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Mid 2 Rhinosporidiosis Lobomycosis Phaeohyphomycosis Chromoblastomyc Sporotrichosis osis colored hyphe (=Chromomycosis) More dangerous than Phaeohyphomycosis Clinical Mucocutaneous fungal Cutaneous – Subcutaneous or brain Abscess caused Lymphocutaneous subcutaneous by dematiaceous fungi and subcutaneous infection fungal infection granulomatous site Nasal, Oral (Palate, Thigh, legs, feet, arms, ....etc, brain extremitees, extremities, joints. epiglottis), (cerebral mainly feet & legs Conjunctiva. any site can be affected In agricultural communities Tyes Neurotropic fungi cerebral PHM as R.mack, C.bant. (here it isolated from brain abscess) Naturally in woody plants, woods, agricultural soils Lesion Polyps, Papillomas, Keloidal – Hyperkeratotic, suppurate, ulcerate. wart-like lesions verrucoid - Verrucous, The lesions are nodular Pedenculus, nodules or ulcers in Violaceous,Caulifl local lymphatics ower, Initially Ulcerative, Autochthonous spread Near swamps Etiology Rhinosporidium Lacazia loboi Dematiaceous imperfect mold fungi. Phialophora Dimorphic, imperfect seeberi (=Loboa loboi) Mainly: Cladosporium, Exophiala, verrucosa, fungus in trees, Wangiella, Fonsecaea shrubs, plant debris Obligately parasitic Obligately pedrosoi, fungus Believed to parasitic fungus Cladophialophora bantiana Exophiala, be (Cladosporium bantianum), Cladosporium Sporothrix schenckii hyphochytridiomycet es, Ramichloridium (Rhinocladiella) Dematiaceous Yeast in human mackenziei, Bipolaris, Drechslera, imperfect mold tissue & at 37oC in Rhinocladiella , C.cladosporoides, fungi in woods culture. Mold in E.jeanselmei, W.dermatitidis and woody plants culture at room temperature with flowerettes of conidia. على شكل ورده But has been grown Does not grow in tissue culture in culture like does not grow on SDA media or artificial (e.g. SDA) tissue culture Lab diagnosis Specimen biopsy tissue biopsy tissue Pus, biopsy tissue Biopsy tissue Biopsy pus from brain tissue,ulcerative materia Direct Stained sections or show chains of KOH & smears brown septate hyphae KOH & smears smear Finger-like Microscop smears or KOH, will cells brown cells with yeast cells or Cigar y: show spherules with With the silver septa, Brown Culture: Some are On endospores stain ( special Muriform cells oval stain ) (=sclerotic bodies) Also asteroid bodies ITs diagnostic may be, seen. Culture Culture on SDA Culture of On SDA & Mycobiotic – very slow On SDA and SDA at Also room negative specimen will growing Mycobiotic Very temperature to grow be negative for black or grey colonies. slow growing be mold, SDA and tissue Dematiaceous . culture fungi )where the flower is In KOH characteristic ) and on blood agar at 37oC to grow yeast. Manageme Cryosurgical Surgical Management: Phaeophypho. & ➢ Treatment: Septrin, nt: excision of lesion. excision of Chromoblasto. KI - relapse common. lesion ➢ Subcutaneous: Clean surgical excision of the lesion + Antifungal ➢ Cerebral phaeohypho: Aspiration of Pus - Antifungals ▪ Amphotericin B, 5- Fluorocytosine (5-FC) ▪ Azoles (e.g. Voriconazole, Posaconazole) ▪ Caspofungin Zygomycosis I Subcutaneous zygomycosis II- Rhinocerebral zygomycosis III IV =Entomophthoromycosis (=Mucoromycosis) III- Gastrointestinal (GI) (= Phycomycosis) Zygomycosis IV- or Pulmonary Zygomycosis ➢ This. is a chronic nfections Mucorales & zygomycete infection caused Entomophthorales. effecting the GI., mainly by Zygomycete Zygomycetes liver and intestine , the fungi of are: lesion re masses or the orders abscesses in these sites . Fast growing, moniliaceous molds, nonseptate hyphae, perfect ➢Seen in children (6 -12 - Year old) often . Clinical Chronic localized Paranasal sinusitis, orbital cellulitis This is chronic or acute Subcutaneous masses, Rhinofacial – orbital – craneal Other aspects similar to Usually acute, affects compromised mucoromycosis host especially Diabetics with acidosis. Opportunistic Acquired Via nasal mucosa VERY SERIOUS – ACUTE - FATAL Sites cellulitis Rhinofacial or other like Hand,Arm,Leg, thigh. Firm swelling of site with intact skin-Distortion. Cases Acquired via nasal mucosa or insect bite, Cont. debris Etiology Conidiobolus coronatus, Fast growing Zygomycetes have ➢Etiology : Caused by Nonseptate hyphae , of the Mucorales Basidiobolus ranarum Basidiobolus ranarum order maily; primarily. and few mucorales. Rhizopus, Mucor, Absidia, These are perfect fungi that Rhizomucor, others. form Sporangia (conidia) and Zygospores. Rhizopus arrhizus Reproduce sexually and asexually forming Sporangia with sporangiospores & Zygospores Lab diagnosis Specimen Biopsy tissue Biopsy tissue ➢Specimen: fine needle biopsy Direct Stained section or smear will Stained sections or smears will show ➢ Direct Microscopy will show broad nonseptate hyphae show nonseptate hyphae broad non-septate hyphae with eosinophils. culture Culture on SDA (no Culture on SDA (no antifungal ➢& culture grow will the antifungals), fungi will grow “Cycloheximide”).The fungi willgrow fungus fast. Zygomycetes are fast within 2-3 days. inhibited by Cycloheximide Prompt Dx & action are essential to save life Treatment: KI orally or KI + Ampho B or Aggressive surgical debridement + ➢Treatment: Medical with Septrin Amphotericin B – other antifungals. Itraconazole —— ➢ prognosis is good ➢ There is mucorales G.I. Zygo which acute and fetal it is rare . Aspergillosis ➢This is any infection caused by Aspergillus–Affecting compromised individuals. ▪ The systemic forms of this infection are opportunistic infections. ▪ In few occasions it is non opportunistic ▪ The clinical manifestations vary from allergy to skin to systemic forms. ▪ Clinical Types: 1- Allergic Aspergillosis − Asthma − Allergic Bronchopulmonary Aspergillosis (ABPA) IgE antibodies present. In ABPA also IgG Best test : —— 2- Colonizing aspergillosis Pulmonary aspergilloma signs include:Cough,hemoptysis, variable fever (=Aspergilloma = Aspergillus fungus ball) ▪ CXR will show coin – like mass in the lung Pulmonary aspergilloma ▪ There the mass will be a radiolucent crescent (=Monod’s sign = Grelot) over Best specimen : —— lung biopsy 3- Invasive Aspergillosis - pulmonary -more sever pulmonary Signs: Cough , hemoptysis, Fever, Pneumonia, Leukocytosis Lab investigation (direct then 2 microscopy and culture) may be negative especially if specimen is noninvasive like sputum Hard to distinguish with pneumonia ——- 4- Aspergillus sinusitis (= Nasal-orbital): Nasal polyps – sinusitis – eye – craneum (Rhinocerebral) The most common cause is Aspergillus flavus (also other fungi can cause sinusitis) 5- Eye infection Corneal ulcer – endophthalmitis 6- Ear infection Otitis externa – otitis media 7- Nail & skin infection 8- Toxicosis due to ingestion of aflatoxin + H.W 9- Disseminated form rare, in debilitated patients. Etiology ▪ Any species of Aspergillus. ▪ It is a moniliaceous imperfect mold – Ubiquitous in distribution ▪ It has hyaline septate hyphae, conidiospores with chains of unicellular conidia. ▪ The common species are Aspergillus fumigatus, A. flavus, A. niger, A.terreus, and others ▪ The perfect stage is: Eurotium species an Ascomycete fungus. specimen ▪ Respiratory, specimens (Sputum, bronchoscopic, Lung biopsy), Surgically removed Aspergilloma , Mass, Scrapings, Blood, etc. Direct KOH, Giemsa, Grecott methenamine silver stain (GMS) Periodic Acid Schiff (P.A.S); will show Septate hyphae with Dichotomous branching Culture Culture on SDA(no cycloheximide) fast growing– If nonsterile specimen (e.g. sputum) rule-out contaminant possibility by repeat specimen Serology ▪ Primarily test for Antibody using. Aspergillus polyvalent Ag, Aspergillys terreus Ag, Aspergillus nidulans Ag ▪ Using I.D (Immunodiffusion)and/or C.I.E (Counterimmunoelectrophoresis).SP-RIA (Solid phase radioimmunoassay) more sensitive. ▪ Multiband identity lines will be seen in aspergilloma ▪ E.I.A. test for Antigen is available. ▪ ▪ There is latex agglutination test available Treatment ▪ Surgical + Medical – Or Medical only ▪ Drugs Used: Amphotericin B, Liposomal Ampho. B, Itraconazole, Voriconazole, Caspofungin Pneumocystosis ➢ Opportunistic fungal pneumonia ▪ It is interstitial pneumonia of the alveolar area. ▪ Signs include; Dyspnea. Cyanosis ▪ Affect compromised host ▪ Especially common in AIDS patients. ▪ Infection commonly known as PCP (should be PJP) why ? ➢ Etiology: ➢ Etiology: Pneumocystis jirovecii ——- thats why it shoaled be PJP ▪ Previously thought to be a protozoan parasite ▪ . ▪ It has been proven to be a fungus based on: 1- RNA studies – similar to fungi 2- Chitinase enzyme attacks the cell wall of the cyst so it has chitin like fungi ▪ Other species naturally found in rodents and other mammals. P. cariniii in rats. Humans contract it during childhood. Does not grow in media like SDA, others ➢Laboratory ➢Patient specimen: Bronchoscopic specimens (B.A.L.), Sputum, Lung biopsy tissue. Diagnosis: Histologic sections or smears stained by Silver stain (GMS). If (+) there will be cysts of : hat- shape, cup shape, crescent, parentheses, comma ▪ Can be detected by specific antibodies ▪ Treatment ▪ Trimethoprim – sulfamethoxazole (septrin) : •.
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  • In Vitro and in Situ ACTIVATION of the COMPLEMENT SYSTEM by the FUNGUS Lacazia Loboi

    In Vitro and in Situ ACTIVATION of the COMPLEMENT SYSTEM by the FUNGUS Lacazia Loboi

    Rev. Inst. Med. trop. S. Paulo 49(2):97-101, March-April, 2007 In vitro AND in situ ACTIVATION OF THE COMPLEMENT SYSTEM BY THE FUNGUS Lacazia loboi Fátima Regina VILANI-MORENO(1), Érika MOZER(2), Ana Márcia Guedes de SENE(2), Margarete de Oliveira FERASÇOLI(2), Tânia Cristina PEREIRA(2), Márcia Garcia MIRAS(2), Gláucia Heloísa de Paula SOUZA(3) & Andréa de Faria Fernandes BELONE(3) SUMMARY Since there are no studies evaluating the participation of the complement system (CS) in Jorge Lobo’s disease and its activity on the fungus Lacazia loboi, we carried out the present investigation. Fungal cells with a viability index of 48% were obtained from the footpads of BALB/c mice and incubated with a pool of inactivated serum from patients with the mycosis or with sterile saline for 30 min at 37 oC. Next, the tubes were incubated for 2 h with a pool of noninactivated AB+ serum, inactivated serum, serum diluted in EGTA-MgCl2, and serum diluted in EDTA. The viability of L. loboi was evaluated and the fungal suspension was cytocentrifuged. The slides were submitted to immunofluorescence staining using human anti-C3 antibody. The results revealed that 98% of the fungi activated the CS by the alternative pathway and no significant difference in L. loboi viability was observed after CS activation. In parallel, frozen histological sections from 11 patients were analyzed regarding the presence of C3 and IgG by immunofluorescence staining. C3 and IgG deposits were observed in the fungal wall of 100% and 91% of the lesions evaluated, respectively. The results suggest that the CS and immunoglobulins may contribute to the defense mechanisms of the host against L.