|Year : 2017 | Volume
| Issue : 5 | Page : 492-496
Ecthyma gangrenosum like lesions in disseminated mycobacterial tuberculosis infection in a renal transplant recipient
Navjyot Kaur, Aditya Vikram Pachisia, Puneet Saxena, VK Sashindran, Pankaj Puri
Department of Medicine, Armed Forces Medical College, Pune, Maharashtra, India
|Date of Submission||24-Oct-2016|
|Date of Acceptance||27-Dec-2017|
|Date of Web Publication||14-Nov-2017|
Department of Medicine, Armed Forces Medical College, Sholapur Road, Pune - 410 040, Maharashtra
Source of Support: None, Conflict of Interest: None
Ecthyma gangrenosum (EG) is a relatively rare skin manifestation that is most commonly described in Pseudomonas aeruginosa bacteremia. It is more frequently seen in immunocompromised individuals. We report a case of 60-year-old renal transplant recipient on triple immunosuppressants and diabetes mellitus type 2 on insulin therapy who developed EG-like lesions due to disseminated mycobacterial tuberculosis (MTB) infection. To the best of our knowledge, this is the first case report of EG-like lesions associated with disseminated kochs.
Keywords: Disseminated mycobacterial tuberculosis infection, ecthyma gangrenosum-like lesion, immunocompromised
|How to cite this article:|
Kaur N, Pachisia AV, Saxena P, Sashindran V K, Puri P. Ecthyma gangrenosum like lesions in disseminated mycobacterial tuberculosis infection in a renal transplant recipient. Med J DY Patil Univ 2017;10:492-6
| Introduction|| |
The term ecthyma gangrenosum (EG) is often used synonymous with severe bacteremia due to Pseudomonas aeruginosa ough it has also been reported with other organisms such as Klebsiella, Burkholderia cepacia, Morganella morganii, Escherichia More Details coli, other Pseudomonas species, Staphylococcus aureus, Candida albicans, Mucor, Aspergillus fumigatus, and herpes simplex virus.,,,, EG due to P. aeruginosa has been reported in previously healthy pediatric patients also. Techatawepisarn et al. reported EG-like lesion in a case of disseminated nontuberculous mycobacterial infection in an immunocompromised individual. A typical EG lesion consists of a black necrotic center surrounded by an erythematous halo. These lesions occur more commonly in patients with immunocompromised state including those on immunosuppressive therapy and diabetes mellitus. Immunocompromised state favors the invasion of microorganisms into the media and adventitia of subcutaneous vasculature, precipitating a hemorrhagic occlusive vasculitis leading to ischemic necrosis.
| Case Report|| |
Our patient was a 60-year-old male, 3 months postrenal transplant on triple immunosuppressive therapy (tablet tacrolimus 2 mg BD, tablet MMF 500 mg BD, and tablet prednisolone 40 mg - drug [OD]) and a case of diabetes mellitus Type 2 on insulin therapy. He presented with fever, productive cough, cervical lymphadenopathy, and multiple blackish cutaneous lesions of 2 weeks duration. Before admission to our center, he was being managed at some other tertiary care center where he was administered meropenem, teicoplanin, and amikacin for 14 days. He was documented to have left submandibular abscess which was managed with incision and drainage. The pus from abscess did not reveal any organism both on staining and culture. Despite 14 days of carbapenems, aminoglycosides, and teicoplanin, the patient continued to have a high-grade intermittent fever, productive cough, and fresh crops of black-colored skin lesions. The skin lesions started behind the left ear [Figure 1]; over the next few days, he developed multiple similar lesions on his back and lower limbs [Figure 2], [Figure 3], [Figure 4]. These lesions started as macule; over next 12–24 h became papulovesicular, and finally, the center of the lesion turned into black eschar. Examination of the patient at our center revealed a body temperature of 101°F, tachycardia with a pulse rate of 116 beats per minute, and pallor. There was a surgical wound at Lt submandibular region (postincision and drainage) with some pus discharge. He had multiple skin lesions, which were characteristically punctate, well-circumscribed plaques with black, necrotic center, and erythematous margins suggestive of EG. New crops of such lesions continued to appear on a daily basis over the next few days. Respiratory system examination revealed bronchial breath sounds at the right infrascapular region.
Investigations showed a hemoglobin of 10.1 g/dL, a white blood cell count of 29,700/mm 3 with a differential count of 90% polymorphs and 10% lymphocytes, and a platelet count of 153,000/mm 3. C-reactive protein level was 18.50 mg/dL (normal: <5.00 mg/dL). Renal function tests revealed a urea level of 125 mg/dL (normal: <40 mg/dL) and a creatinine level of 2.4 mg/dL (normal: <1.00 mg/dL), electrolytes were within normal limits (Na: 135 meq/L [normal: 135–145 meq/L], K: 4.9 meq/L [normal: 3.5–5.5 meq/L], Ca: 9.5 mg/dL [normal: 8–10 mg/dL], P: 4.0 mg/dL [normal: 2.5–4.5 mg/dL]). Liver function tests and clotting parameters were normal. An evaluation for the presence of HIV, hepatitis B, and hepatitis C infection was negative and repeated blood cultures (pyogenic, mycobacterial, and fungal) and urine cultures were sterile. Chest X-ray revealed dense near homogeneous opacity involving right middle and lower zones [Figure 5]. High-resolution computed tomography chest showed segmental consolidation of superior segment of right lower lobe, with multiple areas of patchy consolidations, bronchial cuffing, and surrounding ground glass opacities in the anterior segment of right upper lobe, anterior and superior lingular segment of left upper lobe, right middle lobe, and basal segments of both lower lobes suggestive of active pulmonary kochs [Figure 6]. Multiple enlarged lymph nodes were also noted in the right paratracheal, pretracheal, subcarinal, and left tracheobronchial stations. Pus swab from left submandibular abscess was sent for gram, Ziehl–Neelsen (ZN) and KOH stain and for pyogenic, mycobacterial (both Lowenstein-Jensen [LJ] and mycobacterial growth indicator tube (MGIT)], and fungal cultures. Gram and KOH stain did not reveal any organism; however, acid-fast bacilli (AFB) were seen on ZN stain with a Revised National Tuberculosis Control Program (RNTCP) grading of + 3 which was confirmed by growth of Mycobacterium tuberculosis (MTB) on MGIT and LJ medium. The pyogenic culture showed no growth. Four plus AFB was reported on sputum sample sent for ZN stain [Figure 7] and the growth of MTB on MGIT confirmed the presence of active MTB infection. Line probe assay showed MTB in both pus and sputum sensitive to isoniazid and resistant to rifampicin. The skin biopsy from the site of EG-like lesion revealed neutrophilic vasculitis [Figure 8]. There was perivascular mixed inflammatory infiltrate composed of lymphocytes, plasma cells, and eosinophils in the dermis; neutrophils were seen transmigrating across the capillary wall and there were no granulomas, AFB, or any fungal element. The cultures (pyogenic, mycobacterial, and fungal) from skin specimen were sterile.
|Figure 5: Chest X-ray showing dense near homogeneous opacity involving right middle and lower zones|
Click here to view
|Figure 6: High-resolution computed tomography chest - lung window showing patchy multifocal air space consolidation|
Click here to view
|Figure 8: Skin biopsy from the site of ecthyma gangrenosum-like lesion showing neutrophilic vasculitis|
Click here to view
Management: While the patient was being evaluated, he was continued to carbapenem, teicoplanin, and amikacin for 7 more days (total of 21 days). With the availability of report of presence of MTB in pus and sputum samples, the patient was started on treatment with antitubercular (ATT) drugs: tablet isoniazid 300 mg OD, tablet pyrazinamide 1500 mg, tablet ethambutol 1000 mg, tablet levofloxacin 500 mg, and injection kanamycin 500 mg every 48 hourly along with tablet pyridoxine 50 mg OD. His tacrolimus level was 3.27 μg/L (normal: 5–10 μg/L at 1–3 months of renal transplant); therefore, he was continued on immunosuppressive therapy and was given subcutaneous insulin for blood sugar control. Over the next 4 days, fever subsided and cough improved, and there were no fresh crops of skin lesions. During subsequent reviews and outpatient department visits, all his constitutional symptoms resolved, skin lesions regressed, [Figure 9] and serum creatinine reduced to 1.3 mg/dL. The monthly sputum samples for 5 months have come negative for MTB. The plan is to give intensive phase for 6 months and continuation phase for 12 months (as per RNTCP guidelines for management of multidrug-resistant and rifampicin-resistant MTB).
| Discussion|| |
Tuberculosis is endemic in developing countries and is reemerging in the industrialized world. With the increasing incidence of immunocompromised patients, unusual presentations of tuberculosis including cutaneous TB may be observed more often. Although many type of skin lesions are reported in MTB infection such as tuberculosis chancre, lupus vulgaris, scrofuloderma, tuberculosis verrucosa cutis, and erythema nodosum, EG and EG-like lesions have never been reported. The lesion of EG starts as a painless round macule which evolves into an edematous papule, and subsequently, this papule becomes erythematous forming hemorrhagic bulla or pustule. The lesion finally turns into necrotic ulcer characterized by a black eschar with a surrounding erythematous halo. The lesion of EG may be present in a patient at any stage of development. The EG occurs because of skin necrosis secondary to vascular occlusion. Most of the times, the microexamination of skin biopsy is seen teaming with the organism responsible for EG. However, in some cases, the organism is demonstrated only on culture of skin biopsy.
In our case, skin lesions were well circumscribed with necrotic base. Clinically, the skin lesions could be safely classified as EG. The skin biopsy revealed normal epidermis with perivascular mixed inflammatory infiltrate composed of lymphocytes, plasma cells, and eosinophils in the dermis; neutrophils were seen transmigrating across the capillary wall, and there were no granuloma, AFB, or any fungal element nor did the cultures grew any organism. Hence, our impression was vasculitis leading to vascular occlusion and skin infarction, but we did not find any organism in these lesions. The patient was administered 21 days of carbapenems, teicoplanin, and aminoglycosides. However, he failed to respond and continued to have a high-grade intermittent fever and new crops of skin lesions. He improved only when he was started on ATT, and skin lesions also disappeared which made us believe that these EG-like lesions were indeed because of disseminated Kochs. Vaiman et al. in 2015 accepted a broader definition of EG emphasizing the fact that EG can occur because of diverse microorganisms and not only because of Pseudomonas. We called the skin lesions in our patient as EG-like lesions and not classical EG because of the fact that we could not demonstrate the organism in the skin biopsy lesion. At present, our patient is on 6th month of treatment, and he has gained weight (10 kg) and is asymptomatic on triple immunosuppression and insulin. His creatinine has settled down to 1.2 mg/dL.
Purpose of reporting: A rare skin manifestation of disseminated Kochs in an immunocompromised individual. To the best of our knowledge, EG-like lesions have never been reported earlier in disseminated MTB infection.
Written informed consent has been taken from the patient for writing this case.
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
Conflicts of interest
There are no conflicts of interest.
| References|| |
Aygencel G, Dizbay M, Sahin G. Burkholderia cepacia
as a cause of ecthyma gangrenosum-like lesion. Infection 2008;36:271-3.
Del Pozo J, García-Silva J, Almagro M, Martínez W, Nicolas R, Fonseca E. Ecthyma gangrenosum-like eruption associated with Morganella morganii
infection. Br J Dermatol 1998;139:520-1.
Sen H, Inangil G, Sahin L, Dere K, Ozkan S, Dagli G. Ecthyma-gangrenosum-like lesions associated with methicillin-resistant Staphylococcus aureus
infection. Int J Infect Dis 2009;13:173-5.
Leslie KS, McCann BG, Levell NJ. Candidal ecthyma gangrenosum in a patient with malnutrition. Br J Dermatol 2005;153:847-8.
Kimyai-Asadi A, Tausk FA, Nousari HC. Ecthyma secondary to herpes simplex virus infection. Clin Infect Dis 1999;29:454-5.
Bucak IH, Tümgör G, Mengen E, Temiz F, Turgut M. Ecthyma gangrenosum in a previously healthy pediatric patient and associated facial paralysis and persistent hyperplastic primary vitreous. Am J Case Rep 2012;13:250-3.
Techatawepisarn T, Chiewchanvit S, Salee P, Mahanupab P, Baosoung V, Praparattanapan J. Ecthyma gangrenosum-like lesions associated with disseminated nontuberculous mycobacterial infection in an HIV-infected patient. Southeast Asian J Trop Med Public Health 2013;44:649-54.
Weber DJ, Cohen MS, Rutala WA. The acutely ill patient with fever and rash. In: Mandell GL, Bennett JE, Dolin R, editors. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 6th
ed. Philadelphia: Elsevier; 2005. p. 730-42.
Greene SL, Su WP, Muller SA. Ecthyma gangrenosum: Report of clinical, histopathologic, and bacteriologic aspects of eight cases. J Am Acad Dermatol 1984;11(5 Pt 1):781-7.
Bravo FG, Gotuzzo E. Cutaneous tuberculosis. Clin Dermatol 2007;25:173-80.
Zomorrodi A, Wald ER. Ecthyma gangrenosum: Considerations in a previously healthy child. Pediatr Infect Dis J 2002;21:1161-4.
Weiel JJ, Zhang CZ, Smith JA, Wang W, DuPont J, Lian F. Clinicopathologic aspects of ecthyma gangrenosum in pediatric patients: A case series and review of the literature. J Clin Anat Pathol 2013;1:1-5.
Vaiman M, Lasarovitch T, Heller L, Lotan G. Ecthyma gangrenosum versus ecthyma-like lesions: Should we separate these conditions? Acta Dermatovenerol Alp Pannonica Adriat 2015;24:69-72.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]