|Year : 2017 | Volume
| Issue : 1 | Page : 14-17
Methicillin-resistant Staphylococcus aureus in community-acquired pyoderma in children in South India
Umashankar Nagaraju, Belliappa Pemmanda Raju
Department of Dermatology, Venereology and Leprosy, Rajarajeswari Medical College and Hospital, Bengaluru, Karnataka, India
|Date of Web Publication||12-Dec-2016|
Belliappa Pemmanda Raju
Department of Dermatology, Venereology and Leprosy, Rajarajeswari Medical College and Hospital, Kambipura, Mysore Road, Bengaluru - 560 074, Karnataka
Source of Support: None, Conflict of Interest: None
Background: Emergence of methicillin-resistant Staphylococcus aureus (MRSA) infections among previously healthy persons in community settings (without exposure to healthcare facilities) has been noted recently. Limited studies have been carried out from India in an exclusive pediatric population on MRSA in community-acquired pyoderma.
Aims: The objective of this study was to evaluate different types of primary pyoderma in children caused by S. aureus and to determine the incidence of MRSA in community-acquired primary pyoderma in children.
Materials and Methods: Children aged ≤ 16 years with pyoderma caused by S. aureus who attended camps conducted in schools around Bengaluru were inducted. They were evaluated for a variety of skin infections which were cultured and analyzed for antimicrobial susceptibilities. Swabs from the anterior nares were also collected from each patient.
Results: Of the total 372 children with pyoderma caused by S. aureus studied, 232 were boys and 140 were girls. Impetigo contagiosum (47%) was the most common form of pyoderma, followed by ecthyma (19.9%) and folliculitis (18.5%). The most common site involved was face in 48.4% patients, followed by legs in 32.5% patients. MRSA was isolated in 6.5% patients. Nasal colonization with S. aureus was observed in 59.7% patients.
Conclusion: MRSA in community-acquired pyoderma in children was 6.5% and nasal colonization with S. aureus was 59.7% in our study. High resistance to commonly used antimicrobials in methicillin-sensitive S. aureus was also observed. Judicious use of antimicrobials is essential to control the emergence and spread of antimicrobial resistance.
Keywords: Community-acquired pyoderma, methicillin-resistant Staphylococcus aureus, nasal colonization
|How to cite this article:|
Nagaraju U, Raju BP. Methicillin-resistant Staphylococcus aureus in community-acquired pyoderma in children in South India. Indian J Paediatr Dermatol 2017;18:14-7
|How to cite this URL:|
Nagaraju U, Raju BP. Methicillin-resistant Staphylococcus aureus in community-acquired pyoderma in children in South India. Indian J Paediatr Dermatol [serial online] 2017 [cited 2020 Aug 11];18:14-7. Available from: http://www.ijpd.in/text.asp?2017/18/1/14/188425
| Introduction|| |
Pyodermas in children constitute one of the most common cutaneous diseases. Primary pyodermas include impetigo, folliculitis, furuncle, carbuncle, ecthyma, erythrasma, and sycosis barbae. Changing trends are being noted in the etiological aspects of primary pyoderma, and the problem of emergence of drug resistance strains is an ever increasing one. Most common organism usually isolated in pyoderma is Staphylococcus aureus, which may be either methicillin-sensitive S. aureus (MSSA) or methicillin-resistant S. aureus (MRSA). For approximately three decades until the late 1980s, MRSA remained a predominantly nosocomial infection. Since the 1990s, however, new strains of community-acquired methicilllin-resistant Staphyloccus aureus (CA-MRSA) caused infections in previously healthy people with varied prevalence. Therefore, MRSA infections are now classified as healthcare-associated MRSA infections and community-associated MRSA (CA-MRSA) infections. Community-acquired MRSA (CA-MRSA) infections are increasing as a clinical problem worldwide, with skin and soft-tissue infections being the most common manifestations.,, Knowledge of prevalence of CA-MRSA and their current antimicrobial profile becomes necessary in the selection of appropriate empirical treatment of these infections. Limited studies have been carried out from India in an exclusive pediatric population on CA-MRSA pyoderma. The present study was carried out to evaluate different types of primary pyoderma in children caused by S. aureus and to study the incidence of MRSA in community-acquired primary pyoderma in children.
| Materials and Methods|| |
Three hundred and seventy-two children aged ≤16 years with primary pyoderma caused by S. aureus who attended camps conducted in schools around Bengaluru, South India, were included in the study. Inclusion criteria were positive bacterial culture, history of being untreated during the past 1 month, and nonhospitalization during the preceding year. The patients were evaluated for a variety of skin infections which were cultured and analyzed for antimicrobial susceptibilities. After clinical examination, pus was collected after cleaning the wounds with normal saline using a sterile cotton swab. Swabs from the anterior nares were also collected from each patient.
Clinical samples were processed within 1 h after collection. Gram staining was performed with all samples to determine the likely organisms present. The samples were inoculated on blood agar and MacConkey agar. The inoculated plates were incubated at 37°C for 24–48 h and the bacterial isolates were identified using a standard procedure.S. aureus was identified on the basis of colony morphology, Gram stain, catalase test, slide and tube coagulase test, and modified Hugh Leifson's oxidation fermentation test.
Antimicrobial sensitivity testing was performed on all S. aureus isolates using the Kirby–Bauer disk diffusion method. S. aureus ATCC 25923 was used as control. All S. aureus isolates were also tested for methicillin resistance by oxacillin agar screen. The minimum inhibitory concentration (MIC) of oxacillin was determined using agar dilution.S. aureus ATCC 29213 was used as control.
| Results|| |
A total of 372 patients of primary pyoderma caused by S. aureus were included in the study. The age group varied from 5 to 16 years. The male: female ratio was 1.6:1 (n = 232 boys, n = 140 girls). Mean duration of lesions was 6.2 days.
Impetigo contagiosum was the most common form of pyoderma, followed by ecthyma and folliculitis [Table 1]. The most common site involved was face in 180 (48.4%) patients, followed by legs in 121 (32.5%) patients. S. aureus was isolated as single organism in 346 patients, whereas polybacterial infection was observed in 26 cases [Table 2].
As per the antibiogram of isolates from pyoderma [Table 3], the highest resistance was shown to penicillin followed by erythromycin and co-trimoxazole. All isolates were susceptible to vancomycin. Multidrug-resistant (MDR; resistant to three or more drugs tested)S. aureus was observed in 52 (13.98%) patients. MRSA was isolated in 24 (6.5%) patients from pyoderma. All MRSA isolates had an MIC of oxacillin of ≥ 4 µg/mL. Antimicrobial susceptibility testing was quality controlled using S. aureus ATCC 25923 and ATCC 29213. Nasal colonization with S. aureus was observed in 222 (59.7%) patients. As per the antibiogram of isolates from anterior nares [Table 4], all isolates were susceptible to vancomycin and highest resistance was shown to penicillin followed by erythromycin and co-trimoxazole. MRSA was present in 17 (7.7%) isolates from anterior nares. S. aureus isolated from pus and the anterior nares had a similar antibiogram in 89 (40.1%) patients.
|Table 4: Antibiotic resistance of Staphylococcus aureus isolated from anterior nares|
Click here to view
| Discussion|| |
Methicillin, the first β-lactamase stable semi-synthetic penicillin, was introduced in 1960. MRSA was detected soon after methicillin came into clinical use in 1961. Mucin appears to be the critical surface that is colonized in a process involving interactions between staphylococcal protein and mucin carbohydrate. Cases of community-acquired infections caused by MRSA were reported in the early 1980s. The epidemiology of MRSA has changed since its appearance more than 30 years ago. In contrast to nosocomial-acquired (MRSA) infections, CA-MRSA infections (a) often occur in individuals who are immunocompetent without MRSA-associated risk factors, (b) tend to be susceptible to most non-β-lactam antibiotics, (c) can be virulent and fatal, and (d) have a Type IV staphylococcal cassette chromosome (SCCmec) genetic element (which carries mec A, the methicillin resistance gene) that is distinct from Types I, II, and III SCCmec elements, which are associated with hospital-acquired MRSA infections.,, In addition, CA-MRSA has the pvl gene, a virulence gene encoding a leukocyte-killing toxin, Panton–Valentine leukocidin. The rate of MRSA varies in different populations studied, ranging from 1% to 74%., A study from India revealed a rate of 11.8% of CA-MRSA from a general population study group.
A recent study from North India reported the rate of MRSA in community-acquired pyoderma in children as 6.9%. In this study, the rate of MRSA in community-acquired pyoderma in children was 6.5% which is comparable with published data. The present study clearly shows that MRSA has become a significant community pathogen in and around Bengaluru, South India. The incidence of MRSA can change depending on the usage of antimicrobials. The changing epidemiology of MRSA in the community is likely to be due to the movement of nosocomial strains into the community or the appearance of drug-resistant strains due to gene transfer from resistant to sensitive bacteria.
We observed a high rate of resistance to commonly used antimicrobials, such as penicillin, erythromycin, and co-trimoxazole even in MSSA isolates. Similar findings of high resistance to commonly used antimicrobials in MSSA isolates has been reported from North India by Sardana et al. MDR S. aureus was observed in 13.98% patients, which is similar to another study which reported it to be 16.9%. Antimicrobial resistance is an unavoidable consequence of the selective pressure of antimicrobial exposure. Indiscriminate use and over-counter availability of different antibiotics may be the reason for such a high resistance in these MSSA isolates. Infection with drug-resistant bacteria is favored by drug abuse, underlying illness, and previous hospitalization and antimicrobial treatment.
S. aureus carriage is an important risk factor for infection, and colonizing strains are often similar to those isolated from infected tissue. The prevalence of nasal colonization of S. aureus in healthy children aged 5–15 years in urban, rural, and semi-urban slums of North India has been reported to be 52.3%, and resistance of these nasal isolates to common antibiotics was low. In the present study, nasal colonization with S. aureus was observed in 59.7% of patients, and a similar antibiogram from isolates of pus and the anterior nares was seen in 40.1% of patients. A study from India on MRSA in community-acquired pyoderma from a general population group reported nasal colonization in 54.4% of patients and similar antibiogram in 49% of patients.
Treatment of carriers may help to prevent endogenous infections. Timely detection permits nasal mupirocin therapy to eradicate nasal carriage and thereby control spread of MRSA, especially in high-dependency units. A correct antimicrobial policy based on the knowledge of resistance patterns of the commonly isolated organisms is mandatory to prevent unnecessary medication and further emergence of drug-resistant organisms.
More representative community-based studies are required to: (a) Assess the true prevalence of CA-MRSA in various parts of the country, (b) identify specific risk factors for CA-MRSA acquisition, and (c) target measures to prevent transmission.
| Conclusion|| |
The present study showed that the rate of MRSA in community-acquired pyoderma in children in South India was 6.5% and nasal colonization with S. aureus was observed in 59.7% of patients. We also observed high resistance to commonly used antimicrobials in MSSA isolates. Judicious use of antimicrobials is essential to control the emergence and spread of antimicrobial resistance.
Financial Support and Sponsorship
Conflicts of Interest
There are no conflicts of interest.
| References|| |
Gandhi S, Ojha AK, Ranjan KP, Neelima. Clinical and bacteriological aspects of pyoderma. N Am J Med Sci 2012;4:492-5.
Centers for Disease Control and Prevention (CDC). Community-associated methicillin-resistant Staphylococcus aureus
infections in Pacific Islanders – Hawaii, 2001-2003. MMWR Morb Mortal Wkly Rep 2004;53:767-70.
Gosbell IB. Methicillin-resistant Staphylococcus aureus
: Impact on dermatology practice. Am J Clin Dermatol 2004;5:239-59.
Iyer S, Jones DH. Community-acquired methicillin-resistant Staphylococcus aureus
skin infection: A retrospective analysis of clinical presentation and treatment of a local outbreak. J Am Acad Dermatol 2004;50:854-8.
Sardana K, Manchanda V, Rajpal M, Garg VK, Chauhan DS. Bacterial pyoderma in children and therapeutic options including management of community-acquired methicillin resistant Staphylococcus aureus
. Int J Dermatol 2007;46:309-13.
Kloos WE, Bannerman TL. Staphylococcus
. In: Murray PR, Baron JE, Pfaller AM, Tenover FC, Yolken RH. editors. Manual of Clinical Microbiology. 6th
ed. Washington, DC: American Society for Microbiology; 1995. p. 282.
Collee JG, Miks RS, Watt B. Tests for the identification of bacteria. In: Collee JG, Freser AG, Marmion BP, Simmons A. editors. Mackie and McCartney Practical Medical Microbiology. 14th
ed. New York: Churchill Livingstone; 1996. p. 131.
National Committee for Clinical Laboratory Standards. Performance Standards for Antimicrobial Disk Tests. Approved Standards M2-A4. 4th
ed. Villanova, PA: National Committee for Clinical Laboratory Standards; 1993.
Hindler JA, Jorgensen JH. Procedures in antimicrobial testing. In: Mahon CR, Manuselis G, editors. Textbook of Diagnostic Microbiology. 2nd
ed. Philadelphia: W. B. Saunders; 2000. p. 62-95.
National Committee for Clinical Laboratory Standards. Performance Standard for Antimicrobial Susceptibility Testing. NCCLS Approved Standard M100-59. Wayne, PA: National Committee for Clinical Laboratory Standards; 2003.
Bradley JM, Noone P, Townsend DE, Grubb WB. Methicillin-resistant Staphylococcus aureus
in a London hospital. Lancet 1985;1:1493-5.
Thind P, Prakash SK, Wadhwa A, Garg VK, Pati B. Bacteriological profile of community-acquired pyodermas with special reference to methicillin resistant Staphylococcus aureus
. Indian J Dermatol Venereol Leprol 2010;76:572-4.
Shuter J, Hatcher VB, Lowy FD. Staphylococcus aureus
binding to human nasal mucin. Infect Immun 1996;64:310-8.
Boyce JM, Causey WA. Increasing occurrence of methicillin-resistant Staphylococcus aureus
in the United States. Infect Control 1982;3:377-83.
Cohen PR, Grossman ME. Management of cutaneous lesions associated with an emerging epidemic: Community-acquired methicillin-resistant Staphylococcus aureus
skin infections. J Am Acad Dermatol 2004;51:132-5.
Chambers HF. Community-associated MRSA – Resistance and virulence converge. N Engl J Med 2005;352:1485-7.
Fang YH, Hsueh PR, Hu JJ, Lee PI, Chen JM, Lee CY, et al.
Community-acquired methicillin-resistant Staphylococcus aureus
in children in Northern Taiwan. J Microbiol Immunol Infect 2004;37:29-34.
Nagaraju U, Bhat G, Kuruvila M, Pai GS, Jayalakshmi, Babu RP. Methicillin-resistant Staphylococcus aureus
in community-acquired pyoderma. Int J Dermatol 2004;43:412-4.
Gardam MA. Is methicillin-resistant Staphylococcus aureus
an emerging community pathogen? A review of the literature. Can J Infect Dis 2000;11:202-11.
Cookson BD. Methicillin-resistant Staphylococcus aureus
in the community: New battlefronts, or are the battles lost? Infect Control Hosp Epidemiol 2000;21:398-403.
Kluytmans J, van Belkum A, Verbrugh H. Nasal carriage of Staphylococcus aureus
: Epidemiology, underlying mechanisms, and associated risks. Clin Microbiol Rev 1997;10:505-20.
Chatterjee SS, Ray P, Aggarwal A, Das A, Sharma M. A community-based study on nasal carriage of Staphylococcus aureus
. Indian J Med Res 2009;130:742-8.
[Table 1], [Table 2], [Table 3], [Table 4]