Saksenaea vasiformis
Scientific classification
Kingdom:
Fungi
Division:
Zygomycota
Class:
Mucoromycotina
Order:
Mucorales
Family:
Saksenaeaceae
Genus:
Saksenaea
Species:
S. vasiformis

S.B.Saksena (1953)
Binomial name
Saksenaea vasiformis
S.B.Saksena (1953)

Saksenaea vasiformis is an infectious fungus associated with cutaneous or subcutaneous lesions following trauma.[1][2] It causes opportunistic infections as the entry of the fungus is through open spaces of cutaneous barrier[3] ranging in severity from mild to severe or fatal.[1] It lives in soils worldwide,[3] but is considered as a rare human pathogen since only 38 cases were reported as of 2012.[4] Saksenaea vasiformis usually fails to sporulate on the routine culture media,[3] creating a challenge for early diagnosis, which is essential for a good prognosis.[4] Infections are usually treated using a combination of amphotericin B and surgery.[4] Saksenaea vasiformis is one of the few fungi known to cause necrotizing fasciitis or "flesh-eating disease".[5]

Description

Saksenaea vasiformis was initially described as a new mucoraceous fungus in a new genus Saksenaea in 1953 by Dr. S. B. Saksena.[6] It was isolated from Patharia forest soil in India and distinguishably different from other species in morphology of sporangia (flask-shaped) and the method of spore discharge.[6] The name "vasiformis" came from the flask-shape of sporangiophore.[7] Since 1953, it has been isolated from various countries including Panama, Israel, Honduras, and the southern United States.[3] This species is the only species belong to genus Saksenaea,[3] although two new species, which are Saksenaea oblongispora and Saksenaea erythrospora, were proposed in 2010.[8] Detailed microscopic observation displayed similar flask shape of sporangiophores and the phylogenic analysis indicated that these isolates (S. vasiformis, S. oblongispora and S. erythrospora) belong to the same genus Saksenaea.[8]

This species is associated with Apophysomyces elegans, a member of family Mucoraceae. Despite the significant differences of morphological characteristics of sporangia and the manner of sporangium formation, these two species are associated, usually in medical literature, due to similar disease manifestation in human: cutaneous or subcutaneous infections.[3][7] Infections involving these two species (S. vasiformis and A. elegans) cause rapid necrotizing vasculitis that leads to thrombosis and tissue necrosis in organisms’ vascular lumen.[9]

Cultural characteristics

Saksenaea vasiformis very rapidly grows in growth media, producing sterile hyphae.[3][8] Induction of sporulation is difficult with routine fungal media used in the most of clinical laboratories, but it can be stimulated to sporulate rapidly (5 to 7 days) by incubating the yeast-malt-dextrose agar at 32 °C.[10] The identification of this species is not problematic after sporulation event because of its characteristic flask-shaped sporangium with spherical venter and a distinct dome-shped columella and dichotomously branched rhizoid complex.[3][6] On top of the venter, there is a neck with closed apex with a mucilaginous plug.[6] Inside of the neck are the sporangiophores, which are liberated by the dissolution of the mucilaginous plug.[6]

Pathogenesis

Saksenaea vasiformis is normally present in soil and does not cause human infection unless it is introduced to the open site where the cutaneous barrier no longer exists.[11] This is why this species causes an opportunistic infection following a traumatic event that breaks the cutaneous barrier. Infections were reported in the United States, Australia, Norway, New Zealand, Spain, India, French Guiana, France, India and Greece.[1][4] The first human infection by S. vasiformis was reported in 1976 in a 19-year-old male with cranial and facial wounds incurred during an automobile accident.[12]

Saksenaea vasiformis usually causes cutaneous or subcutaneous zygomycosis, but can also cause primary sinusitis and rhinocerebral disease.[1] Cutaneous diseases by S. vasiformis present red blisters.[13] with necrotic ulcers[14] or raised red to purple lesions.[15] Infections by S. vasiformis are normally localized and indolent, but in some cases infection is disseminated or becomes highly invasive, and these cases were all fatal.[3]

Early diagnosis is the key to survival of the patients, but the diagnosis of the disease is hard due to difficulties in stimulating sporulation. Furthermore, there has been only 38 cases of infections reported as of 2012[4] and the author of the paper suggested that low number of cases reported can be due to lack of awareness of this species in clinical environment, high mortality rate, and largely, microbiological and clinical bias resulted from difficulties in stimulating sporulation of this species. To ease the identification of fungus producing sterile mycelium such as S. vasiformis and A. elegans, exoantigen test has been developed. For S. vasiformis, even though exoantigen testing is helpful with positive test, it is rarely used because of the high false-negative rate, requiring confirmation by sporulating morphology with all the negative tests.[3] — see cultural characteristics.

Human hosts are usually immunocompetent with open lesion that acts as a portal entry of the fungus into the body. There has been some reported cases of immunocompromised hosts due to steroid treatment, antibiotic therapy, and compromised immune system due to underlying disease is also known as a risk factor.[3] For example, S. vasiformis infection has been seen in some patients with preleukemia,[14] bladder cancer[16] and diabetes mellitus.[17] Moreover, S. vasiformis causes infections in bovines[18] and cetaceans such as bottlenose dolphins, killer whales, and Pacific White-sided dolphins in with A. elegans.[7]

Treatment

Infections by S. vasiformis are mainly treated with drug amphotericin B because this species is resistant to many antifungal agents.[4] The side effect of amphotericin B is renal toxicity, but the chances of side effect can be reduced by administering amphotericin B in incremental doses to reach maximum daily dose of 0.5 to 0.75 mg/kg.[4] Furthermore, amphotericin B deoxycholate is more nephrotoxic than liposomal amphotericin B; due to the expense of liposomal amphotericin B, many of the patients were unable to afford this therapy, resulting in fatal outcome.[4] In addition, another antifungal agent, posaconazole, was able to successfully treat disseminated infection by S. vasiformis in vitro, suggesting that it could be used as an alternative to amphotericin B for the treatment of the infections.[19]

Along with the drug treatment, patients are recommended to receive an aggressive surgical debridement or an amputation in some severe cases. This is an important for the infection to be treated efficiently and effectively[3][4] because necrotic tissues may act as a barrier to penetration of drug to the site of infection.[4]

It is essential to treat infections appropriately and as soon as possible to decrease the mortality rate as mortality rate of untreated cases is almost 100% and that of properly treated cutaneous diseases is only around 10%.[20][21]

References

  1. 1 2 3 4 Vega W; Orellana M; Zaror L; Gené J; Guarro J. (2006). "Saksenaea vasiformis infections: case report and literature review". Mycopathologia. 162 (4): 289–94. doi:10.1007/s11046-006-0061-6. PMID 17039275. S2CID 4672160.
  2. ↑ Padmaja IJ; Ramani TV; Kalyani S. (2006). "Cutaneous zygomycosis: necrotising fascitis due to Saksenaea vasiformis". Indian Journal of Medical Microbiology. 24 (1): 58–60. doi:10.1016/S0255-0857(21)02474-9. hdl:1807/7251. PMID 16505559.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 Ribes, J. A.; Vanover-Sams, C. L.; Baker, D. J. (1 April 2000). "Zygomycetes in human disease". Clinical Microbiology Reviews. 13 (2): 236–301. doi:10.1128/CMR.13.2.236. PMC 100153. PMID 10756000.
  4. 1 2 3 4 5 6 7 8 9 10 Kaushik, Robin; Chander, Jagdish; Gupta, Sanjay; Sharma, Rajeev; Punia, Rajpal Singh (1 April 2012). "Fatal Primary Cutaneous Zygomycosis Caused by Saksenaea vasiformis: Case report and review of literature". Surgical Infections. 13 (2): 125–129. doi:10.1089/sur.2010.078. PMID 22280152.
  5. ↑ Bashford, C; Yin, T; Pack, J (February 2002). "Necrotizing fasciitis: a model nursing care plan". Medsurg Nursing. 11 (1): 37–42, quiz 43. PMID 11901612.
  6. 1 2 3 4 5 Saksena, SB (1953). "A New Genus of the Mucorales". Mycologia. 45 (3): 426–436. doi:10.1080/00275514.1953.12024280. JSTOR 4547711.
  7. 1 2 3 Chakrabarti, A.; Kumar, P.; Padhye, A. A.; Chatha, L.; Singh, S. K.; Das, A.; Wig, J. D.; Kataria, R. N. (1 April 1997). "Primary Cutaneous Zygomycosis Due to Saksenaea vasiformis and Apophysomyces elegans". Clinical Infectious Diseases. 24 (4): 580–582. doi:10.1093/clind/24.4.580. PMID 9145731.
  8. 1 2 3 Alvarez, E.; Garcia-Hermoso, D.; Sutton, D. A.; Cano, J. F.; Stchigel, A. M.; Hoinard, D.; Fothergill, A. W.; Rinaldi, M. G.; Dromer, F.; Guarro, J. (6 October 2010). "Molecular Phylogeny and Proposal of Two New Species of the Emerging Pathogenic Fungus Saksenaea". Journal of Clinical Microbiology. 48 (12): 4410–4416. doi:10.1128/JCM.01646-10. PMC 3008438. PMID 20926710.
  9. ↑ Robeck, T. R; Dalton, L. M (2002). "Saksenaea vasiformis and Apophysomyces elegans Zygomycotic Infections in Bottlenose Dolphins (Tursiops truncatus), a Killer Whale (Orcinus orca), and Pacific White-Sided Dolphins (Lagenorhynchus obliquidens)". Journal of Zoo and Wildlife Medicine. 33 (4): 356–366. doi:10.1638/1042-7260(2002)033[0356:SVAAEZ]2.0.CO;2. PMID 12564534. S2CID 29488757.
  10. ↑ Ellis, J. J; Ajello, L (1982). "An Unusual Source for Apophysomyces elegans and a Method for Stimulating Sporulation of Saksenaea vasiformis". Mycologia. 74 (1): 144–145. doi:10.2307/3792640. JSTOR 3792640.
  11. ↑ Adam, R. D.; Hunter, G.; DiTomasso, J.; Comerci, G. (1 July 1994). "Mucormycosis: Emerging Prominence of Cutaneous Infections". Clinical Infectious Diseases. 19 (1): 67–76. doi:10.1093/clinids/19.1.67. PMID 7948560.
  12. ↑ Ajello, Libero; Dean, David F; Irwin, Richard S (1976). "The Zygomycete Saksenaea vasiformis as a Pathogen of Humans with a Critical Review of the Etiology of Zygomycosis". Mycologia. 68 (1): 52–62. doi:10.2307/3758897. JSTOR 3758897. PMID 945456.
  13. ↑ Pritchard, RC; Muir, DB; Archer, KH; Beith, JM (1–15 Dec 1986). "Subcutaneous zygomycosis due to Saksenaea vasiformis in an infant". The Medical Journal of Australia. 145 (11–12): 630–1. doi:10.5694/j.1326-5377.1986.tb139516.x. PMID 3796372.
  14. 1 2 Torell, J; Cooper, BH; Helgeson, NG (July 1981). "Disseminated Saksenaea vasiformis infection". American Journal of Clinical Pathology. 76 (1): 116–21. doi:10.1093/ajcp/76.1.116. PMID 6942651.
  15. ↑ Lye, GR; Wood, G; Nimmo, G (November 1996). "Subcutaneous zygomycosis due to Saksenaea vasiformis: rapid isolate identification using a modified sporulation technique". Pathology. 28 (4): 364–5. doi:10.1080/00313029600169364. PMID 9007959. S2CID 22179099.
  16. ↑ Padhye, A.A.; Koshi, G.; Anandi, V.; Ponniah, J.; Sitaram, V.; Jacob, M.; Mathai, R.; Ajello, L.; Chandler, F.W. (February 1988). "First case of subcutaneous zygomycosis caused by Saksenaea vasiformis in India". Diagnostic Microbiology and Infectious Disease. 9 (2): 69–77. doi:10.1016/0732-8893(88)90099-5. PMID 3289825.
  17. ↑ Bearer, EA; Nelson, PR; Chowers, MY; Davis, CE (July 1994). "Cutaneous zygomycosis caused by Saksenaea vasiformis in a diabetic patient". Journal of Clinical Microbiology. 32 (7): 1823–4. doi:10.1128/jcm.32.7.1823-1824.1994. PMC 263809. PMID 7929783.
  18. ↑ HILL, BD; BLACK, PF; KELLY, M; MUIR, D; DONALD, WAJ MC (1 July 1992). "Bovine cranial zygomycosis caused by Saksenaea vasiformis". Australian Veterinary Journal. 69 (7): 173–174. doi:10.1111/j.1751-0813.1992.tb07509.x. PMID 1445086.
  19. ↑ Salas, Valentina; Pastor, F. Javier; Calvo, Enrique; Sutton, Deanna; García-Hermoso, Dea; Mayayo, Emilio; Dromer, Françoise; Fothergill, Anette; Alvarez, Eduardo; Guarro, Josep (1 October 2012). "Experimental murine model of disseminated infection by Saksenaea vasiformis: successful treatment with posaconazole". Medical Mycology. 50 (7): 710–715. doi:10.3109/13693786.2012.673137. PMID 22458251.
  20. ↑ Prabhu, R. M.; Patel, R. (March 2004). "Mucormycosis and entomophthoramycosis: a review of the clinical manifestations, diagnosis and treatment". Clinical Microbiology and Infection. 10 (s1): 31–47. doi:10.1111/j.1470-9465.2004.00843.x. PMID 14748801.
  21. ↑ Spellberg, B.; Edwards, J.; Ibrahim, A. (14 July 2005). "Novel Perspectives on Mucormycosis: Pathophysiology, Presentation, and Management". Clinical Microbiology Reviews. 18 (3): 556–569. doi:10.1128/CMR.18.3.556-569.2005. PMC 1195964. PMID 16020690.
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