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Nosocomial fungal infections
Nosocomial fungal infections are infections acquired in a healthcare setting. Candida species are a common cause of nosocomial fungal infections, with C. albicans being the most frequent cause. However, non-albicans Candida species are emerging as more drug-resistant species due to selective pressure from antifungal treatments. Catheter-associated urinary tract infections are a frequent type of nosocomial Candida infection, which can be difficult to diagnose due to the challenges differentiating colonization from true infection based on urine culture results alone.
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Nosocomial fungal infections
- 1. Nosocomial fungal infections Dr. ROUMI GHOSH PG,3rd Yr, MAMC, New Delhi
- 2. What’s meant byNosocomial infections or Healthcare-associated Infections ? • Comes from 2 Greek words. “Nocos”= disease + “komeion” =take care of • A localized or systemic condition 1) that results from adverse reaction in presence of an infectious agent(s) or its toxin(s) and 2) that was not present or incubating at the time of admission to the hospital or other health care facility. • Infection are considered nosocomial if they first appear 48 hrs or more after hospital admission without proven prior incubation or within 30 days after discharge. • This also includes occupational infections among staff of the facility and patient companions.
- 3. • Two specialsituations in which an infection is considered nosocomial: (a) infection that is acquired in the hospital but does not become evident until after hospital discharge (b) infection in a neonate that results from passage through the birth canal • But infection transplacentally (e.g., toxoplasmosis, rubella, cytomegalovirus, or syphilis), becomes evident after birth not considered nosocomial.
- 4. • There aretwo conditions that are not infections: 1)Colonization, presence of microorganisms (on skin, mucous membranes, in open wounds, or in excretions or secretions) not causing adverse clinical signs or symptoms. 2)Inflammation, a condition that results from tissue response to injury or stimulation by noninfectious agents, such as chemicals.
- 5. Factors associated withrising trend of nosocomial infections: • Crowded hospital conditions • Increasing number of people with compromised immune systems •New microorganisms •Increasing bacterial resistance
- 6. Why do nosocomialinfection occur? Presence of microbes in hospital environment Immunocompromised patients Transmission between staff and patients and among patients Nosocomial infection
- 7. Five major routesof transmission 1. Contact: Direct (person-person) Indirect (through an object) 2. Droplet 3. Airborne 4. Common vehicle 5. Vector borne The same organism may be transmitted by more than one route
- 8. • Variety offungi of medical importance were recovered from cockroaches (Blattella germanica) from hospital and residential area. Cockroaches (Blattella germanica) as carriers of microorganisms of medical importance in hospitals. R. FOTEDAR', U. BANERJEE SHRINIWAS' AND A. VERMA2. Epidemiol. Infect. (1991)t 107, 181-187 181. All India Institute of Medical Sciences, New Dehli 110029, India
- 9. Types of infections CAUTI 35% Surgicalwound infection 19% Central Line- associated Bloodstream Infection (CLABSI) 15% 12% others 5% Antibiotic associated diarrhea Catheter-associated Urinary Tract Infections (CAUTI) Pneumonia 14% In general 5–10% of patients develop nosocomial infections. Magnifies several folds depending on high risk patient population
- 10. Fungal infections accountfor 9% of all nosocomial infections. Wider use of aggressive modalities of treatments hematopoietic stem cell transplantation (HSCT) solid organ transplantation (SOT) new chemotherapeutic & broad spectrum antimicrobial agents immunomodulatory agents Increases immunocompromised patient population at risk for invasive fungal infection Incidence of infections in health care facilities by moulds risen dramatically in recent years more in developing countries.
- 11. Frequently identified riskfactors for fungemia in hospitalized patients • Antimicrobial agents: Number and Duration • Adrenal corticosteroid • Chemotherapy • Hematological/solid organ malignancy • Previous colonization • Indwelling catheter • Central venous catheter • Pressure transducer/Swan-Ganz • Total parenteral nutrition • Neutropenia (polymorphonuclear cells,500/mm3) • Extensive surgery or burns • Assisted ventilation • Hospitalization or intensive care unit stay • Hemodialysis • Malnutrition • Hospitalization during construction activity
- 12. The majority ofnosocomial fungal infections are caused by Candida spp. and Aspergillus spp.
- 13. EMERGING NOSOCOMIAL FUNGALPATHOGENS Yeasts Moulds Hyalohyphomycosis Aspergillus Mucormycotina Fusarium Acremonium Scedosprorium Pseudallescheria Paecilomyces Phaeohyphomycosis Exserohilum Cladophialophora Curvularia Alternaria Bipolaris Chaetomium Candida Trichosporon Rhodotorula Saccharomyces Malassezia Pichia Geotrichum Cryptococcus
- 14. YEAST & YEASTLIKE FUNGI
- 15. Candida Spectrum of diseasescaused: Catheter associated UTI (CAUTI) Catheter related blood stream infection (CRBSI) Antibiotic associated diarrhea And other disseminated diseases: arthritis, osteomyelitis, endocarditis, endophthalmitis, meningitis.
- 16. • C. albicansis the mc cause of invasive fungal infections in hospital settings (50% - 70%) • Emergence of non-albicans species due to selection pressure (overall 46%) • Global Antifungal Surveillance Program- C. albicans most common (63–70%) C. glabrata (44%), C. tropicalis (6%), and C. parapsilosis (5%). • Fluconazole resistance was noted in • C. krusei (78%) • C. glabrata (16%) • C. guilliermondii (11%)
- 17. Candida spp. causingnosocomial infections Candida species Affected patient population C. tropicalis bone marrow transplantation hematologic malignancies C. glabreta patients with solid tumors C. parapsilosis Parenteral nutrition Post-op endophthalmitis by contaminated iol-irrigating Sol C. krusei Hematologic malignancies, Granulocytopenia Having antifungal prophylaxis Others C. kefyr C. lusitaniae C. guilliermondii C. dubliniensis C. rugosa C. pelliculosa C. Lipolytica C. viswanathii C. nivariensis hematologic malignancies Catheter-related BSI can be acquired from hospital gardens or potted plants
- 18. Reservoirs and Modesof Transmission • Endogenous: • major reservoir: g.i. tract skin • through a breakdown in mucosal or epithelial tissue colonized flora is the source of infection • Strategies for prevention: decrease mucosal colonization decreased use of broad- spectrum antimicrobials • Exogenous: • contaminated infusates, • hands of health care workers • indwelling catheter • MC species isolated from hands of nurses was C. parapsilosis
- 19. Reasons for Candida’svirulence 1. Versatility in adaptation to various different habitats, and formation of biofilms. – C. albicans forms fungal biofilms most often, – non-albicans Candida species also, specially C. parapsilosis or C. tropicalis. 2. Secretion aspertyl proteinase (Sap): facilitate hyphal entry 3. Phenotypic switching: from budding yeast cells to hyphae or pseudohyphae reduce phagocytosis
- 20. Fluconazole Voriconazole AMP-BCaspofungin C glabrata Susceptible (dose dependent) to resistant Susceptible (dose dependent) to resistant Susceptible to intermediate Susceptibility Susceptible* C tropicalis Susceptible Susceptible Susceptible Susceptible* C parapsilosis Susceptible Susceptible Susceptible Susceptible to resistant* C krusei Resistant Susceptible (dose dependent) to resistant Susceptible to intermediate Susceptibility Susceptible Candida kefyr Susceptible Susceptible Susceptible Susceptible* C lusitaniae Susceptible Susceptible Resistant Susceptible* C dubliniensis Susceptible (71%) to resistant Susceptible(91%) Susceptible Susceptible Candida rugosa Very low activity Low activity Susceptible Susceptible C guilliermondii Low activity Susceptible Susceptible Susceptible
- 21. • C parapsilosis,C lipolytica, C lusitaniae, C glabrata and C tropicalis can cause breakthrough mycoses despite prophylactic or therapeutic use of echinocandins. • Reports of reduced susceptibility or resistance in – immunosuppression, – recurrent candidaemia, and – prolonged exposure to echinocandins. • Resistance to amphotericin B appears to be the hallmark of C. lusitaniae
- 22. Drug-resistant fungi newhospital menace Feb 4, 2013 • NEW DELHI: After the superbug, it might soon be the 'superfungi'. The organisms, known to be opportunistic pathogens causing infection in critically-ill patients, are fast turning drug-resistant. • A study by microbiologists at Ganga Ram Hospital revealed several new species of fungi, become difficult to treat even with most potent antifungal medicine, such as amphotericin B. • One particular species C. haemulonii, has also proved untreatable.
- 23. Catheter-associated UTI • 10-15%nosocomial UTI are due to Candida spp. • Always in a diagnostic dilemma whether contamination, colonization or true infection • No reliable methods of differentiating colonization or true UTI with Candida. • Candida infection is more common during extreme of ages. • Hematogenous spread is the most common route of renal candidiasis. • Ascending infection follows catheterisation, introduce peri-urethral commensal and allow migration into bladder along surface. • Risk of developing candemia following candiduria varies (2-50%).
- 24. • Risk factors: urinary tract instrumentation. (27% of all indwelling catheter associated UTI) Use of antibiotics> suppress endogenous flora> colonization by candida Previous surgical procudure Diabetes mellitus> glycosuria> increase fungal growth Predominant species isolated from our hospital: C. tropicalis (46%), C. albicans (30%),C. kefyr, C. krusei, C. sphaerica. In a recent study in GB Pant Hospital shows prevalence of 71.4% non-albicans Candida spp. causing UTI in ICU patients. Mixed isolates found in 10% of patients.
- 25. Diagnosis: Positive candida urine culture colonization Confirmby 2nd urine sample Check for pyuria Absent If colony count < 103 cfu/ml Rule out Candida infection Present Candida infection Localise anatomic site of infection Asymptomatic candiduria Candida cystitis Renal candidiasis > 10⁵ CFU/ml+ Urine sample from asymptomatic pts without indwelling catheter
- 26. Urine sample frompts long-term indwelling or intermittent catheters •Diagnosis of a UTI due to Candida species very difficult. •Pyuria or quantitative urine cultures for UTI of little use. Catheterisation low-grade Inflammation Presence of WBCs As few as 10⁴ cfu/mL may mean infection 2x10⁴-10⁵ cfu/mL may mean only colonization Many tried to co-relate with •presence of pseudohyphae •antibody-coated yeasts in the urine •casts containing yeasts
- 27. Diagnosis: • Collection ofsecond sample • Second sample collection after changing catheter or by suprapubic aspiration Helps to rule out contamination from perineal colonization or asymptomatic adherence on catheter or foreign bodies
- 28. Bundled Interventions toPrevent Urinary Tract Infections • Place bladder catheters only when absolutely needed, not solely for the provider's convenience. • Use aseptic technique for catheter insertion and urinary tract instrumentation. • Minimize manipulation or opening of drainage systems. • Ask daily: Is the bladder catheter needed? • Remove catheter if not needed.
- 29. Management: • Removal ofcatheter is strongly recommended as soon as possible. • Amphotericin B bladder irrigation highly effective for Candida cystitis • Oral fluconazole, 200 to 400 mg/day for 14 days. • In case of C. glabrata or C. krusei: Flucytocine shows excellent activity with high urinary concentration • Echinocandins poor glomerular filtration, not very useful. • High dose i.v. Ampho B or fluconazole recommended for pyelonephritis, but duration is not determined. • Nephrostomy tube can be used to administer high dose of drugs locally.
- 30. Blood stream infection: •In developed countries Candida species are 4th most common cause of BSI. • A study from Maulana Azad Medical College, found an incidence rate of 6.9% for Candida species in BSI. • Study from UCMS gave a prevalence rate of 18% for Candida species among blood culture isolates • AIIMS, New Delhi, found a prevalence rate of 6% for Candida species in a 5-year study (2001- 2005).
- 31. • C. albicans,most common species from BSI worldwide • Among the non-albicans species, C. glabrata has emerged as an important opportunistic pathogen worldwide. • It for 75% of cases of fungemia among patients receiving fluconazole as antifungal prophylaxis. • In India, C. tropicalis is now the most common cause of nosocomial candidemia. (67-90%). Mainly among hematologic malignancies. • C. parapsilosis found to be increasingly implicated in BSI after placement of intravascular devices and TPN infusion.
- 32. • Highest mortalitywas found among patients with C. krusei infection (52.9%) • C. parapsilosis infection had the lowest mortality rate of 23.7%
- 33. Diagnosis: • Most reliablediagnostic method of CRBSI: 1. Semiquantitative (roll plate) >15 cfu 2. Quantitative or (vortex or sonication methods) catheter culture techniques > 10²cfu + • For rapid diagnosis: use of acridine orange stains • Paired cultures of blood drawn through the iv catheter and percuteneous 1. CFU from CVS 5–10-fold greater 2. Positive culture form CVS at least 2 h earlier signs of local or systemic infection
- 34. Bundled Interventions" toPrevent Common Health Care– Associated Infections • Prevention of Central Venous Catheter Infections: 1) Educate personnel about catheter insertion and care. 2) Use chlorhexidine to prepare the insertion site. 3) Use maximal barrier precautions during catheter insertion. 4) Consolidate insertion supplies (e.g., in an insertion kit or cart). 5) Use a checklist to enhance adherence to the bundle. 6) Empower nurses to halt insertion if asepsis is breached. 7) Cleanse patients daily with chlorhexidine. 8) Ask daily: Is the catheter needed? Remove catheter if not needed or used.
- 35. • New 2011CDC guidelines has announced new guidelines to reduce the risk of catheter- associated infections. • The guidelines now designate treatment with chlorhexidine gluconate-impregnated sponge
- 36. Prevention and Therapy •Removal of Central i.v. catheters in patients with candidemia • I. V. AmB or fluconazole, continued for 14 days after blood cultures have yielded no yeast • Patients with candidemia and metastatic foci (eg, eye, bone, heart, liver, spleen) require a longer duration of therapy. • Prophylactic fluconazole among selected leukemia or bone marrow transplant patients effective for all except C. krusei • Posaconazole or echinocandins are preferred for the initial treatment if C. glabrata or C. krusei is identified or suspected
- 37. Antibiotic-associated diarrhea: • Patientsreceiving longterm antimicrobial agents commonly develop a secretory non- bloody diarrhea C. difficile toxin-negative evidence of intestinal overgrowth of Candida spp. • A study from our department reported yeast from 26.7% of nosocomial diarrhea cases. • Respond to oral nystatin therapy • Stoppage of persistent use of intravenous antimicrobial agents
- 38. Trichosporon species: T. asahii,T. mucoides, T. asteroides • Most common non-candidal yeast infection in hematologic cancer patients with mortality >80%
- 39. Trichosporon species: T.asahii, T. mucoides, T. asteroides • Causes superficial infection of hair shafts, white piedra. • Trichosporonosis (bloodstream infections, severe skin infections, endocarditis, peritonitis), becoming more common in hospitalized patients. • Catheter related fungaemia, occur as a breakthrough invasive infection on antifungal therapy with high mortality. • Endophthalmitis after cataract extraction, endocarditis following prosthetic cardiac valves insertion also reported. • Because of shared Ag with the capsule of Cryptococcus neoformans, a positive cryptococcal latex test can occur in patients with trichosporonosis.
- 40. • Abundant pseudohyphae, •arthroconidia • Numerous spherical to oval budding blastoconidia from both corner of arthroconidia • “Rabbit ears” appearence
- 41. Fluconazole Voriconazole AMP-BCaspofungin Flucytosine Trichosporon asahii Low activity Susceptible Resistant Resistant Resistant Trichosporon beigelii (cutaneum) Low activity Low activity Resistant Resistant Resistant Anifungal sensitivity •Clinical and in-vitro studies, suggest that azoles, especially voriconazole and posaconazole, have greatest effectiveness against Trichosporon. spp
- 42. Rhodotorula species: R.mucilaginosa • In immunocompetent patients: • Endophthalmitis • Peritonitis (continuous ambulatory peritoneal dialysis) • Overall mortality from rhodotorula fungaemia is 15%. •Previously regarded as non-pathogenic. •Emerged as opportunistic pathogens •Most cases of rhodotorula infection are fungaemia associated with catheters, endocarditis, and Meningitis.
- 43. Fluconazole Voriconazole AMP-Bflucytosine Caspofungin Rhodotorula species Very low activity Variable susceptibility / very low activity Susceptible Susceptible Resistant • Rhodotorula species, often resistant to fluconazole and voriconazole. • Amphotericin is the antifungal agent of choice for treatment of rhodotorula infections. Anifungal sensitivity
- 44. Malassezia species: M.furfur and M. pachydermatis • Causative agent of Pityriasis versicolor and seborrhoeic dermatitis • Frequently observed as nosocomial pathogens in recent times. • Causes invasive infections especially in NICU patients. • Central line used for infusion of the lipid emulsion tend to grow M. furfur from LBW neonate and adult patients Globose, oblong-ellipsoidal to cylindrical yeast cells with broad base budding from the same site at one pole (unipolar) • Unable to synthesize long-chain fatty acids and requires exogenous lipid for growth
- 45. • Detection enhancedby growing the specimen on Sabouraud agar covered with a thin layer of sterile olive oil (lipophilic) • Alternatively to use specialized media like Dixon's agar which contains glycerol mono-oleate • Removal of the catheter and cessation of lipid infusion main stay of treatment • Systemic antifungal treatment with ampho B, ketoconazole, itraconazole, voriconazole reserved for persistent infection
- 46. Pichia anomala (Hansenulaanomala) • P. anomala first reported as pathogen in nosocomial outbreak among 379 neonates in Chandigarh (Chakrabarti et al 2001)- fungemia, interstitial lung disease, endocarditis, enteritis • Fungaemia associated with a CVC is most common, mainly among neonates and ICUs. • Later outbreak reported in paediatric ICU in Brazil in 2005 Saprophytes in environment, also found In milk, cheese, yoghurt production of one to four hat-shaped ascospores
- 47. Fluconazole Voriconazole AMP-BCaspofungin P anomala Fluconazole: low activity; itraconazole: very low activity Susceptible Susceptible Susceptible •In vitro, amphotericin, fluconazole, voriconazole, and caspofungin have activity against P anomala, although high drug concentrations required for inhibition; •itraconazole is poorly active against this yeast.
- 48. Saccharomyces cerevisiae: • Useof live yeast capsules (Saccharomyces boulardii), taken for prevention of Clostridium difficile associated diarrhoea, leads to Fungaemia. • Patients at risk:-in ICU,with CVC - had broad spectrum antibiotics • Very few data are available for drug efficacy, • amphotericin and voriconazole seem to be active in vitro. Probiotic!!
- 49. Cryptococcus neoformans • Nosocomialtransmission quite rare. • Pulmonary cryptococcosis case Direct inhalation 2ndry infection in close contact • Needlestick injury localized cuteneous cryptococcal granuloma in lab worker • Proper sterilization hospital equipment mandatory. Also...
- 50. Principal Criteria andTests for Identifying Yeasts 1. Culture characteristics - Colony color, shape, texture 2. Asexual structures: a) Shape and size of cells b) Bipolar, fission, multipolar or unipolar "budding" c) Absence or presence of arthroconidia, ballistoconidia, blastoconidia, clamp connections, endoconidia, germ tubes, hyphae, pseudohyphae, or sporangia and sporgangiospores. 3. Sexual structures - Arrangement, cell wall ornamentation, number, shape and size of ascospores or basidiospores 4. Physiological studies a) Sugar Assimilation b) Sugar Fermentation c) Cycloheximide resistance d) Tetrazolium reduction test e) Diazonium Blue B test f) Nitrogen utilization g) Urea hydrolysis h) Temperature studies i) CHROME Agar
- 51. YEAST MORPHOLOGY Brown toblack colony Direct Mount Yeast only Phaeococcomyces Yeast and hyphae Aureobasidium Exophiala Wangiella Pink to red colony Satellite colonies Present Forcibly discharged conidia Sporobolomyces Absent Urease+ Capsule+ Inositol- Rhodotorula White, creamy colony Germ Tube Test Positive C albicans C dubliensis Negative Other Candida Moist mycelial colony Direct Mount Arthroconidia Blastoconidia Trichosporon Geotrichum
- 52. If Germ Tubetest Negative Corn Meal Agar or Rice Starch Agar Incubate at 25 C X 2-3 days Only yeasts present Hypae, Pseudohypae Or both present C. Glabrata C. Famata Cryptococcus Rhodotorula Ascomycetous yeasts
- 53. Chlamydospore present (thick wall,refractile, round) Single, terminal Chlamydospore Terminal, cluster of Chlamydospore C. albicans C. dubliensis Arthroconidia present Blastoconidia present Trichosporon Rabbit ears” appearence Geotrichum “Hockey stick” appearence No Chlamydospore No Arthroconidia Other Candida Saccharomycec Pichia Malassezia Hypae, Pseudohypae Or both present Ascospore + On Malt extract agar Or Na-acetate agar At 25 C Ascospore are acid fast Spaghetti & meat ball app
- 54. Candida species Identification C.albicans C.dubliniensis C.glabrata C.krusei C.kefyr C.parapsilosis C.tropicalis C.guilliermondii C.famata C.lipolytica Chlamydospore+ + - - - - - - - - Germ tube + + - - - - - - - - Pellicle On broth + + Urease + + Fermentation Glu Mal Suc Lac Gal Tre F F - - F F F - - F F F - - - - F F - - - - - F - F F F - F - - - - - F F F - F F F - F - F F W - W - - W - - - - - - Assimilation Glu Mal Suc Lac Tre + + + + + + + - - - + - - - + + - - - - + - + + - + + + - + + + + - + + + + - + + + + + + + - - - -
- 55.
- 56. ASPERGILLUS SPECIES • Sourcesof Aspergillus spores in the hospital air: – Inadequate filtration of outside air or malfunctionning of ventilation – Dust and places infrequently cleaned – Vacuum cleaning – Plants, flowers, etc. – Periods of hospital constructions, renovations, demolition 56 No uniform definition of nosocomial aspergillosis till now, due to unknown incubation period of invasive aspergillosis Working definition: invasive disease occurs after 1 week of Hospitalization or within 2 weeks of hospital discharge
- 57. Common Aspergillus spp.causesnosocomial infection Aspergillus fumigatus Aspergillus flavus Aspergillus terreusAspergillus nidulans
- 58. Predisposing host factors •autologous bone marrow transplants • graft versus host disease • solid organ transplants • Acute leukemia, myelodyaplastic syndrome, aplastic anaemia • Advanced AIDS (reduced CD4 cell count < 100) • Chronic granulomatous disease • Pre-existing structural lung diseases (emphysema, COPD, cavitory tuberculosis) Immunosuppressive therapy Defective NADPH oxidase Co-existing diabetes, malnutrition, Steroid therapy Severe long term granulocytopenia. Chemotherapy & underlying hematologic disease 1,000/mm3
- 59. Clinical Diseases • Predominately(77%)respiratory and includes necrotizing bronchopneumonia • Postcardiac surgery endocarditis • Surgical site Infection (5%): Burn wound, aortic graft sites, peritoneal catheter sites (use of dressings contaminated with spores) • Cutaneous infections associated with the use of arm boards for patients with iv catheters
- 60.
- 61. Diagnosis • Chest radiograph:single or multiple rounded densities • Histopathology: tissue invasion by fungal hyphae in skin or lung biopsy specimens confirm diagnosis. • Culture from bronchoalveolar lavage, sputum, or endotracheal aspirates: may represent colonization, but in conjunction with a clinical diagnosis, positive cultures probably indicate pulmonary aspergillosis • Blood cultures are very insensitive for detecting Aspergillus spp. • Role of routine surveillance cultures of immunocompromised patients has not been well established.
- 62. • Rapid Antigendetection: Galactomannan, Cell-wall polysaccharide specific to Aspergillus species, correlate with clinical diagnosis and response to antifungal therapy. Immune complexes dissociation(Heat, Acid, Alkali) and use of monoclonal antibodies increases sensitivity A sandwich ELISA, most sensitive methods currently available to detect galactomannan (0.5 to 1.0 ng per ml of serum).
- 63. Management: • Until recentlyAmpho B considered gold standard drug for invasive pulmonary aspergillosis. • Now Voriconazole is used as 1st line therapy (ASM & I D S A g u i d e l i n e s) • Empirical antifungal therapy: with AMB, itra, vori, or caspofungin recommended for high-risk patients with prolonged neutropenia who remain persistently febrile despite broad-spectrum antibiotic therapy. not for patients, have short durations of neutropenia (<10 days)
- 64. PREVENTION AND CONTROL •CDC has published revised recommendations for preventing nosocomial pulmonary aspergillosis • Interrupt Transmission of Aspergillus sp. Spores: 1) maintenance of a) HEPA filtration (99.97% efficient in filtering particles >0.3um), b) directed room airflow, c) positive air pressure in patients' rooms relative to the air pressure in the corridor, d) properly sealed rooms, and e) high rates of room-air changes (100-400/hr) 2) Minimize exposures of high-risk patients to potential sources of Aspergillus sp. (e.g., hospital construction and renovation, cleaning activities, carpets, food, potted plants, and flower arrangements) 3) Collect environmental samples from potential sources.
- 66. Mucormycotina Recent rising incidencedue to continued rise of diabetics, increased use of immunosuppressive agents and Voriconazole a broadspectrum antifungal as prophylaxis
- 67. Epidemiology Developed countries • thedisease is still a rare finding • mostly seen in patients with • haematological malignancies undergoing chemotherapy, • in bone marrow transplant recipients, • in patients receiving voriconazole therapy or prophylaxis. Developing countries • Increasing number of mucormycosis cases • occurring commonly in patients with uncontrolled diabetes • Cases are also seen in patients with haematological malignancies or in transplant recipients In India, more than 30 million poorly compliant diabetics, at risk of developing opportunistic mucormycosis
- 68. • Modes ofinfection: 1) Aerosolization of the spores > tissue invasion via the respiratory tract (in most patients). 2) acquisition is through disrupted skin(trauma and burn) 3) Ingestion of contaminated foodstuffs • Risk factors : 1) poorly controlled diabetes mellitus, 2) Hematologic malignancies (especially with neutropenia), 3) solid-organ or hematopoietic stem cell transplant (HSCT), 4) Deferoxamine therapy for iron or aluminum overload 5) burn wounds 6) corticosteroid therapy. • The most dramatic presentations are in patients with diabetic ketoacidosis, tend to have rhinocerebral (rather than pulmonary) mucormycosis.
- 69.
- 70. • Poor infectioncontrol practices associated with injury mode of entry of mucormycetes in hospital. • Interestingly from India many cases of cutaneous mucormycosis were reported at the site of intramuscular injection • Very disturbing and indicates poor medical care practices in developing countries. • It may be gradual and slowly progressive or may be aggressive and fulminant leading to necrotizing lesions and haematogenous dissemination. • Outbreak of gastrointestinal zygomycosis due to contaminated food and drugs or even tongue depressor.
- 71. • Patients witha dual mycotic infection, i.e. Aspergilllus and a mucormycete, are not uncommon. • Rhizopus oryzae is commonest • Apophysomyces and Saksenaea can initiate invasive disease in apparently normal hosts who have sustained penetrating trauma during accidents. • After the tsunami disaster in 2004, victims were found to be infected with Apophysomyces in Sri Lanka and Thailand
- 72. • The biopsyspecimen should be taken from the centre of the lesion especially from black eschar area and include subcutaneous fat, as frequently invade blood vessels of the dermis and subcutis. Irregular, broad, ribbon-like, (6-50 microns in width) Hyphae, usually devoid of septae, to invade blood vessels
- 73. Rapidly grownon agarin gray-white, brown cottony or wooly colonies Sporangiophores may be septate Columella and rhizoids, shape of the apophysis important in genus identification
- 74. Apophysomyces elegans: • isan emerging zygomycete in India distinctive funnel- or bell-shaped apophyses, hemispherical-shaped columellae, a conspicuous pigmented sub-apical thickening which constricts the lumen of sporangiophore below the apophysis, and distinctive foot cells.
- 75. Saksenaea vasiformis flask-shaped Sporangiawith a distinct spherical venter and long-neck, darkly pigmented rhizoids. Sporangiospores discharged through the neck following the dissolution of an apical mucilaginous plug. •Sporulate rarely on routine media •Difficult to differentiate from Apophysomyces
- 76. • A specialnutrient deficient growth medium (Czapek Dox agar, cornmeal-glucose-sucrose-yeast extract agar), high temperature and prolonged incubation may be used to induce sporulation. •By using the agar block method described by Ellis and Ajello (1982). a small block of agar is cut from a well established culture grown on PDA and is placed in the centre of petri dish containing 1% distilled water agar. After 21 days at 26°C look for sporangium formation at the periphery of the petri dish.
- 77. Management • Rapid diagnosis:Diagnosis at the early stage is desirable as the mortality 83- 94% in disseminated disease. • Remove or reduce risk factors: • rectifying diabetic ketoacidosis, • withdrawing desferrioxamine therapy • reducing the level of immunosuppression. • Antifungal therapy and surgical debridement: • Till date Amphotericin B is the only drug effective. • Posaconazole as a substitute gaining popularity in recent years • fluconazole, voriconazole, flucytosine and the echinocandins have no efficacy. • The best management for cutaneous zygomycosis is extensive surgical debridement combined with antifungal. • Adjunctive therapies: hyperbaric oxygen (HBO) treatment
- 78. Bundled Interventions" toPrevent Common Health Care– Associated Infections • Prevention of Surgical-Site Infections: • Choose a surgeon wisely. • Administer prophylactic antibiotics within 1 h before surgery; discontinue within 24 h. • Limit any hair removal to the time of surgery; use clippers or do not remove hair at all. • Prepare surgical site with chlorhexidine- alcohol. • Maintain normal perioperative glucose levels (cardiac surgery patients). • Maintain perioperative normothermia (colorectal surgery patients).
- 79. Fusarium species: • Disseminatedinfections among severely immunocompromised patients • Postoperative endophthalmitis and peritonitis associated with continuous ambulatory peritoneal dialysis (CAPD) • Local invasive infection of wound, burn, ulcer. • Diagnosis is usually made by culture of biopsy specimens or other normally sterile sites. Hyaline, 2- to several-celled, fusiform- to sickle-shaped macroconidia, with an elongated apical cell and pedicellate basal cell
- 80. Clinical manifestations similarwith disseminated aspergillosis except • Associated with concomitant cellulitis or subcutaneous lesions • More readily isolated from cultures of blood than are Aspergillus spp. • Resistance to Amphotericin B leads to treatment and prevention failure
- 81. Clinical manifestations similarwith disseminated aspergillosis, except • Associated with concomitant cellulitis or subcutaneous lesions • More readily isolated from cultures of blood than are Aspergillus spp. • Resistance to Amphotericin B leads to treatment and prevention failure Microscopically similar fungal species Cylindrocapron: Chlamydospore +ve Acremonium: microconidia in early stage of culture
- 82. Management: • Recovery fromunderlying neutropenia is main stay of treatment. • Voriconazole and Posaconazole effective. • Combination of caspofungin with amphotericin B showed synergistic to additive effect.
- 83. Acremonium species: A.kiliense, A. strictum •Endophthalmitis following cataract surgery as colonize soft contact lenses long awl-shaped phialides producing cylindrical, one-celled conidia, mostly aggregated in slimy heads at the apex of each phialide •Rarely disseminated infections in immunosuppressed patients Fluconazole was shown to be completely inactive against Acremonium in vitro •Recurrent cutaneous infection in renal transplant cases Drug of choice is Ampho B
- 84. Paecilomyces lilacinus • Associatedwith intrinsic contamination of a neutralizing solution for synthetic intraocular lenses, resulting postoperative endophthalmitis
- 85. Scedosporium prolificans: • Outbreaksreported in patients with leukemia undergoing chemotherapy (anti-TNFα ) • Scedosporium is generally resistant to all available antifungal agents. • Infection associated with nearly 100% mortality • A Case of Scedosporium Prolificans Osteomyelitis in a Child reported from our department, Misdiagnosed as Tubercular Osteomyelitis single-celled, clavate to ovoid conidia, borne singly or in small groups on elongate conidiophores or laterally on hyphae
- 86. Pseudallescheria boydii • Anascomycete (anamorphs are Scedosporium apiospermum and Graphium) • corneal ulcers, endophthalmitis, otitis externa, sinusitis, pneumonia, and many invasive infections in immunocompromised hosts • commonly resistant to amphotericin B but susceptible to miconazole and newer azoles
- 87. Phaeoid/ Dematiaceous/ Melanizedfungi • dark pigmentation due to presence of dihydroxynaphthalene melanin in their cell walls • Ubiquitous saprobes, often considered contaminants • Curvularia spp, isolated from saline-filled breast implants, resulting from contamination of saline stored beneath a water-damaged ceiling. • Cladophialophora bantiana causes cerebral pheohyphomycosis
- 88. • Exserohilum dermatitidis,recently causes fatal meningitis outbreak after use of contaminated injection •closely resemles Bipolaris •strongly protruding truncate hilum (i.e. exserted hilum)
- 89. Pneumocystis jiroveci • Recentreports of possible person-to-person airborne transmission of infection suggested by PCR testing. • Close contacts of HIV+ patients with Pneumocystis pneumonia, including HCWs • Outbreaks particularly among renal transplant recipients • But specific isolation of hospitalized patients with Pneumocystis pneumonia still not recommend. • For Prevention: trimethoprim-sulfamethoxazole prophylaxis is recommended for HSCT and SOT recipients especially the first 100 days after transplantation.
- 90. Isavuconazole • a newand promising antifungal triazole for the treatment of invasive fungal infections • currently in Phase III clinical trial
- 91.