Dimorphic Fungal Infections

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Dimorphic Fungal Infections

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Dimorphic Fungal Infections

  1. 1. DIMORPHIC FUNGI BASICS DR.T.V.RAO MD10/22/2011 1Dr.T.V.Rao MD
  2. 2. DIMORPHIC FUNGUS CAUSE SYSTEMIC MYCOSISDeep seated fungalinfectionsInhalation of air bornespores produced by casualmouldsPresent as saprophytes insoil and on plant materialThey are caused byDimorphic fungiOccurs mainly Americancontinent.10/22/2011 2Dr.T.V.Rao MD
  3. 3. IMPORTANT FUNGI IN SYSTEMIC MYCOSISCoccidioidomycosis.HistoplasmosisBlast mycosisParacoccidioidomycosis.Others can also manifest withsystemic infection ( Not Dimorphic ) Aspergillus,Candida,Cryptococcus10/22/2011 spp 3Dr.T.V.Rao MD
  4. 4. DIMORPHIC FUNGIHISTOPLASMOSISBLASTOMYCOSISCOCCIDIODOMYCOSISPARACOCCIDIODOMYCOSISSPOROTRICHOSIS 4
  5. 5. DIMORPHIC FUNGIThere are five genera of dimorphic fungi: • Histoplasma capsulatum • Blastomyces dermatitidis Systemic •Coccidioides immitis • Paracoccidioides braziliensis • Sporothrix schenckii Subcutaneous
  6. 6. DIMORPHIC FUNGIDimorphic fungi grow innatural environments assaprobic moldsWhen they gain entranceinto the human body andcause an infection they growas yeast, or in the case of C.immitis, as a spherule(round structure resemblinga sporangium withoutsporangiophores withinwhich spores develop
  7. 7. DIMORPHIC FUNGIThese fungal pathogens can generally overcome the physiological and cellular defenses of the normal human host by changing their morphological form. They are geographically or occupationally restricted.Human infections of the four most common systemic dimorphic is by inhalation of conidia from environmental saprobesPrimary disease is in the lung but all can disseminate throughout the body to any organ system (i.e. systemic)
  8. 8. OVER VIEW OF DIAGNOSIS OF DIMORPHIC FUNGUS10/22/2011 8Dr.T.V.Rao MD
  9. 9. DIMORPHIC FUNGILab confirmation requires three (or four) steps: 1. Detect and presumptively identify the “tissue” form (yeast?) in clinical specimens 2. Culture the mold form on primary media and identifying characteristic hyphae and conidia
  10. 10. DIMORPHIC FUNGILab confirmation requires three (or four) steps: 3. Convert the mold form to “tissue” form (yeast) in vitro using rich media (usually containing blood and glucose) incubated at body temperature C. immitis requires a special medium incubated at 42o C in CO2)
  11. 11. DIMORPHIC FUNGILab confirmation requires three (or four) steps: •If the first three steps fail to definitively identify the organism, an exoantigen test can be done • Many hospital labs send isolates to reference labs for this test • It involves extracting water soluble antigens from young mold cultures
  12. 12. DIMORPHIC FUNGI•Exoantigen testThis is an example of a “precipitin test” in which a visible opaque “lattice” forms at the “zone-of-equivalence.” Monoclonal Ab is added and the lattice occurs where the concentration Ag and Ab are equal.An Ouchterlony type double Immunodiffusion procedure is usually used on a commercially available product.Ouchterlony can be ran in this manner or can be ran using patients serum & bottled Ag in an attempt to detect Abs in a patients serum.
  13. 13. 1310/22/2011Dr.T.V.Rao MD
  14. 14. HISTOPLASMOSIS AND COCCIDIOIDOMYCOSISHistoplasmosis andCoccidioidomycosis are similarfungal organisms that both produce adisease that resembles tuberculosis. Both are caused by fungi that growas spore producing hyphae atenvironmental temperatures, but asyeasts (spherules or ellipses) at bodytemperature within the lungs. 1410/22/2011Dr.T.V.Rao MD
  15. 15. COCCIDIOIDOMYCOSISCoccidioidomycosis is initially, arespiratory infection, resulting from theinhalation of conidia, that typically resolvesrapidly leaving the patient with a strongspecific immunity to re-infection. However,in some individuals the disease mayprogress to a chronic pulmonary conditionor to a systemic disease involving themeninges, bones, joints and subcutaneousand cutaneous tissues. 1510/22/2011Dr.T.V.Rao MD
  16. 16. COCCIDIOIDOMYCOSISDimorphic fungipresent in soilCoccidioides imitis,Prevalent in USAand MexicoDark skinned andAgriculturalworkers, 1610/22/2011Dr.T.V.Rao MD
  17. 17. COCCIDIOIDOMYCOSIS 1710/22/2011Dr.T.V.Rao MD
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  19. 19. CULTURINGIn culture / Soil as moldsBarrel shapedArthoconidaDisperses through wind.In the lungs arthoconidabecomes spherules 30-60 micronsContains end spores. 1910/22/2011Dr.T.V.Rao MD
  20. 20. PATHOGENESISC.imitis can beasymptomatic or selflimited.Pulmonary involvement.Fatal illnessPulmonary 7-28 daysSkin rashesChronic cavitations,Pulmonary infectionLocal infection 2010/22/2011Dr.T.V.Rao MD
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  22. 22. DEVASTATING LESIONS ARE PRODUCED 2210/22/2011Dr.T.V.Rao MD
  23. 23. PATHOGENESIS ( CONT )Generalized infection inimmune suppressed.Organ transplant recipientsLymphoma patientsAIDSCNS Skin, Joints,Poor prognosis in immunesuppressed and Meningitispatients. 2310/22/2011Dr.T.V.Rao MD
  24. 24. LABORATORY DIAGNOSISMicroscopy Sputum Pus, Biopsy, Mature spherules,Grown in test tube slopes at 25 -30 c 3 weeksMorphology thick walled ArthoconidaFine Septate hyphae.Arthoconida are highly infectious.Skin test with Coccid odes 2410/22/2011Dr.T.V.Rao MD
  25. 25. SEROLOGYPrecipitationtest.Latexagglutinationtest.Complementfixation test. 2510/22/2011Dr.T.V.Rao MD
  26. 26. TREATMENTIVAmphotericin BFluconazole,Itraconazole 2610/22/2011Dr.T.V.Rao MD
  27. 27. HISTOPLASMOSISHistoplasmosis is an intracellular mycoticinfection of the reticuloendothelial systemcaused by the inhalation of conidia fromthe fungus Histoplasma capsulatum.Histoplasmosis has a world widedistribution, however, the Mississippi-OhioRiver Valley in the U.S.A. is recognized as amajor endemic region. Africa, Australia andparts of East Asia, in particular India andMalaysia are also endemic regions 2710/22/2011Dr.T.V.Rao MD
  28. 28. HISTOPLASMOSISSoil – Enriched with Birddroppings and Batdroppings,Spread through inhalationof sporesPrevalent in Eastern USA– 95%Causative agentHistoplasma duboisii, 28 10/22/2011 Dr.T.V.Rao MD
  29. 29. 2910/22/2011Dr.T.V.Rao MD
  30. 30. CLINICAL MANIFESTATIONS:Approximately 95% of cases ofHistoplasmosis are in apparent,subclinical or benign. Five percent ofthe cases have chronic progressivelung disease, chronic cutaneous orsystemic disease or an acutefulminating fatal systemic disease.All stages of this disease may mimictuberculosis. 3010/22/2011Dr.T.V.Rao MD
  31. 31. LUNG INVOLVEMENT A MAJOR MANIFESTATION IN HISTOPLASMOSIS 3110/22/2011Dr.T.V.Rao MD
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  34. 34. CULTURINGGrows as mould at 25 – 30 cAnimal tissues as Yeast and37 cGrows in Blood agar,Enriched medium Sabouraud dextrose agarMould looks fluffy, wheatbrown colored.Produce Unicellular, asexualsporesTuberculate Microcondia 8-14 microns 3410/22/2011Dr.T.V.Rao MD
  35. 35. PATHOLOGYActive influenza like illnessCalcified lesions in lungs,Lung cavities develop.Looks like TuberculosisWide spread infection in RESDisseminated infection in infants and old age.Aggregation in Neutropenia and Hematologicalmalignancies, 3510/22/2011Dr.T.V.Rao MD
  36. 36. LABORATORY DIAGNOSISMicroscopic appreance insputum,pus,Giemsas stainingBlood cultures,Liver and lung biopsy,Culturing on Sabouraudagar at 37 and 25-30 c 1-2weeksRecognize Macrocondiaand Micro conidia 36 10/22/2011 Dr.T.V.Rao MD
  37. 37. LABORATORY DIAGNOSISCulture at 37 c showsyeast phaseMold form at 25-30 cSkin test HistoplasminSerology titers above1in 8 > 32CF test. RadioimmunoassayELISA 3710/22/2011Dr.T.V.Rao MD
  38. 38. BLASTOMYCOSISBlast mycosis is a chronic granulomatousand suppurative disease having a primarypulmonary stage that is frequently followedby dissemination to other body sites,chiefly the skin and bone. Although thedisease was long thought to be restrictedto the North American continent, in recentyears autochthonous cases have beendiagnosed in Africa, Asia and Europe. 3810/22/2011Dr.T.V.Rao MD
  39. 39. BLASTOMYCOSISPrevalent in USA andCanadaCaused byBlastomycosisdermatitidis,Inhalation of spores,Men between 30 to 50years are affected,Cool wet climatecondition 3910/22/2011Dr.T.V.Rao MD
  40. 40. MORPHOLOGYBlastomycosis dermatitidis-Dimorphic fungusMould Septate mycelium 25 –30 cAsexual conidiaConidia are 2-10 microns /Dumbbell shapedYeast at 37 c with broadbased buds 40 10/22/2011 Dr.T.V.Rao MD
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  42. 42. PATHOLOGYPulmonary formsDisseminated to otherorgans,X rays looks likeTuberculosis / CarcinomaCutaneous lesions occur80% patients withpulmonary infection 4210/22/2011Dr.T.V.Rao MD
  43. 43. LABORATORY DIAGNOSISMicroscopy – pusScrapping from the lesions sputumThick walled yeast cells 8- 15 micronsBuds on broad base.PAS / Methenamine silver stain,Sabouraud dextrose agar – Blood agar,Retained for 6 weeksGrow in test tubes,ELISA test 4310/22/2011Dr.T.V.Rao MD
  44. 44. TREATMENTIVAmphotericin BItraconazoleKetoconazole 4410/22/2011Dr.T.V.Rao MD
  45. 45. PARACOCCIDIOIDOMYCOSISParacoccidioidomycosis is a chronicgranulomatous disease thatcharacteristically produces a primarypulmonary infection, often in apparent, andthen disseminates to form ulcerativegranulomata of the buccal, nasal andoccasionally the gastrointestinal mucosa..The only etiological agent,Paracoccidioides brasiliensis isgeographically restricted to areas of Southand Central America 4510/22/2011Dr.T.V.Rao MD
  46. 46. PARCOCCODIOMYCOSISChronic granulomatusinfectionParacoccodioidesbrasilensis,Lungs- Mucosa – Skin –Lymphatic vesselsEnter through the lungsSaprophytic in nature,Humid forests of South andCentralCommon in 20 – 40 years, 46 10/22/2011 Dr.T.V.Rao MD
  47. 47. MORPHOLOGYMycelium at 25 – 30 cYeast forms at 37 cConversion from mycelialforms to yeast.The yeast forms consistsof Oval or globose cells 2-30 microns, in diameter,with small buds attachedby a narrow neckencircling the parent cells. 47 10/22/2011 Dr.T.V.Rao MD
  48. 48. PATHOGENESISUlceration ,Granulomatousinfection of oralNasal MucosaLymphatic systemspleen, IntestinesLiver involvement 48 10/22/2011 Dr.T.V.Rao MD
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  50. 50. LABORATORY DIAGNOSISMicroscopy – Sputum , Pus,Biopsy of glaucomatous lesionsPresence of Numerous multipolar buddingcells is diagnosticStaining with PAS / Silver methenamineCultures kept for 6 weeks25 c moulds37 c yeastsSerology Precipitation tests, Complementfixation 5010/22/2011Dr.T.V.Rao MD
  51. 51. TREATMENTAmphotericin BOralKetaconazole,Itraconazole. 5110/22/2011Dr.T.V.Rao MD
  52. 52. Created by Dr.T.V.Rao MD for the Medical and Paramedical students in Developing world Email doctortvrao@gmail.com 5210/22/2011Dr.T.V.Rao MD

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