- Email: [email protected]
A case of fibrocalculous pancreatic diabetes (FCPD) with pelvic and scrotal abscess caused by Candida glabrata
Indian Journal of Medical Specialities 7 (2016) 90–92
Contents lists available at ScienceDirect
Indian Journal of Medical Specialities journal homepage: www.elsevier.com/locate/injms
Case report
A case of fibrocalculous pancreatic diabetes (FCPD) with pelvic and scrotal abscess caused by Candida glabrata Shukla Das a, Rumpa Saha a, Priyamvada Roy a,*, Vivek Hada b, Iqbal Rajinder Kaur a, Gaurav Muktesh c, S.V. Madhu d a
Department of Microbiology, University College of Medical Sciences & Guru Teg Bahadur Hospital, Delhi 110095, India Department of Microbiology, All India Institute of Medical Sciences, Jodhpur 342005, India Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India d Department of Medicine, University College of Medical Sciences & Guru Teg Bahadur Hospital, Delhi 110095, India b c
A R T I C L E I N F O
A B S T R A C T
Article history: Received 18 February 2016 Received in revised form 25 May 2016 Accepted 27 May 2016 Available online 13 June 2016
Fibrocalculous pancreatic diabetes (FCPD) is a peculiar form of diabetes secondary to chronic pancreatitis and usually affects young individuals. It is mostly seen in the developing countries of the world where protein-calorie malnutrition is prevalent. FCPD has an aggressive course and may be responsible for pancreatic calculi, steatorrhoea and other complications of diabetes as well as makes the patient immunocompromised in the majority of cases. Candida glabrata is an important cause of invasive candidiasis in immunocompromised hosts. Here we report the first case of intra-abdominal and scrotal abscess caused by C. glabrata in a patient suffering from FCPD. ß 2016 Published by Elsevier, a division of Reed Elsevier India, Pvt. Ltd on behalf of Indian Journal of Medical Specialities.
Keywords: Candida glabrata Fibrocalculous pancreatic diabetes Invasive candidiasis
1. Introduction Fibrocalculous pancreatic diabetes (FCPD) is a form of diabetes secondary to tropical calcific pancreatitis usually affecting the poorer strata of society. The patients are often lean and malnourished.1 FCPD is one of the 2 subtypes of malnutrition-related diabetes mellitus (MRDM), a rare type of diabetes associated with long-term malnutrition. FCPD usually occurs below 30 years of age and is characterized by clinical evidence of malnutrition, insulinrequirement, radiological evidence of pancreatic calcification and/ or exocrine pancreatic dysfunction. The other subtype of MRDM is protein-deficient diabetes mellitus (PDDM), in which there is no clinical or radiological evidence of pancreatic dysfunction.2 Here we report the first case of intra-abdominal and scrotal abscess caused by Candida glabrata in a patient with FCPD. 2. Case report A 24-year-male from north India, a known diabetic on insulin therapy since 6 years, presented with hypoglycemia to the * Corresponding author at: C/o Group Captain Dev Dutta Roy, Flat no. C-115, Jalvayu Vihar (Near AWHO), Plot no. 8, Pocket P-4, Greater Noida 201310, Uttar Pradesh, India. E-mail addresses: [email protected] (S. Das), [email protected] (R. Saha), [email protected] (P. Roy), [email protected] (V. Hada), [email protected] (I.R. Kaur), [email protected] (G. Muktesh), [email protected] (S.V. Madhu).
emergency room of our hospital and was evaluated in the endocrine unit after correction of hypoglycemia. The patient had steatorrhea since 5 years and grayish white urethral discharge since 1 year, involuntary dribbling of urine since 1 year and high grade fever on and off since 4 months. The discharge which was distinct from urine was semisolid in consistency with a distinct offensive odor. Patient complained of involuntary passage of the white urethral discharge 7–8 times per day. The patient was anemic, emaciated and had a toxic look. His blood pressure on presentation was 101/69 mm of mercury with a pulse rate of 152/min. The body mass index was calculated to be 12.5 kg/m2 and temperature of 101 8F was recorded. His systemic examination revealed a mass visible and palpable in the hypogastric region that was non-tender. Rest of the systemic examination was unremarkable. Investigations revealed the following: total leukocyte count – 15,200 with neutrophils 81%, lymphocytes 16%, erythrocyte sedimentation rate – 70 mm/h, hemoglobin – 7.9 g%, reticulocyte count 1%. Peripheral smear showed moderate hypochromic microcytic anemia. Blood urea was 95 mg/dl and serum creatinine was 2.2 mg/dl. Liver function tests were normal. Stool for routine examination showed plenty of yeast cells. Urine examination showed 25–30 pus cells/high power field and few yeast cells. Culture of the urethral discharge using standard techniques grew Candida species.3,4 Blood culture at the time of admission was sterile. Fundus examination was suggestive of moderate non-progressive diabetic retinopathy in both eyes, with right eye being more affected than left. Serology for HIV antibody
http://dx.doi.org/10.1016/j.injms.2016.05.004 0976-2884/ß 2016 Published by Elsevier, a division of Reed Elsevier India, Pvt. Ltd on behalf of Indian Journal of Medical Specialities.
S. Das et al. / Indian Journal of Medical Specialities 7 (2016) 90–92
Fig. 1. Contrast-enhanced CT scan of abdomen with noniodinated contrast suggesting lesion in relation to the atrophic pancreas with multiple calculi in the pancreatic duct, and left lower ureteric stricture with left hydroureteronephrosis.
and HBsAg was negative. Ultrasonography of abdomen showed bilateral grade 2 renal disease and cystitis. Left kidney was enlarged (11.5 cm 4.5 cm) and showed left sided gross hydrouretronephrosis. Right kidney was found to be contracted (7.5 cm 2.5 cm). An ill defined mass anterosuperior to the bladder was seen, suggestive of either an abscess or urachal mass. Contrast-enhanced CT scan of abdomen with noniodinated contrast was done which suggested a lesion in relation to the dome of bladder, likely thick walled focal collection or a necrotic urachal mass (Figs. 1 and 3). The findings also included atrophic pancreas with multiple calculi in the pancreatic duct and left lower ureteric stricture with left hydroureteronephrosis (Figs. 2 and 3). During the course of stay while under investigation, patient developed hospital acquired urinary tract infection caused by E. coli which was sensitive to imipenem and nitrofurantoin. Subsequently, he also developed bacteremia caused by Methicillin-resistant Staphylococcus aureus (MRSA). The patient was administered vancomycin, fluconazole and high dose of insulin to control blood glucose. However, the patient continued to be febrile and toxic, even though urethral discharge had ceased. Considering the deteriorating condition of the patient, an exploratory laparotomy was undertaken with high risk consent. Approximately 50–100 ml walled off abscess containing thick yellowish pus was identified in the pelvis. The drained pus was
91
Fig. 3. Contrast-enhanced CT scan of abdomen with noniodinated contrast suggesting lesion in relation to the dome of bladder, likely thick walled focal collection or a necrotic urachal mass, atrophic pancreas with multiple calculi in the pancreatic duct, and left lower ureteric stricture with left hydroureteronephrosis.
subjected to laboratory analysis using standard techniques.3,4 Gram staining of pus revealed yeast cells with few pus cells. Growth on Sabouraud dextrose agar at 30 8C produced smooth, glistening, cream colored colonies suggestive of Candida spp., which was subsequently identified by growth on cornmeal agar, germ-tube test and biochemical reactions as C. glabrata. On the 6th postoperative day, patient complained of a painful scrotal swelling which was drained percutaneously under sonological guidance taking all aseptic precautions. The yellowish-brown aspirate was subjected to microbiological analysis. C. glabrata was isolated after 48 h. Both the isolates of C. glabrata (i.e. from pelvic abscess and scrotal collection) were resistant to fluconazole with high MIC of more than 164 mg/ml, but susceptible to all three echinocandins as per CLSI M44-A2 guidelines.5 An attempt was made to study colonization status of patient, and swabs from oral cavity, axilla and groin were subjected to culture.3,4 Stool sample showed predominant growth of C. glabrata. The patient was started on intravenous caspofungin 50 mg once a day for 2 weeks. After the surgery and the course of caspofungin, the insulin requirement reduced drastically and the patient became symptomatically much better. Patient was discharged once he was afebrile, not having any urethral discharge, and without evidence of any recurrent abscess at any other site. 3. Discussion
Fig. 2. Contrast-enhanced CT scan of abdomen with noniodinated contrast suggesting lesion in relation to the pancreas.
This patient is described as a case of fibrocalculous pancreatic diabetes (FCPD) as per the diagnostic criteria proposed by Mohan et al.1 The severe malnutrition due to long standing steatorrhea and secondary diabetes caused by FCPD may have contributed to his immunocompromised state, thereby predisposing to repeated urinary tract infections. Invasive candidiasis encompasses a variety of conditions including acute disseminated candidiasis (ADC), renal candidiasis, intraabdominal disease etc. and most of these are due to hematogenous spread. C. glabrata is now increasing in frequency among non-Candida albicans Candida (NCAC) spp. as a cause of invasive candidiasis, especially in immunocompromised hosts.6 C. glabrata has been shown to be the causative organism in infections of urinary tract, retroperitoneal soft tissue, vertebrae and other soft tissues.7–10 With its intrinsically decreased
92
S. Das et al. / Indian Journal of Medical Specialities 7 (2016) 90–92
susceptibility to azoles derivative mostly due to higher expression of efflux pump, C. glabrata poses a challenge to treatment.11 In this case, the patient had plenty of yeast cells in the stool at time of admission, which along with prevailing steatorrhea and mucosal breach due to repeated inflammation, may have led to the dissemination of C. glabrata into the genitourinary tract. Oral fluconazole with other broad spectrum antimicrobials may have led to further selecting out of C. glabrata. Although yeast was not isolated from blood sample of this case, similar strains were isolated from abdominal and scrotal collection along with stool, thus indicating gut as the site of colonization and subsequent dissemination. There are studies which suggest gastrointestinal tract colonization as a risk factor for invasive candidasis.12,13 Amphotericin B and echinocandins are the available treatment options for azole resistant NCAC spp. Caspofungin is shown to be safe and effective in treatment of deep invasive candidiasis, including intraabdominal abscesses, peritonitis and arthritis caused by C. albicans and NCAC spp.14 In this patient caspofungin was chosen over amphotericin B in view of renal dysfunction and the patient responded well. FCPD has numerous other complications including proliferative retinopathy and maculopathy, neuropathy, nephropathy, left ventricular dysfunction, tuberculosis, urinary tract infections, and cataract.15 The nature of diabetes in FCPD is usually severe and requires insulin treatment. However, patients with FCPD rarely develop ketoacidosis.15 FCPD has been found to share susceptibility genes in common with non-insulin dependent diabetes mellitus and insulin-dependent diabetes mellitus patients.15 However, the World Health Organization (WHO) has recently recommended to delete the class MRDM and to classify FCPD as fibrocalculus pancreatopathy which is a disease of the exocrine pancreas.16 The present case is the first reported case of intra-abdominal and scrotal abscess caused by C. glabrata in patients suffering from FCPD. This case highlights the significance of species specific identification of Candida spp. and routine antifungal susceptibility testing in management of invasive candidiasis. Also this case exemplifies the need for evaluating Candida spp. colonization status in patients at risk of invasive candidiasis.
Author’s contribution Concepts: SD, RS, PR; design: SD, RS, PR, VH, IRK; definition of intellectual content: SD, RS, PR, VH, GM, SVM; literature search: SD,
RS, PR; experimental studies: SD, RS, IRK; data acquisition: SD, RS, PR, IRK, GM, SVM; data analysis: SD, RS, PR; statistical analysis: SD, RS, PR; manuscript preparation: SD, RS, PR, VH; manuscript editing: SD, RS, PR, VH; manuscript review: SD, RS, PR, VH, IRK, GM; guarantor: PR. Conflicts of interest The authors have none to declare. References 1. Mohan V, Nagalotimath SJ, Yajnik CS, Tripathy BB. Fibrocalculous pancreatic diabetes. Diabetes Metab Rev. 1998;14:153–170. 2. Taksande A, Taksande B, Kumar A, Vilhekar KY. Malnutrition-related diabetes mellitus. J Mahatma Gandhi Inst Med Sci. 2008;13:19–24. 3. Bacteria and related organisms.Collee JG, Fraser AG, Marmion BP, Simmons A, eds. In: Mackie & McCartney Practical Medical Microbiology 14th ed. New Delhi: Elsevier South Asia Edition; 2008:151–423. 4. (a). Rippon JW, ed. In: Medical Mycology: The Pathogenic Fungi and the Pathogenic Actinomycetes 2nd ed. Philadelphia: W.B. Saunders Co.; 1982; (b). Rippon JW, ed. In: Medical Mycology: The Pathogenic Fungi and the Pathogenic Actinomycetes 3rd ed. Philadelphia: W.B. Saunders Co.; 1988. 5. Clinical and Laboratory Standards Institute. Method for Antifungal Disk Diffusion Susceptibility Testing of Yeasts; Approved Guideline. 2nd ed. Wayne, PA, USA: CLSI Document; 2009:M44-A2. 6. Silva S, Negri M, Henriques M, Oliveira R, Williams DW, Azeredo J. Candida glabrata, Candida parapsilosis and Candida tropicalis: biology, epidemiology, pathogenicity and antifungal resistance. FEMS Microbiol Rev. 2012;36(2):288–305. 7. Kauffman CA, Fisher JF, Sobel JD, Newman CA. Candida urinary tract infections – diagnosis. Clin Infect Dis. 2011;52(suppl 6):S452–S456. 8. Patel BC, Wayangankar SA, Ngo E, Chakrabarty S, Bronze MS. Primary retroperitoneal abscess caused by Candida glabrata. Am J Med Sci. 2012;344(4):332–334. 9. Dailey NJ, Young EJ. Candida glabrata spinal osteomyelitis. Am J Med Sci. 2011;341(1):78–82. 10. Celik AD, Yulugkural Z, Kuloglu F, Akata F. Candida glabrata: etiologic agent of soft tissue abscess in a diabetic patient. Indian J Pathol Microbiol. 2010;53(3): 590–591. 11. Panackal AA, Gribskov JL, Staab JF, Kirby KA, Rinaldi M, Marr KA. Clinical significance of azole antifungal drug cross-resistance in Candida glabrata. J Clin Microbiol. 2006;44(5):1740. http://dx.doi.org/10.1128/JCM.44.5.1740-1743.2006. 12. Nucci M, Anaissie E. Revisiting the source of candidemia: skin or gut? Clin Infect Dis. 2001;33:1959–1967. 13. Segireddy M, Johnson LB, Szpunar SM, Khatib R. Differences in patient risk factors and source of candidaemia caused by Candida albicans and Candida glabrata. Mycoses. 2011;54:e39–e43. http://dx.doi.org/10.1111/j.1439-0507.2009.01824.x. 14. Cornely OA, Lasso M, Betts R, Klimko N, Vazquez J, Dobb G. Caspofungin for the treatment of less common forms of invasive candidiasis. J Antimicrob Chemother. 2007;60(2):363–369. 15. Mohan V. Fibrocalculus pancreatic diabetes (FCPD) in India. Int J Diabetes Dev Ctries. 1993;13:14–21. 16. Khatib OMN, ed. In: Guidelines for the Prevention, Management and Care of Diabetes Mellitus. Geneva: World Health Organization; 2006.
Contents lists available at ScienceDirect
Indian Journal of Medical Specialities journal homepage: www.elsevier.com/locate/injms
Case report
A case of fibrocalculous pancreatic diabetes (FCPD) with pelvic and scrotal abscess caused by Candida glabrata Shukla Das a, Rumpa Saha a, Priyamvada Roy a,*, Vivek Hada b, Iqbal Rajinder Kaur a, Gaurav Muktesh c, S.V. Madhu d a
Department of Microbiology, University College of Medical Sciences & Guru Teg Bahadur Hospital, Delhi 110095, India Department of Microbiology, All India Institute of Medical Sciences, Jodhpur 342005, India Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India d Department of Medicine, University College of Medical Sciences & Guru Teg Bahadur Hospital, Delhi 110095, India b c
A R T I C L E I N F O
A B S T R A C T
Article history: Received 18 February 2016 Received in revised form 25 May 2016 Accepted 27 May 2016 Available online 13 June 2016
Fibrocalculous pancreatic diabetes (FCPD) is a peculiar form of diabetes secondary to chronic pancreatitis and usually affects young individuals. It is mostly seen in the developing countries of the world where protein-calorie malnutrition is prevalent. FCPD has an aggressive course and may be responsible for pancreatic calculi, steatorrhoea and other complications of diabetes as well as makes the patient immunocompromised in the majority of cases. Candida glabrata is an important cause of invasive candidiasis in immunocompromised hosts. Here we report the first case of intra-abdominal and scrotal abscess caused by C. glabrata in a patient suffering from FCPD. ß 2016 Published by Elsevier, a division of Reed Elsevier India, Pvt. Ltd on behalf of Indian Journal of Medical Specialities.
Keywords: Candida glabrata Fibrocalculous pancreatic diabetes Invasive candidiasis
1. Introduction Fibrocalculous pancreatic diabetes (FCPD) is a form of diabetes secondary to tropical calcific pancreatitis usually affecting the poorer strata of society. The patients are often lean and malnourished.1 FCPD is one of the 2 subtypes of malnutrition-related diabetes mellitus (MRDM), a rare type of diabetes associated with long-term malnutrition. FCPD usually occurs below 30 years of age and is characterized by clinical evidence of malnutrition, insulinrequirement, radiological evidence of pancreatic calcification and/ or exocrine pancreatic dysfunction. The other subtype of MRDM is protein-deficient diabetes mellitus (PDDM), in which there is no clinical or radiological evidence of pancreatic dysfunction.2 Here we report the first case of intra-abdominal and scrotal abscess caused by Candida glabrata in a patient with FCPD. 2. Case report A 24-year-male from north India, a known diabetic on insulin therapy since 6 years, presented with hypoglycemia to the * Corresponding author at: C/o Group Captain Dev Dutta Roy, Flat no. C-115, Jalvayu Vihar (Near AWHO), Plot no. 8, Pocket P-4, Greater Noida 201310, Uttar Pradesh, India. E-mail addresses: [email protected] (S. Das), [email protected] (R. Saha), [email protected] (P. Roy), [email protected] (V. Hada), [email protected] (I.R. Kaur), [email protected] (G. Muktesh), [email protected] (S.V. Madhu).
emergency room of our hospital and was evaluated in the endocrine unit after correction of hypoglycemia. The patient had steatorrhea since 5 years and grayish white urethral discharge since 1 year, involuntary dribbling of urine since 1 year and high grade fever on and off since 4 months. The discharge which was distinct from urine was semisolid in consistency with a distinct offensive odor. Patient complained of involuntary passage of the white urethral discharge 7–8 times per day. The patient was anemic, emaciated and had a toxic look. His blood pressure on presentation was 101/69 mm of mercury with a pulse rate of 152/min. The body mass index was calculated to be 12.5 kg/m2 and temperature of 101 8F was recorded. His systemic examination revealed a mass visible and palpable in the hypogastric region that was non-tender. Rest of the systemic examination was unremarkable. Investigations revealed the following: total leukocyte count – 15,200 with neutrophils 81%, lymphocytes 16%, erythrocyte sedimentation rate – 70 mm/h, hemoglobin – 7.9 g%, reticulocyte count 1%. Peripheral smear showed moderate hypochromic microcytic anemia. Blood urea was 95 mg/dl and serum creatinine was 2.2 mg/dl. Liver function tests were normal. Stool for routine examination showed plenty of yeast cells. Urine examination showed 25–30 pus cells/high power field and few yeast cells. Culture of the urethral discharge using standard techniques grew Candida species.3,4 Blood culture at the time of admission was sterile. Fundus examination was suggestive of moderate non-progressive diabetic retinopathy in both eyes, with right eye being more affected than left. Serology for HIV antibody
http://dx.doi.org/10.1016/j.injms.2016.05.004 0976-2884/ß 2016 Published by Elsevier, a division of Reed Elsevier India, Pvt. Ltd on behalf of Indian Journal of Medical Specialities.
S. Das et al. / Indian Journal of Medical Specialities 7 (2016) 90–92
Fig. 1. Contrast-enhanced CT scan of abdomen with noniodinated contrast suggesting lesion in relation to the atrophic pancreas with multiple calculi in the pancreatic duct, and left lower ureteric stricture with left hydroureteronephrosis.
and HBsAg was negative. Ultrasonography of abdomen showed bilateral grade 2 renal disease and cystitis. Left kidney was enlarged (11.5 cm 4.5 cm) and showed left sided gross hydrouretronephrosis. Right kidney was found to be contracted (7.5 cm 2.5 cm). An ill defined mass anterosuperior to the bladder was seen, suggestive of either an abscess or urachal mass. Contrast-enhanced CT scan of abdomen with noniodinated contrast was done which suggested a lesion in relation to the dome of bladder, likely thick walled focal collection or a necrotic urachal mass (Figs. 1 and 3). The findings also included atrophic pancreas with multiple calculi in the pancreatic duct and left lower ureteric stricture with left hydroureteronephrosis (Figs. 2 and 3). During the course of stay while under investigation, patient developed hospital acquired urinary tract infection caused by E. coli which was sensitive to imipenem and nitrofurantoin. Subsequently, he also developed bacteremia caused by Methicillin-resistant Staphylococcus aureus (MRSA). The patient was administered vancomycin, fluconazole and high dose of insulin to control blood glucose. However, the patient continued to be febrile and toxic, even though urethral discharge had ceased. Considering the deteriorating condition of the patient, an exploratory laparotomy was undertaken with high risk consent. Approximately 50–100 ml walled off abscess containing thick yellowish pus was identified in the pelvis. The drained pus was
91
Fig. 3. Contrast-enhanced CT scan of abdomen with noniodinated contrast suggesting lesion in relation to the dome of bladder, likely thick walled focal collection or a necrotic urachal mass, atrophic pancreas with multiple calculi in the pancreatic duct, and left lower ureteric stricture with left hydroureteronephrosis.
subjected to laboratory analysis using standard techniques.3,4 Gram staining of pus revealed yeast cells with few pus cells. Growth on Sabouraud dextrose agar at 30 8C produced smooth, glistening, cream colored colonies suggestive of Candida spp., which was subsequently identified by growth on cornmeal agar, germ-tube test and biochemical reactions as C. glabrata. On the 6th postoperative day, patient complained of a painful scrotal swelling which was drained percutaneously under sonological guidance taking all aseptic precautions. The yellowish-brown aspirate was subjected to microbiological analysis. C. glabrata was isolated after 48 h. Both the isolates of C. glabrata (i.e. from pelvic abscess and scrotal collection) were resistant to fluconazole with high MIC of more than 164 mg/ml, but susceptible to all three echinocandins as per CLSI M44-A2 guidelines.5 An attempt was made to study colonization status of patient, and swabs from oral cavity, axilla and groin were subjected to culture.3,4 Stool sample showed predominant growth of C. glabrata. The patient was started on intravenous caspofungin 50 mg once a day for 2 weeks. After the surgery and the course of caspofungin, the insulin requirement reduced drastically and the patient became symptomatically much better. Patient was discharged once he was afebrile, not having any urethral discharge, and without evidence of any recurrent abscess at any other site. 3. Discussion
Fig. 2. Contrast-enhanced CT scan of abdomen with noniodinated contrast suggesting lesion in relation to the pancreas.
This patient is described as a case of fibrocalculous pancreatic diabetes (FCPD) as per the diagnostic criteria proposed by Mohan et al.1 The severe malnutrition due to long standing steatorrhea and secondary diabetes caused by FCPD may have contributed to his immunocompromised state, thereby predisposing to repeated urinary tract infections. Invasive candidiasis encompasses a variety of conditions including acute disseminated candidiasis (ADC), renal candidiasis, intraabdominal disease etc. and most of these are due to hematogenous spread. C. glabrata is now increasing in frequency among non-Candida albicans Candida (NCAC) spp. as a cause of invasive candidiasis, especially in immunocompromised hosts.6 C. glabrata has been shown to be the causative organism in infections of urinary tract, retroperitoneal soft tissue, vertebrae and other soft tissues.7–10 With its intrinsically decreased
92
S. Das et al. / Indian Journal of Medical Specialities 7 (2016) 90–92
susceptibility to azoles derivative mostly due to higher expression of efflux pump, C. glabrata poses a challenge to treatment.11 In this case, the patient had plenty of yeast cells in the stool at time of admission, which along with prevailing steatorrhea and mucosal breach due to repeated inflammation, may have led to the dissemination of C. glabrata into the genitourinary tract. Oral fluconazole with other broad spectrum antimicrobials may have led to further selecting out of C. glabrata. Although yeast was not isolated from blood sample of this case, similar strains were isolated from abdominal and scrotal collection along with stool, thus indicating gut as the site of colonization and subsequent dissemination. There are studies which suggest gastrointestinal tract colonization as a risk factor for invasive candidasis.12,13 Amphotericin B and echinocandins are the available treatment options for azole resistant NCAC spp. Caspofungin is shown to be safe and effective in treatment of deep invasive candidiasis, including intraabdominal abscesses, peritonitis and arthritis caused by C. albicans and NCAC spp.14 In this patient caspofungin was chosen over amphotericin B in view of renal dysfunction and the patient responded well. FCPD has numerous other complications including proliferative retinopathy and maculopathy, neuropathy, nephropathy, left ventricular dysfunction, tuberculosis, urinary tract infections, and cataract.15 The nature of diabetes in FCPD is usually severe and requires insulin treatment. However, patients with FCPD rarely develop ketoacidosis.15 FCPD has been found to share susceptibility genes in common with non-insulin dependent diabetes mellitus and insulin-dependent diabetes mellitus patients.15 However, the World Health Organization (WHO) has recently recommended to delete the class MRDM and to classify FCPD as fibrocalculus pancreatopathy which is a disease of the exocrine pancreas.16 The present case is the first reported case of intra-abdominal and scrotal abscess caused by C. glabrata in patients suffering from FCPD. This case highlights the significance of species specific identification of Candida spp. and routine antifungal susceptibility testing in management of invasive candidiasis. Also this case exemplifies the need for evaluating Candida spp. colonization status in patients at risk of invasive candidiasis.
Author’s contribution Concepts: SD, RS, PR; design: SD, RS, PR, VH, IRK; definition of intellectual content: SD, RS, PR, VH, GM, SVM; literature search: SD,
RS, PR; experimental studies: SD, RS, IRK; data acquisition: SD, RS, PR, IRK, GM, SVM; data analysis: SD, RS, PR; statistical analysis: SD, RS, PR; manuscript preparation: SD, RS, PR, VH; manuscript editing: SD, RS, PR, VH; manuscript review: SD, RS, PR, VH, IRK, GM; guarantor: PR. Conflicts of interest The authors have none to declare. References 1. Mohan V, Nagalotimath SJ, Yajnik CS, Tripathy BB. Fibrocalculous pancreatic diabetes. Diabetes Metab Rev. 1998;14:153–170. 2. Taksande A, Taksande B, Kumar A, Vilhekar KY. Malnutrition-related diabetes mellitus. J Mahatma Gandhi Inst Med Sci. 2008;13:19–24. 3. Bacteria and related organisms.Collee JG, Fraser AG, Marmion BP, Simmons A, eds. In: Mackie & McCartney Practical Medical Microbiology 14th ed. New Delhi: Elsevier South Asia Edition; 2008:151–423. 4. (a). Rippon JW, ed. In: Medical Mycology: The Pathogenic Fungi and the Pathogenic Actinomycetes 2nd ed. Philadelphia: W.B. Saunders Co.; 1982; (b). Rippon JW, ed. In: Medical Mycology: The Pathogenic Fungi and the Pathogenic Actinomycetes 3rd ed. Philadelphia: W.B. Saunders Co.; 1988. 5. Clinical and Laboratory Standards Institute. Method for Antifungal Disk Diffusion Susceptibility Testing of Yeasts; Approved Guideline. 2nd ed. Wayne, PA, USA: CLSI Document; 2009:M44-A2. 6. Silva S, Negri M, Henriques M, Oliveira R, Williams DW, Azeredo J. Candida glabrata, Candida parapsilosis and Candida tropicalis: biology, epidemiology, pathogenicity and antifungal resistance. FEMS Microbiol Rev. 2012;36(2):288–305. 7. Kauffman CA, Fisher JF, Sobel JD, Newman CA. Candida urinary tract infections – diagnosis. Clin Infect Dis. 2011;52(suppl 6):S452–S456. 8. Patel BC, Wayangankar SA, Ngo E, Chakrabarty S, Bronze MS. Primary retroperitoneal abscess caused by Candida glabrata. Am J Med Sci. 2012;344(4):332–334. 9. Dailey NJ, Young EJ. Candida glabrata spinal osteomyelitis. Am J Med Sci. 2011;341(1):78–82. 10. Celik AD, Yulugkural Z, Kuloglu F, Akata F. Candida glabrata: etiologic agent of soft tissue abscess in a diabetic patient. Indian J Pathol Microbiol. 2010;53(3): 590–591. 11. Panackal AA, Gribskov JL, Staab JF, Kirby KA, Rinaldi M, Marr KA. Clinical significance of azole antifungal drug cross-resistance in Candida glabrata. J Clin Microbiol. 2006;44(5):1740. http://dx.doi.org/10.1128/JCM.44.5.1740-1743.2006. 12. Nucci M, Anaissie E. Revisiting the source of candidemia: skin or gut? Clin Infect Dis. 2001;33:1959–1967. 13. Segireddy M, Johnson LB, Szpunar SM, Khatib R. Differences in patient risk factors and source of candidaemia caused by Candida albicans and Candida glabrata. Mycoses. 2011;54:e39–e43. http://dx.doi.org/10.1111/j.1439-0507.2009.01824.x. 14. Cornely OA, Lasso M, Betts R, Klimko N, Vazquez J, Dobb G. Caspofungin for the treatment of less common forms of invasive candidiasis. J Antimicrob Chemother. 2007;60(2):363–369. 15. Mohan V. Fibrocalculus pancreatic diabetes (FCPD) in India. Int J Diabetes Dev Ctries. 1993;13:14–21. 16. Khatib OMN, ed. In: Guidelines for the Prevention, Management and Care of Diabetes Mellitus. Geneva: World Health Organization; 2006.