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Mucormycosis
Mucormycosis is a rare but aggressive fungal infection caused by fungi of the class Zygomycetes, including Rhizopus, Mucor, and Absidia. It mainly affects immunocompromised patients or those with uncontrolled diabetes. The fungi thrive in high glucose, acidic conditions. Common forms include rhinocerebral affecting the sinuses and orbit, pulmonary, gastrointestinal, cutaneous from skin injuries, and disseminated infection of multiple organs. Diagnosis involves tissue biopsy and culture. Treatment requires intravenous amphotericin B antifungal therapy and surgical debridement of infected tissues.
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Mucormycosis
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- 2. Mucormycosis • Mucormycosis isan uncommon but aggressive opportunistic fungal infection that afflicts patients with severe underlying immunosuppression, uncontrolled hyperglycemia and/or ketoacidosis, patients with iron overload resulting from frequent blood transfusions or blood disorders and occasionally healthy patients who are inoculated with fungal spores through traumatic injuries. • a/w high mortality
- 3. • third mostcommon cause of invasive fungal infections following Aspergillosis and Candidiasis with an increase of mucormycosis in the adult population and in infants less than 1 year old
- 4. Zygomycosis or mucormycosis •Fungi of class zygomycetes • Rhizpous or mucor or absidia • These fungi form aseptate or coenocytic hyphae. • They reproduce sexually by zygospore formation • They reproduce asexually by sporangiospore formation. • Predisposing factors • Leukemia/lymphoma/metabolic acidosis/DM
- 5. • thermo-tolerant • growingon decaying organic matter
- 6. RHIZOPUS RHIZOIDS ARISE OPPOSITE SPORANGIOPHOREIN RHIZOPUS ABSIDIA RHIZOIDS ARISE IN TERNODAL
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- 8. MUCOR NORHIZOIDS
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- 10. • Mucor areubiquitous in nature and can be found on decaying vegetation and in the soil. These fungi grow rapidly and release large numbers of spores that can become airborne
- 11. • The morphologyshows aseptate/pauci septate broad (3–25 μm), ribbon-like, hyaline hyphae with irregular or right angle branching
- 12. Growth of theFungus Role of Iron Acquisition of Iron by Using Siderophores Hemoglobin as a Source of Iron Evasion of Host Defenses Resistance to AntifungalAgents
- 13. ketone reductase • Rhizopusorganisms have an enzyme, ketone reductase, which allows them to thrive in high glucose, acidic conditions. Serum from healthy individuals inhibits growth of Rhizopus, whereas serum from individuals in diabetic ketoacidosis stimulates growth
- 14. CF • Rhinocerebral • Seriousfuminating infection / angioinvasive /thrombosis/ischemic necrosis of tissues • Pulmonary / gastrointestinal/disseminated/ dermal/ sc
- 15. • Specimen tissue biopsy • Staining • H& E best • Aseptate hyphae irregular branching of hyphae at OBTUSE angle • Culture • SDA @37*c • Dense hairy colony with aseptate hyphae sporangiophore and sporangiospores
- 18. Risk factors • Diabetesmellitus, particularly with ketoacidosis • Treatment with glucocorticoids • Hematologic malignancies • Hematopoietic cell transplantation • Solid organ transplantation • Treatment with deferoxamine • Iron overload • AIDS • Malnutrition • Injection drug use These risk factors impair host defenses and permit growth and dissemination of fungus resulting in invasive disease
- 19. • The individualsat highest risk of developing invasive disease are those who have decreased numbers (quantitative defects) of mononuclear and polymorphonuclear phagocytes as in neutropenia or who have diseases that impair the function (qualitative defects) of phagocytes as in hyperglycemia/ acidosis or administration of glucocorticoid
- 21. Coronavirus disease 2019-associated •but the relationship of these two infections is unclear
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- 23. Host Defenses • intactskin/mucosal barrier and innate immunity • mucus layer of sinus/lung has anti-microbial properties and poor in nutrients • nutrient immunity of mucosa and skin • host keeps the essential nutrient iron firmly bound to the serum proteins to restrict access to pathogens in a process called nutrient immunity and keeps an iron poor environment as a defense strategy against fungal invasion • Mononuclear cells • Tissue macrophages phagocytose the inhaled spores and kill them
- 26. Altered Host Factors •Neutropenia and immunosuppression • hamper the host defenses and allow growth of the fungus • Administration of corticosteroids impairs host’sability to prevent germination of spores, whereas exposure to voriconazole makes the organism highly virulent, possibly due to an epigenetic modification
- 28. • exposure tovoriconazole makes the organism highly virulent, possibly due to an epigenetic modification
- 30. • In healthyindividuals, cilia transport these spores to the pharynx and they are cleared through the gastrointestinal tract. In susceptible individuals, infection usually begins in the nasal turbinates or the alveoli
- 32. • The sporesenter the body by • I. inhalation • II. ingestion of contaminated food • III. implantation in injured skin by trauma/burns/surgery, or • IV. percutaneous route by contaminated needles or catheters
- 34. • Inhaled orinoculated Mucorales spores elicit a robust inflammatory response in healthy hosts
- 35. Rhinocerebral Mucormycosis • Mostcommon form • diabetic ketoacidosis/uncontrolled diabetes is the most common risk factor • Acquired by inhalation of spores
- 37. • The hallmarksof spread beyond the sinuses are tissue necrosis of the palate resulting in palatal eschars, destruction of the turbinates, perinasal swelling, and erythema and cyanosis of the facial skin overlying the involved sinuses and/or orbit
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- 43. Diagnosis of Rhino-orbital-cerebralinfection • Endoscopic evaluation of the sinuses should be performed to look for tissue necrosis and to obtain specimens.
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- 46. Diagnosis of Pulmonaryinfection • radiographic evidence to support the diagnosis • Chest radiographs or CT scans • demonstrate focal consolidation, masses, pleural effusions, or multiple nodules • halo sign (ground-glass attenuation surrounding a nodule) is characteristic of angioinvasive fungi, • reversed halo sign, a focal area of ground-glass attenuation surrounded by a ring of consolidation
- 47. Gastrointestinal mucormycosis Stomach isthe most common site of involvement, followed by colon and ileum, though any part of the gastro intestinal tract may be involved. It may also involve liver, spleen, and pancreas
- 49. • In prematureneonates, it causes necrotizing enterocolitis whereas in neutropenic patients, it forms mass lesions. Microscopically, it shows angioinvasion leading to hemorrhage, gangrene, perforation, and peritonitis
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- 51. cutaneous mucormycosis • cutaneousmucormycosis is almost always associated with trauma or wounds. The entry of the fungi into the dermis can result from seemingly innocuous insults, such as the entry site for an intravenous catheter, spider bites, and insulin injection sites
- 52. • Majority ofthe patients are immunocompetent who have disruption of skin barrier due to injury • Patients have necrotic eschar, ulcer, or fasciitis • It is locally invasive with involvement of subcutaneous tissue, adipose tissue, muscle, and fascia • Involvement of vessels may lead to hematogenous dissemination to other organs and skin may be involved secondarily in disseminated disease. Necrosis with suppurative inflammation and infarction may be seen
- 54. Disseminated Mucormycosis • Itinvolves two or more noncontiguous organs and lung is the most common organ involved. Patients with iron overload and severe immunosuppression develop disseminated disease • The infection may spread from lung, GIT, or skin to other organs by hematogenous dissemination. Microscopically, angioinvasion with hemorrhagic infarcts and necrosis are seen
- 55. Uncommon Forms ofMucormycosis • Intravenous drug use is the most common risk factor. • The involvement may be osteomyelitis, pyelonephritis, endocarditis, peritonitis, or focal involvement of any organ
- 56. Diagnosis • identification oforganisms in tissue by histopathology with culture confirmation • Serum tests, such as the 1,3-beta-D-glucan assay and the Aspergillus galactomannan assay • polymerase chain reaction (PCR)-based techniques on histologic specimens
- 58. Rx • Intravenous (IV)amphotericin B (lipid formulation) is the drug of choice for initial therapy • Posaconazole or isavuconazole is used as step-down therapy for patients who have responded to amphotericin B
- 60. • Surgery —Aggressive surgical debridement of involved tissues should be considered as soon as the diagnosis of any form of mucormycosis is suspected. Surgical intervention with removal of necrotic tissue and debulking infection has been associated with improved survival in anecdotal clinical reviews of rhinocerebral and pulmonary infection
- 61. Infection in immunocompetentindividual causes • skin injuries, burns, trauma • natural calamities like tornadoes, tsunami, volcanic eruption • combat-related injuries • contaminated bandages, tongue depressors • injection drug use • prolonged hospital stay
- 62. Combat-associated • Usually inmilitants in Afghanistan
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