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maduramycosis
This document provides information about Maduramycosis, also known as Madura foot or mycetoma. It is a chronic fungal or bacterial infection that enters through the skin, usually on the foot, and causes swelling, draining sinuses, and grain-like structures. It is most common in tropical areas and affects adult males. Diagnosis involves examining these grains microscopically and through cultures. Treatment involves long-term antifungal medications for fungal causes or antibiotic regimens for bacterial causes. Surgery may be needed for extensive or bone-involved cases. Prevention focuses on protecting the feet from minor skin trauma.
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maduramycosis
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- 2. HISTORY Gill first describedthe disease in Madura District - India in 1842. Hence the name Madura foot/Madura mycosis.
- 3. DEFINITION • Madura footor mycetoma • Chronic Slowly Progressive post traumatic infection of subcutaneous tissue usually occurring in foot and rarely in other parts of the body • Caused by fungi and bacteria
- 4. EPIDEMIOLOGY • Overall actinomycetomais more common (60%)than eumycetoma(40%). • More common in tropics and subtropics. • In India maximum no of mycetoma cases reported in Rajasthan Followed by Tamilnadu. • Adult male are usually affected. • Maximum incidence 21 to 40 yrs of age. • Male :female ratio – 3:1to5:1
- 5. CAUSES Eumycetoma Madurella mycetomatis, Madurella grisea, Scedosporium, Aspergillus, Fuscarium. Actinomycetoma(filamentous bacteria) Streptomyces, Nocardia. Botryomycosis Staphylococcus aureus. •
- 6. PATHOGENESIS • Organism enterthrough minor trauma in farmers(thorn prick, contaminated soil, walking with barefoot) • Begins – small subcutaneous swelling of the foot. • Enlarge – burrowing into deeper tissue and tracking to the surface as multiple discharging sinuses(viscid seropurulent fluid containing granules).
- 7. CLINICAL FEATURES • Triadof mycetoma ; Tumour like swelling(tumefaction), Discharging sinuses, Granules.
- 8. CONTD • Start withmultiple hard deep seated and fixed papule&nodule soft at centre and form abscess. • Abscess rupture – persistently draining fistula. • Because of very slow extension – infection spread involving tendons bone, muscles proximally toward the ankle upto leg. • Skin may be hypo/hyperpigmented with sign of both healed and active sinuses. • Swelling is often firm non tender overlying skin is not erthyematous. • Extension to underlying bone give rise to periostitis ostemyelitis Arthritis.
- 9. LAB DIAGNOSIS • Granulesand grains are microcolonies of causative agent. • Look for colour and consistency of grains(macroscopic). • In actinomycotic-grains composed of very thin (less than 1um in diameter) GRAM STAIN. • Mycotic lesion-broader and often show septae and chlamydospores(2-6um width) KOH mount. • Culture-granules obtained from biopsy best suitable for culture. • Fungal(SDA) bacteria (lowenstein jensen media).
- 10. • Histopathological staining.Of granules. • eumycetoma-granulomatous relation with palisade arrangement of hyphae and cement substance. • actinomycetoma-show granulomatous reaction with filamentous bacteria.
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- 12. DIFFERENTIATING FEATURES CLINICAL MANIFESTATIONEumycetoma Actinomycetoma Tumour Single well defined margin Multiple tumour mass with ill- defined margin Sinuses Appear late few in number Appear early numerous with raised inflamed openings Discharge /granules Serous /blackish/white Purulent/white /red Bone Osteosclerotic Osteolytic
- 13. RADIOLOGIC FEATURE • Earlystage—soft tissue granuloma appear as soft tissue shadow with calcification and obliteration of facial plane. • Bone scalloping from external pressure seen. • Periosteal reaction seen. • Late stage-punched out cavities after multiple may appear that have well defined margin. • Actinomycetic-cavity small numerous with no defined margin (moth eaten appearance).
- 15. • Usg-differentiate themycetoma from osteomyelitis tumour. • Eumycetoma-sharp hyperechoic focus. • Actinomycetoma-fine hyperechoic focus. • MRI-dot in circle sign.
- 16. COMPLICATION • Secondary bacterialinfection, • Local abscess formation, • Cellulitis • Bacterial and tubercular osteomyelitis, • Septic death, • Lymphoedema.
- 17. TREATMENT • It’ isimportant to characterise the etiological agent to determine the nature of infection whether it is bacteria or Fungal and to evaluate the extent of this disease. • Specific therapy depend upon the identification of causative agent and determination of drug sensitivity. • Therapy should be continued for several month after clinical cure to prevent release. • Generally eumycetoma has lesser successful rate than actinomycetona.
- 18. TREATMENT • Eumycetoma –antifungal drug. • ketoconazole400mg/day. • Itraconazole 200 – 500mg/day. • Amphotericin50mg/kg iv daily. • Actinomycetoma-Welsh regimen. • Amikacin +clotrimazole. • Isolated case treated with voriconazole200mgpoBD for several month combined with posaconazole400mg bid. • Therapy suggested for one or two years for complete eradication unless adverse effect Warrant the cessation of medication.
- 19. SURGERY • Excision ofthe affected tissue. • Localised mycetoma-can be excised completely without Residual disability. • Healthy tissue removed – to prevent recurrence. • Extensive surgery-followed by skin grafting (cover large open area). • Extensive bone involvement – surgical amputation.
- 20. PREVENTION • It isbest accomplished by impacting on the incidence of the traumatic inoculation of causative agent. • Wearing of shoes and clothing to protect against the splinter and thorn prick should be stressed. • Complication can be prevented by Early identification and treatment of lesion usually with minor surgery and chemotherapy.
- 21. REFERRENCE Tureks orthopaedics Varshney –essential orthopaedics
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