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Year : 2014  |  Volume : 16  |  Issue : 2  |  Page : 77-80

Necrotizing fasciitis due to Apophysomyces elegans

Department of Microbiology, Kamineni Institute of Medical Sciences, Narketpally, Nalgonda, Andhra Pradesh, India

Date of Web Publication14-Nov-2014

Correspondence Address:
Lakshmi P Vasantha
Department of Microbiology, Kamineni Institute of Medical Sciences, Narketpally, Nalgonda, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-1282.144720

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Mucormycosis caused by Apophysomyces elegans is an emerging disease not only in immunocompromised hosts but also in the immunocompetent. Here, we report a case of invasive necrotizing fasciitis of left thigh due to Apophysomyces elegans in a diabetic. Below knee amputation of gangrenous right leg was done 20 days before this developed. Broad aseptate hyphae were observed in necrosed tissues. Surgical debridement was done and Amphotericin B was recommended. Isolate recovered in culture was identified as A. elegans based on induction of sporulation on water agar and other modified methods. Patient expired due to sepsis.

Keywords: Apophysomyces elegans , Immunocompromised people, Necrotizing fasciitis

How to cite this article:
Vasantha LP, Leela SK. Necrotizing fasciitis due to Apophysomyces elegans. J Acad Clin Microbiol 2014;16:77-80

How to cite this URL:
Vasantha LP, Leela SK. Necrotizing fasciitis due to Apophysomyces elegans. J Acad Clin Microbiol [serial online] 2014 [cited 2021 Jan 26];16:77-80. Available from: https://www.jacmjournal.org/text.asp?2014/16/2/77/144720

  Introduction Top

Mucormycosis is a rapidly spreading and often fatal infection, especially in immunocompromised hosts. Zygomycetes implicated in causing mucormycosis belong to genera Rhizopus, Rhizomucor, Lichtheimia (Absidia), Mucor, Apophysomyces, Saksenaea, Cunninghamella, Cokeromyces and Syncephalastrum. Rhizopus, Rhizomucor and Lichtheimia are commonly reported pathogens compared to others. Apophysomyces elegans even though reported infrequently, is an emerging zygomycete that causes human infections. Like other zygomycetes, it causes infections mainly in immunocompromised people but for the past few decades, primary cutaneous or subcutaneous infections by A. elegans in immunocompetent people were increasing especially after trauma. [1] Early suspicion and intervention like extensive debridement and antifungal therapy is needed in these cases. A total of approximately 74 well-documented cases were reported from India and abroad, [1] but from India more number of cases were from north India. [2],[3],[4] Here, we report a case of invading necrotizing fasciitis due to A. elegans in a diabetic individual with ketoacidosis from south India.

  Case report Top

A 35-year-old man was admitted in the hospital with the complaints of shortness of breath, fever and cough for 4 days. Patient had bimalleolar fracture of right ankle 20 days back, for which a plaster of Paris cast was put. He was a known diabetic since 10 years. He was not a known hypertensive or asthmatic. Patient complained of pain over right ankle at the fractured site. On physical examination, there was blackening of entire right foot along with subcutaneous emphysema extending two inches above the ankle joint.

Laboratory tests


Random blood sugar −403 mg/dl

Urine for ketone bodies - positive

HbA 1 c −12.5%

Alkaline phosphatase −362 IU/L

Serum creatinine −0.8 mg/dl

Blood picture showed a total count of 26,700/mm 3 with neutrophils −80%, lymphocytes −15%, eosinophils −2%, monocytes −3%, basophils −0% and haemoglobin level was 13.6 g%, ESR −22 mm in first hour. Serology for HIV and Hepatitis B were negative.

The ankle wound was debrided and fasciotomy was done. Piperacillin-Tazobactam, Amikacin, Clindamycin and Metrogyl were started. Debrided tissue was sent for bacterial culture. Gram stain showed the presence of Gram-negative bacilli along with inflammatory cells.  Escherichia More Details coli were isolated in culture. As the isolate was sensitive to Piperacillin-Tazobactam and Amikacin, same treatment was continued. Patient remained febrile. Below knee amputation was done on the next day. After two days, a well defined tender hyperpigmented macule appeared on posterolateral aspect of left thigh. This macule increased in size to 8 × 6 cm and became indurated within 3 to 4 days giving the picture of cellulitis. This lesion was incised and debrided. Extensive dissection of dead and necrotic tissue including devitalized muscle was done on next day. Infected tissues were sent for fungal culture. Broad, aseptate or pauci septate hyphae were observed on KOH mount after overnight incubation of tissue in 10% KOH. Debrided tissue sent on first day and muscle tissue sent on second day were inoculated separately in Sabouraud's dextrose agar with antibiotics. Both yielded same growth. Growth appeared within 2 days and was fast growing, floccose, filamentous growth. Colonies were white in colour in the beginning and turning to slight yellow on prolonged incubation [Figure 1].
Figure 1: White, cottony, fl uffy growth of A. elegans on Sabouraud's dextrose agar with antibiotics

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Fungal colony on tease mount with Lacto phenol cotton blue (LPCB) showed hyaline broad, aseptate hyphae with no asexual spores. As they failed to sporulate on routinely used media, special sporulating media for zygomycetes group i.e., water agar [5] and modified method by Padhye et al.,[6] were used to induce sporulation. The following procedures were adopted for inducing sporulation.

Fungal isolate was first cultured on Sabouraud's dextrose agar dispensed in a petridish. Three agar blocks approximately 1 cm΂ each permeated with hyphae were cut and placed on the surface of sterilized and solidified 1% water agar in a petridish. In the second method, three 1 cm΂ agar blocks permeated with hyphae were cut and kept in a petridish containing 20 ml distilled water with 0.2 ml of 10% yeast extract. Duplicate plates using these two methods were incubated at 25°C, 30°C, and 37°C for 2 weeks. Abundant sporulation was observed when plates were incubated at 30° & 37°C.

Sporangiophores were aroused at right angles to hyphae and often from septate basal segment, foot cell [Figure 2]. They were unbranched bearing prominent, dark champanulate or champagne glass-shaped apophyses [Figure 3]. Sporangiophores below the apophyses had shown light to dark brown thickening [Figure 4]. Sporangia were pyriform in shape. Sporangiospores were oblong or subglobose. Delicate, unbranched rhizoids were observed which were below the sporangiophore and sometimes arising from foot cell [Figure 5]. Isolate was identified as A. elegans.
Figure 2: LPCB mount of growth on water agar showing unbranched sporangiophore arising from a foot cell (arrow). (×400)

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Figure 3: LPCB mount of growth showing characteristic champanulate or champagne glass shaped apophysis of A. elegans (arrow). (×800)

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Figure 4: LPCB mount showing sporangiophore with hyperpigmented region of thickening just below the apophysis of A. elegans (arrow). (×400)

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Figure 5: LPCB mount showing prominent, unbranched, tuft of rhizoids at the base of sporangiophore and also adjacent to foot cell (arrows). (×400)

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Patient was advised intravenous Amphotericin B. But patient developed features of sepsis and died.

  Discussion Top

0A. elegans was considered as a rare pathogen but over the past few decades, mucormycosis caused by A. elegans was increasing especially in immune-competent hosts. [1]

A. elegans belongs to order Mucorales, family Saksenaeaceae and genus Apophysomyces (A. elegans complex). A. elegans is now considered as a part of complex of four species, containing other three species, A. ossiformis, A. trapeziformis and A. variabilis along with it. [1]

A. elegans was first isolated in 1979 from soil samples in a mango orchard in north India. [7] It was also isolated from soil and air filter dust samples in Australia in association with human infections. In 1982, A. elegans was isolated from bronchial washings of a patient in United States. Two cases of traumatic zygomycosis caused by A. elegans and involving the extremities were reported in 1982. Another case of human A. elegans infection was reported in Arizona, in United States in 1985. [8] Afterwards, a total of 74 cases were reported from different countries with a maximum from India i.e., 36 cases [2],[3],[4],[9],[10] , followed by United states (24) [8] , Australia (5), Mexico (2), central America (2), South America (2), Sri Lanka (1), Thailand (1), Kuwait (1). In India, more number of cases were reported from north India [2],[3],[4] compared to south India. [9],[10]

The most common clinical presentation by A. elegans is cutaneous and subcutaneous involvement with local invasion into neighbouring tissues particularly fat, muscle, nerves and bone. Other presentations include rhino cerebral and renal zygomycosis. Cutaneous involvement generally presents as pain, erythema and induration with a varying degree of central necrosis. More advanced lesions take on the appearance of necrotizing fasciitis with mortality around 80%. This can progress to gangrene and disseminated forms. [3]

This case of necrotizing fasciitis first presented as a patch of erythema followed by induration and central necrosis. Afterwards it had invaded fascia and muscles.

Like in other zygomycoses, immunocompromised individuals are more prone to A. elegans infection. But from the reported cases globally, it is evident that immunocompetent people were affected as commonly as the immunocompromised. [1],[3],[4],[9] The most common systemic conditions predisposing to A. elegans infection are uncontrolled diabetes mellitus (hyperglycaemia), ketoacidosis, malignancy, leucopoenia, immunosuppressive therapy, organ transplantation and alcoholic cirrhosis. [1] The present case is a diabetic for the past 10 years who was in a ketoacidotic condition at the time of presentation.

Percutaneous inoculation of pathogen after trauma is the most common mode of A. elegans infection acquisition. Other modes of entry include burns, surgery, surgical splints, arterial lines, injection sites, biopsy sites, tattoos, and insect and spider bites. Disruption of the cutaneous barrier is needed for the entry of this fungus to cause necrotizing fasciitis. [1]

In the present case, the area of skin that was macerated because of prolonged immobilisation may be the portal of entry of this infective agent.

The presenting case had progressed from simple erythema, induration to necrotizing fasciitis within 12 days. Rapid progression in A. elegans infection can be explained by angioinvasion and growth of fungus in vascular lumen leading to thrombus formation and ischemic tissue. [1]

A. elegans infection can disseminate from primary site of infection. As a part of dissemination, A. elegans has a predilection to involve the kidney compared to other organs. In renal involvement, A. elegans invades renal vessels causing vessel necrosis and thrombosis leading to infarction and necrosis of cortex and medulla and thereby abscess formation. Hyphae may also be found within glomeruli, tubules and interstitium.

As A. elegans spreads rapidly early suspicion and diagnosis can save the patient. Direct demonstration of hyaline aseptate or pauci septate hyphae by KOH mount in the sample, culture on SDA with antibiotics and induction of sporulation by special methods will help in identification of etiological agent. As A. elegans does not sporulate on routinely used fungal culture media, 1% water agar [5] or modified method by Padhye et al.,[6] will be needed for the induction of asexual spores. A. elegans differs from Absidia by having foot cell from which sporangiophore arises, prominent champagne glass-shaped apophysis and dark brown or greyish brown sub-apical thickening in sporangiophore. Sporangiospores are oblong or subglobose.

Extensive surgical debridement and parenteral antifungal therapy is the main mode of treatment. Amphotericin B is the most commonly used drug for treatment of A. elegans infections. But other alternatives such as Posaconazole in Amphotericin B-resistant cases and Isavuconazole or Itraconazole are used in susceptible strains.

  References Top

Gomes MZ, Lewis RE, Kontoyiannis DP. Mucormycosis caused by unusual Mucormycetes, non-Rhizopus, -Mucor, and -Lichtheimia species. Clin Microbiol Rev 2011; 24:411-45.  Back to cited text no. 1
Chakrabarti A, Ghosh A, Prasad GS, David JK, Gupta S, Das A, et al. Apophysomyses elegans: An emerging zygomycete in India. J Clin Microbiol 2003;41:783-8.  Back to cited text no. 2
Chander J, Kaur J, Attri A, Mohan H. Primary cutaneous zygomycosis from a tertiary care centre in north-west India. Indian J Med Res 2010;131:765-70.  Back to cited text no. 3
[PUBMED]  Medknow Journal  
Jain D, Kumar Y, Vasishta RK, Rajesh L, Pattari SK, Chakrabarti A. Zygomycotic necrotizing fasciitis in immunocompetent patients: A series of 18 cases. Mod Pathol 2006;19:1221-6.  Back to cited text no. 4
Ellis JJ, Ajello L. An unusual source for Apophysomyces elegans and a method for stimulating sporulation of Saksenaea vasiformis. Mycologia 1982;74:144-5.  Back to cited text no. 5
Padhye AA, Ajello L. Simple method of inducing sporulation by Apophysomyces elegans and Saksenaea vasiformis. J Clin Microbiol 1988;26:1861-3.  Back to cited text no. 6
Misra PC, Srivastava KJ, Lata K. Apophysomyces, a new genus of Mucorales. Mycotaxon 1979;8:377-82.  Back to cited text no. 7
Wieden MA, Steinbronn KK, Padhye AA, Ajello L, Chandler FW. Zygomycosis caused by Apophysomyces elegans. J Clin Microbiol 1985;22:522-6.  Back to cited text no. 8
Lakshmi V, Rani TS, Sharma S, Mohan VS, Sundaram C, Rao RR, et al. Zygomycotic necrotizing fasciitis caused by Apophysomyces elegans. J Clin Microbiol 1993;31:1368-9.  Back to cited text no. 9
Reddy IS, Rao NR, Shankar Reddy VM, Rao R. Primary cutaneous mucormycosis (zygomycosis) caused by Apophysomyces elegans. Indian J Dermatol Venereol Leprol 2008;74:367-70.  Back to cited text no. 10
[PUBMED]  Medknow Journal  


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]


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