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| CASE REPORT |
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| Year : 2018 | Volume
: 7
| Issue : 4 | Page : 301-304 |
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Methicillin-resistant Staphylococcus aureus, Cytomegalovirus, and mucosal Candida albicans coinfection in a postrenal transplant recipient
Nupur Pal, Kalidas Rit, Munmun Sarkar
Department of Microbiology, Institute of Post-Graduate Medical Education and Research, Kolkata, West Bengal, India
| Date of Web Publication | 10-Jan-2019 |
Correspondence Address:
Dr. Kalidas Rit
Department of Microbiology, Institute of Post-Graduate Medical Education and Research, Kolkata, West Bengal
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/JDRNTRUHS.JDRNTRUHS_152_15
Here, we report a rare case of methicillin-resistant Staphylococcus aureus (MRSA), Cytomegalovirus (CMV), and mucosal Candida albicans coinfection in a post-renal transplant recipient. The patient presented with a cheek ulcer with nasal swelling after 2 months of immunosuppressive therapy following renal transplantation. Microbiological investigations revealed MRSA and C. albicans from the respective lesions and polymerase chain reaction for CMV from blood sample was positive. The patient was subsequently treated with appropriate regimen and is on regular follow-up.
Keywords: Candida albicans, CMV, MRSA, renal transplant recipient
How to cite this article:
Pal N, Rit K, Sarkar M. Methicillin-resistant Staphylococcus aureus, Cytomegalovirus, and mucosal Candida albicans coinfection in a postrenal transplant recipient. J NTR Univ Health Sci 2018;7:301-4 |
How to cite this URL:
Pal N, Rit K, Sarkar M. Methicillin-resistant Staphylococcus aureus, Cytomegalovirus, and mucosal Candida albicans coinfection in a postrenal transplant recipient. J NTR Univ Health Sci [serial online] 2018 [cited 2023 Mar 22];7:301-4. Available from: https://www.jdrntruhs.org/text.asp?2018/7/4/301/249823 |
| Introduction | |  |
Infection is an important problem following renal transplantation. Because of immunosuppressive therapy, there are increasing chances of developing infections.[1] Fungal infections are responsible for 5% of all infections in renal transplant recipients.[2] Disseminated fungal infections remain the major cause of death in those individuals. The incidence varies according to the regions involved. Cytomegalovirus (CMV) infection is common after receiving transplantation, and often precipitates the patients to secondary infections due to fungal and bacterial cause.[3] Bacterial infections occur in 47% kidney transplant recipients and usually manifests as urinary tract infections.[4] Here, we report a rare case of combined infections manifested as nasal mucosal candidiasis, ulcer over right cheek by methicillin-resistant Staphylococcus aureus (MRSA), and Cytomegalovirus (CMV) viremia in a post-transplant recipient.
| Case Report | | |
A 27-year-old male patient underwent renal transplantation in May 2015 from a living haploid- identical donor (his brother). He was on tacrolimus (10 mg/day), prednisolone (15 mg/day), and azathioprine (50 mg/day). The patient was readmitted after 2 months of transplantation with complaints of an ulcer at the right lower side of the cheek [Figure 1] of 15–20 days duration. The ulcer was confined to the skin with involvement of subcutaneous tissue. The oral mucosa adjacent to the ulcer was intact. It was associated with redness and swelling of the nose with low-grade fever and occasional serosanguinous discharge [Figure 2]. Blood examination revealed fasting blood sugar level of 110 mg/dl, Hb 9.38 g%, total count 4,900 with neutrophil 80%, lymphocyte 17%, and serum creatinine 2.5 mg/dl. In view of graft dysfunction (serum creatinine: 2.5 mg/dl), graft biopsy was done which showed interstitial fibrosis and tubular atrophy. Serosanguinous discharge was aseptically collected from the base of the ulcer and sent to the microbiology laboratory for bacterial and fungal culture as well as sensitivity testing. Pus was also collected from the nose and subjected to bacteriological and mycological investigations. Intravenous empirical broad-spectrum antibiotic therapy was started, pending further report. Consecutive three cultures of collected pus samples from the cheek ulcer showed growth of MRSA [Figure 3], which was sensitive to vancomycin, linezolid, teicoplanin, and clindamycin. Pus from the nose showed budding yeast on direct microscopy and growth of Candida was observed on Sabouraud dextrose agar (SDA) after 48 hours of incubation which was identified as C. albicans by positive germ tube test [Figure 4] and chlamydospore formation in cornmeal agar. Repeated cultures (more than three times) from the pus of the nose showed similar findings. Repeated isolation of these pathogens from affected sites confirmed the causal association of them with the disease. Polymerase chain reaction for CMV DNA was positive in patient's blood sample and intravenous ganciclovir (GCV) 250 mg/day was started. He was started on oral itraconazole (ITR) 200 mg/day along with linezolid 600 mg twice daily. His cheek and nose lesions gradually dried up after 2 weeks of therapy [Figure 5]. The patient was initiated on hemodialysis and is on regular follow-up. | Figure 3: Characteristic growth of methicillin-resistant Staphylococcus aureus
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 | Figure 4: Microscopic view of germ tube formation suggestive of Candida albicans
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| Discussion | | |
Here, we reported a case of mucosal candidiasis associated with MRSA and CMV infections in a post-renal transplant recipient. To our knowledge, this is the first reported case of simultaneous co-infections of these three organisms in the eastern region of the country. The incidence of fungal infection of recipients of solid organ varies 6–10% with a mortality rate of 70–100% in the Indian subcontinent.[4] Risk factors for fungal infections in transplant recipients include urgent transplantation, preoperative high doses of steroids, and broad-spectrum antibiotics, high creatinine level, length of transplantation operation, and associated coinfections.[5],[6] Risks of acquiring fungal infections are much more in developing countries in comparison to developed world because of higher degree of immunosuppression, delayed diagnosis, and treatment with associated overcrowded unsanitary environmental conditions.[6] Candida, Aspergillus, Zygomycosis (Mucor), Cryptococcus species, and Pneumocystis carinii, and the geographically restricted mycoses (Coccidioidomycosis, Histoplasmosis, etc.) are the major offending fungal pathogens that infect renal transplant recipients presenting as either reactive or newly acquired disease.[1] The manifestations of fungal infections in renal transplant recipients are usually nonspecific. As many of the fungal infections are diagnosed only after autopsy, the clinician must be highly cautious for this type of infections.[7] An extensive diagnostic approach including batteries of tests need to be done to clinch a proper diagnosis.
CMV is one of the most common infections encountered in renal transplant recipients (30–50%). It belongs to beta herpes virus group and is widely distributed in the community. CMV may cause primary or secondary latent reactivation infection after transplantation, but later is more common. Use of corticosteroids alone can cause reactivation of latent CMV infection, with the use of triple or quadruple immunosuppressive therapy CMV infections are more frequent.[8] Those at the highest risk of getting infection include CMV seronegative recipients of CMV seropositive donor kidneys. Reactivation disease in a seropositive recipient is generally less severe clinically, and superinfection is generally rare. The most frequent clinical presentation for CMV is fever, malaise, and leucopenia. In the severe form of disease, there may be life-threatening retinitis or disseminated systemic involvement such as pulmonary, gastrointestinal, or hematological. In these situations, treatment with intravenous ganciclovir is usually needed. CMV infection can often lead to significant immunosuppression, thereby secondary opportunistic infections may occur as in our case.
Patients waiting for transplantation may be colonized with MRSA, vancomycin-resistant Enterococcus, Clostridium defficile, multidrug-resistant gram negative bacteria, and other fungal agents such as Aspergillus species.[9] After transplantation, these agents may cause various types of infections. Similarly, in our case, MRSA strain may colonize the patient before transplantation and manifestations occur thereafter.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Fishman JA, Rubin RH. Infection in organ-transplant recipients. N Engl J Med 1998;338:1741-51.  |
| 2. | Paya C. Fungal infections in solid organ transplantation. Clin Infect Dis 1993;16:677-88. |
| 3. | Rubin RH. Cytomegalovirus in solid organ transplantation. Transpl Infect Dis 2001;3(Suppl 2):1. |
| 4. | Sia IG, Paya CV. Infectious complications following renal transplantation. Surg Clin North Am 1998;78:95-112. |
| 5. | Alangaden GJ, Thyagarajan R, Gruber SA. Infectious complications after kidney transplantation: Current epidemiology and associated risk factors. Clin Transplant 2006;20:401-9. |
| 6. | Brayman KL, Stephanian E, Matas AJ, Schmidt W, Payne WD, Sutherland DE, et al. Analysis of complications occurring after solid-organ transplantation. Arch Surg 1992;127:38-47. |
| 7. | Rubin RH. Infectious disease complications of renal transplantation. Kidney Int 1993;44:221-36. |
| 8. | Avery RK. Prophylactic strategies before solid-organ transplantation. Curr Opin Infect Dis 2004;17:353-6. |
| 9. | Date A, Vaska K, Vaska PH, Pandey AP, Kirubakaran MG, Shastry JC. Terminal infections in renal transplant patients in a tropical environment. Nephron 1982;32:253-7. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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