, Planet
PJ, Lauren CT. 2015. High prevalence of mupirocin
resistance in Staphylococcus aureus isolates from a
pediatric population. AAC; 59(6): 3350-56.
Cadilla A, David MZ, Daum RS, Vavra SB. 2011.
Methicillin-resistant of high-level mupirocin resistance
and Multidrug-resistant Staphylococcus aureus at an
Academic Center in the Midwestern United States. J
Clin Microbiol; 49(1): p. 95-100.
Caft N. 2012. Superficial cutaneous infections and
pyodermas.. In: Goldsmith LA, Katz SI, Gilchrest BA,
Paller AS, Leffell DJ, Wolff K, editors. Fitzpatrick’s
Dermatology in General Medicine. 8
th
ed. New York:
The Mc Graw-Hill Companies, Inc;. p. 2128-60.
Depari LI, Sugiri U, Ilona L. 2016. Relation between risk
factors of pyoderma and pyoderma incidence. AMJ;
3(3): 434-39.
Karimkhani C, Boyers LN, Prescott L, Weich V, Delamere
FM, Nasser MZ, et al. 2014. Global burden of skin
sisease as reflected in Cochrane database of systematic
riview. JAMA Dermatol; 150(9): 945-51.
Koning S, Van Der Sande R, Venagen AP, Van Suijlekom-
Smit LWA, Morris AD, Butler CC, et al.2012.
Intervention of Impetigo (review). Cochrane Database
Systematic Review issue 1. Amsterdam: John Wiley &
Sons.
McNeil JC, Hulten KG, Kaplan SL, Mason EO. 2014.
Decreased susceptiblities to ratapamulin, mupirocin,
and chlorhexidine among Staphylococcus aureus
isolates causing skin and soft tissue infections in
otherwise healthy children. Antimicrob Agents Chem;
58(5): 2878-83.
Milet CR, Halpern AV, Reboli AC, Heymann WR. 2012.
Bacterial diseases. In: Bolognia Jl, Jorizzo JL, Rapini
RP, Schaver JV, editors. Dermatology. 3
rd
ed.
Edinburg: Mosby; p. 1887-1220.
Mohajeri P, Ghalamine B, Rexaei M, Khamisabadi Y.
2012. Frequency of mupirocin resistant Staphylococcus
aureus strains isolated from nasal carriers in hospital
in Kermanshah. Jundisphapus J Microbiol; 5(4): 560-
63.
Nirwati H, Radiono S, Ariwibowo L, Hananta IPY, Tama
LGY, Danarti R. 2013. Sensitivity pattern of S. aureus
isolated from children with pyoderma againts various
antibiotics in Waingapu, Sumba Nusa Tenggara Timur.
In: Nirwati H, Dewi NYA. Proceeding of DAAD-
IGHEP Maternal and Child Health Summer School.
Bali: Udayana University Press; p. 195-203.
Paudel U, Parajuli S, Pokhrel DB. 2013. Clinico-
bacteriological profile and antibiotic sensitivity pattern
in pyodermas: a hospital based study. Nep J Lepr;
11(1): 49-58.
Poovelikunnel T, Gethin G, Humphreys H. 2015.
Mupirocin resistance: clinical implications and
potential alternatives for the eradication of MRSA. J
Antimicrob chem; 70: 2681-92.
Sanchez CE, Moore LSP, Husson F, Holmes AH. 2016.
What are the factors driving antimicrobial resistance?
Perspective from a public event in London, England.
BMC infec Dis; 16(465): 1-5.