Opportunistic Mycoses - DR Santos

MICROBIOLOGY: OPPORTUNISTIC MYCOSES
Reference: Dr. Camilo Santos’ Lecture

Transcriber: [email protected]
“To toil and not to seek for rest... “
OPPORTUNISTIC MYCOSES
137 Slides
INTRODUCTION o Population at Risks: ( Predisposing Factors )

 Non- Immunologic
 Immunosuppressive Therapy – Cytotoxic – Mucosal damage
I. Introduction  Antibiotic
o Opportunistic Fungi or  Invasive Devices  IV lines, Urinary Catheters, Tracheostomy
 Emerging Fungal Pathogen  Invasive procedures  Major Surgery – GI Surgery
 Organisms of low virulence.  Immunologic
 Immunocompromised/weakened patients  Increased Frequency of Infection  Neoplastic Diseases – E.g. Hematologic  Neutropenia
 Morbidity & Mortality  Hospitalized patients  Neutropenia & Impaired T- Cell Function
 Saprophytic/Laboratory Contaminants  Opportunistic  Solid Organ Transplantation
 Fail to induce disease  Immunocompetent  Blood & BM Transplantation (BMT)
 Normal conditions  No disease  Cellular Immune Dysfunction
 Causes:  AIDS, Lymphoma & CMC - Impaired T – Cell Function
 Endogenous – Colonization precedes infection  Immunosuppressive Therapy
 Exogenous – Health Care workers  Advanced Age
 Premature Birth
o Opportunistic Organisms
 Normal resident flora
 Pathogenic only - Host's Immune Defense Altered
 Antibacterial therapy - Upsets the balance of normal flora
o Conditions: Weakened Immune Function:

 Inherited Immunodeficiency Diseases
 Drugs – Suppress Immune System – E.g. Cancer chemotherapy
 Corticosteroids -Prevent Organ Transplant Rejection
 Radiation therapy
 Infections (E.g. HIV)
 Cancer
 Diabetes
 Advanced age & malnutrition.
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o Classical Opportunists o Transmission of Opportunistic Fungi


Candidiasis  Candida, Trichosporon, Malassezia

Cryptococcosis  ENDOGENOUS

Aspergilloses  Unique strain

Zygomycoses  Colonization precedes infection

Pneumocystis Jerovici  Antibiotic – (-) Normal flora  Fungal overgrowth

Penicillioses  EXOGENOUS
o Order of Highest frequency of Opportunistic Fungal Infections  Hands -Health care workers
 Candidiasis  Aspergillus, Zygomycetes, other filamentous fungi, Cryptococcus
 Aspergillosis  EXOGENOUS
 Cryptococcosis  Inhaled conidia
 Ventilation systems, construction, heliports, plants, environment
 Pneumocystis jerovici
 Direct contact - dressings, arm boards, burns, wounds
 Zygomycosis
 NOTE: ANY fungus found in nature MAY GIVE RISE to opportunistic mycoses
CANDIDA SPECIES
II. Candida Species

o Most common Invasive Fungal infection (Immunocompromised )
o 4th most common cause - Nosocomial Bloodstream Infection
o Species Most often Implicated in human disease :
 C. albicans
 C. tropicalis
 C. parapsilosis
 C. krusei  Fluconazole resistant
 C. Glabrata
 C. lusitaniae  Amphotericin B resistant
Candida Albicans
o Dominant Opportunistic Mycoses

 Part of normal flora
 40-80% - Mouth, skin, URT, GUT, Female GT
 Body Temperature , Neutral pH
 Endogenous Infection- infects: Skin & Mucosa
 70% =Nosocomial Fungal Infection
 30% = Death of Nosocomial Infection
o PROPERTIES:
 Tissues
 Yeast forms
 Oval & Budding cells (Blastoconidia )
 Pseudohyphae
 Elongated Yeast
 Resembles hyphae
 Not true hyphae
 CHO Fermentation Tests
 Differentiates from other species:
 E.g. C. tropicalis, C. parapsilosis, C. krusei & C. glabrata
o CLINICAL INFECTION  Localized  Severe Systemic Infection o MORPHOLOGY :

 Thick cell walled  Polymers: Mannan & Glucan
o YEAST:  Dimorphic fungi  Grow : Yeast , Pseudohyphae & True hyphae
Candida spp.  albicans, tropicalis, parapsilosis, krusei, glabrata,  Culture or Tissue
lusitaniae, kefyr, guilliermondii.  Oval, Budding Yeast
 Cryptococcus neoformans  Pseudohyphae
o FILAMENTOUS FUNGI  Constricted or Narrow based buds fail to detach, chains of elongated
 Aspergillus spp. (fumigatus, niger, flavus) blastospores
 Zygomycetes (Rhizopus, Mucor, Rhizomucor, Absidia)  True Hyphae  buds germinate
 Fusarium spp.  Commensals or Pathogens
 Penicillium spp. (marneffei)  Strict aerobe, favors moist surfaces
 Pseudallescheria boydii (Scedosporium apiospermium)  See photo next page.
 Curvularia spp.
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 Surface hydrophobicity
 Virulent
 Hydrophobic C. albicans at 25ᴼ C
 Less Virulent
 Hydrophilic C. albicans at 37 ᴼC
 Shows increase adherence
 More rapid hyphal Germ tube formation
 Surface Virulence Molecules  Receptors, Adhesins, Pyrogens, &

Immunomodulators
 ADHERENCE:
 Epithelial Mucosal Cells
 Buccal, Cervical, Corneal, GUT & GIT, Vascular endothelial cells,
spermatozoa, plastics
 Ligands
 Host components - C3d, iC3b, fibrinogen, Laminin, Fibronectin,
Fucose receptors, N- Acetyl glucosamine Receptors
 Molecular mimicry
 Surface Molecules  Coats Organism - Mimics Host Components
 Decreases Recognizability
 C. albicans  in circulation coated with host platelets via Fibrinogen-
binding ligand.
 Lytic enzymes
 Hydrolases with broad substrate specificities:
 Proteinase, phospholipases
 Lipases , Acid phosphomonoesterase
 Aspartyl proteinase  Most potent.
o TRANSMISSION: Member = Normal flora

 Can be transmitted between individuals
 Vertical transmission
 Sexual contact – NGU in Men
o PATHOGENESIS:
 Local or Systemic Host defense Impairment Diseases
o Virulence Factors
o More virulent than other species
 Rapid switching of expressed phenotype
 Ability
 Reassort & Regulate Genetic expression
 Chromosomal Rearrangement
 Recombination
 Phenotypic
 Nutrient depletion produces different colony form
 Virulence factors
 Antifungal resistance
 E.g. C. lusitaniae - Amphotericin B
 Hyphal Formation
 Correlated  Tissue invasion o CLINICAL PRESENTATION:
 Function: Adherence - Host cells (50x than yeast Cells )  Mucous Membrane Infections
 Yeast formation  Associated: Epithelial Colonization  Thrush (oropharyngeal)
 Non-hyphae-forming Mutant Strains  Decreased pathogenicity in a rat  Esophagitis
Candida vaginitis model  Vaginitis
 Experimental renal infection  Cutaneous Infections
 Yeast & Hyphae initiate renal lesions,  Paronychia (skin around nail bed)
 Hyphae - Essential for invasion of renal pelvis.  Onychomycosis (nails)
 Contact sensing  Diaper rash
 Thigmotropism  Growth of hyphae on filters/membranes pores.  Balanitis
 Tissue penetration  Facilitated Skin breaks & discontinuities  Chronic Mucotaneous Candidiasis
 Children with T-cell abnormalities
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 Systemic Infection
 Disseminated (Systemic, Invasive) infection
 Immunocompromised patients
 Cancer/ Chemotherapy
 Neonatal Candidiasis
 Endophthalmitis (eye)
 Liver and spleen
 Skin, Brain ,Kidneys, Lungs & Bone
o Clinical Manifestations
 Oral Thrush
 Patchy - confluent, adherent, whitish pseudomembrane
 Tongue, lips, gums and palate
 Epith. Cells, Yeasts, pseudohyphae
 Factors:  Esophageal Candidiasis
 Indiscriminate use of antibiotic  Painful, bleeding ulcerations.
 Trauma  Nausea and vomiting
 Impaired or decreased immunity  AIDS patients  70% of AIDS patients
 Newborn (5%) & Elderly patients (10%).
 Vulvovaginitis or Vaginal thrush

 Yeast Infection
 Itching or irritation & yellow-white discharge  (White – Cottage Cheese like
Patches) & Ulceration
 Favored by: High pH , Diabetes, Use of antibiotic, Pregnant Women
 Risk for neonates – childbirth
 Transmitted - Male partners – Sexual intercourse
 Severe Cases  Spread  Vagina  Perineum  Thighs
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 Candidal Blood-borne Infection – Candidemias

 High Mortalities  Serious Assault  Any other fungal pathogen
 Causes of BSI:
 C. albicans & C. parapsilosis  Infants & Children
 C. glabrata  Older patients
 Cutaneous Candidiasis
 Skin & nails
 Complicates burns, Scalded-like rash
 Neonates
 Onychomycosis
 Occupational risks
 Anatomic barrier - Constant immersion : Hands & feet in H2O
 Intertrigenous infection
 Moist areas = Skin rubs against skin
 Beneath the breast, armpit, between folds of the groin
 Erythematous Vasiculo-pustular lesions
o Principal Targets of Systemic Infection:

 GUT
 Endocardium
 Endocarditis
 Risk: Valvular Heart Disease
 Usually: C. tropicalis , C. parapsilosis
 Brain  Cerebromeningeal Infection
o UPDATES:
 Biofilm Formation
 Artificial joints, catheters, Heart valves
 Colonization – very drug resistant
 Remedy: Removal of device
o Candida krusei
 Terminal infection in
 BM transplant patients
 Recipient of Anti-cancer therapy
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o LABORATORY DIAGNOSIS
 Chronic Mucocutaneous Candidiasis  Microscopy
 Chronic Disfiguring Granulomatous Infection  KOH Mount (10-20% )
 Overlapping syndrome  Scrapping – Nails, skin, exudates
 Persistent, severe & diffuse cutaneous infection  With Calcofluor White Staining
 Skin, nails & mucous membranes  Presumptive Diagnosis
 T- Cell Deficiency ( CD4 Cells )  Protection & Control of infections  Spherical or ovoid Budding Yeast Cells & Pseudohyphae
 SUFFICIENT for diagnosis
 PAS – Best
 Superficial  Mixture of Yeast & Pseudohyphae
 Systemic  Few yeast cells; Mostly pseudohyphae
 Chorioretinitis, Endophthalmitis, & Traumatic Keratitis

 Patient at risk: Frequent Ophthalmologic Examination
 Renal Abscess
 Peritonitis
 CNS Infection  Mimics Bacterial Meningitis – VP Shunts
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 Culture
 Fungal Media w/ Trypan Blue
 differentiates Candida spp. from yeast Cryptococcus
 CHROMagar Candida
 Selective media  Morphologic Appearance
 C. albicans – Green colonies
 C. tropicalis – Blue colonies
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 Confirmatory Test - C. albicans

 Germ Tube Test
 Hyphal outgrowths  Serum suspension at 37ᴼC
 Diagnostic for C. albicans  Multi-Panel System
 Presence of Chlamydospores  Biochemical Reaction
 Typical of C. albicans  Sugar Assimilation Panel
 Thick-walled Chlamydoconidia  DNA Amplification Technique
 PNA-FISH
o TREATMENT:
 Oropharyngeal & Esophageal Thrush  DOC: Fluconazole
 Mucocutaneous Candidiasis  Ketoconazole
 Cutaneous Infection  Clotrimazole or Nystatin
 Disseminated candidiasis  Amphotericin B or fluconazole with or without
Flucytosine
 Oral Thrush  Oral Clotrimazole troches nystatin Swish and swallow
 Fluconazole  Prevention in high risk patients – BM transplantation, Neonates
 Vulvovaginitis  Intravaginal antifungal medications – Clotrimazole
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Cryptococcus neoformans
CRYPTOCOCCUS SPECIES
III. Cryptococcus Species

o Basidiomycete Family, Monomorphic organisms
o Other Names: Not Dimorphic
 Busse-Buschke Disease
 Turolosis
 European Blastomycosis
o Two Variants:
 C. neoformans var. neoformans
 Worldwide  Immunocompromised hosts
 Etiologic agent: Cryptococcoses ( 50% of Cases )
 Capsular Serotypes : A, D, AD
 Variants:
 grubii ( Serotype A)
 neoformans ( Serotype B )
 C. gattii
 Immunocompetent individuals
 Outbreaks in California – AIDS patients
 Serotypes: B and C
 CNS Granuloma Formation >> Severe Neurologic complication
o Morphology:
 Yeast
 Only Encapsulated yeast , Spherical-Ovoid Small Constricted Buds (Narrow
Based)
 Can be: Single or rarely multiple buds
 No hyphae nor pseudohyphae
 True Yeast
 India Ink Smears

 Variable in Size, spherical, elliptical
 Huge Clear Halo
 Extracellular Polysaccharide Capsule
 Distinctive Marker
 Mayer Mucicarmine Stain
 Filobasidiella neoformans – Sexual form of Cryptococcus
o Four Serotypes - A,B,C,D o Pathogenesis:

 A and D - C.neofromans var neoformans  Entry: Respiratory – Lung Infection  Inhalation  Yeast or Basidiospores
 B and C - C.neoformans var .gatti.  Subclinical
 Flu-like Symptoms
o Most Infections  Enhance by Several Characteristics:
 C.neofromans var neoformans.  Capsule  Phagocytic-resistant
 Melanin production  inhibits phagocytosis, Fontana- Masson Stain
 Found: Wild & Domesticated birds.
 CNS Predilection
 Pigeons carry C.neofromans
 Birds do not get infected.
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o Human Infection:
 Inhalation:
 Aerosolized Spores or Dried Yeast forms
 Pigeon and chicken droppings
 Proliferates I - High nitrogen content (Droppings )
 Highest rate – AIDS patients
 Defective Cellular Immunity
 CD4+ Lymphocytes =< 100/mm ( <2oomm²)
 Risk of Disseminated & CNS Cryptococcosis
 C. neoformans var. neoformans & var. grubii
 Worldwide
 Soil contaminated with Avian excreta
 C. gattii
 Tropical & Subtropical Climates
 Associated: Bark of Eucalyptus Tree
 Incidence: Early 1990’s = 65.5 Infections /million/year
o Pathogenesis
 Entry:
 Inhalation of Basidiospores
 Result : Pulmonary infections
 Men >>> Infections than women
 Self-limiting - Immunocompetent  Cutaneous Cryptococcosis
 MIMICS TUBERCULOSIS  Rare
 Transcutaneous Inoculation
 10-15% - Mimic Molluscum contagiosum
 Discrete nodules  AIDS – 2nd most common manifestation
 Cryptococcoma  Lesions: Head & Neck
 Solid fungal mass
 Cerebral Hemisphere
 Cerebellum
 Rare – Spinal cord
 Mistaken: Cerebral Tumor
 Virulence Factors:
 Capsule
 Laccase
o Clinical Manifestations:
 Aggravated by: Abnormalities of T lymphocyte function
 Meningeal Signs:
 Head ache
 Low grade fever
 Visual abnormalities o Laboratory Diagnosis:
 Coma – fatal  India Ink Stain – CSF, Tissue biopsy, Bronchial Washings
 CSF = Encapsulated Budding Yeast Cells
 AIDS = 3- 20%  Develop Cryptococcosis  No pseudohyphae formation
 Gram Staining
 Manifestations : Chronic meningitis , Meningoencephalitis
 Disseminated Form:
 Involvement : Skin, Mucosa, Organs – Adrenals , Prostate glands, Bones , eyes
o Clinical manifestations:
 Pulmonary Cryptococcosis - Asymptomatic  Fulminant Pneumonia –
Bilateral, lung nodules & Cavitation - rare Impaired Immunity  Yeast escape
 Circulation
 Cryptococcal Meningitis
 Highly Neurotropic: Brain & meninges
 Tumor-like masses
 Headache, Meningismus, Paralysis, Eye disturbances, Seizures, coma.
 Most common form of cryptococcal infection
 Dissemination - Few cases: Skin, Bones, Viscera
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 Culture
 Blood and CSF
 Flat shiny mucoid colonies color - Creamy to tan & pink colonies
 Carbohydrate Assimilation Testing

 Growth on Niger Seed Agar  C. neoformans - colonies – brown to black
 Phenoloxidase Activity – C. neoformans – positive
 Serologic Tests
 Cryptococcal Antigen detection in CSF
 Rapid, sensitive & specific
 Latex Agglutination – Best Serologic Test
 Enzyme Immunoassay Kits
 DNA Probes & FAT
 NOTE: CSF findings mimic like Tuberculosis
 Mortality: 30%

o Treatment:
 Cryptococcal meningitis & Disseminated Forms
 Induction Therapy
 Amphotericin + Flucytosine x 2 weeks
 Repeat CSF Examination
 Consolidation Therapy
 Oral fluconazole or Itraconazole – 8 weeks
 Repeat CSF Analysis
o AIDS patients
 Lifelong Maintenance  Fluconazole or Itraconazole
 AIDS patients  not totally cured.
 Relapses  Frequent with fatal outcome.
 Rapid resistance with Fluconazole
 Avoid contact with Birds
o Immune Deficient
 Amphotericin B & Flu cytosine
o Immune competent
 Fluconazole & Itraconazole
 Treatment reduces the morbidity &
 Cure in non- immunosuppressed is expected
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o Organ Involvement:
PNEUMOCYSTIS JEROVICI  Spleen, Lymph Nodes, Bone Marrow, Liver, S.I. Gut, Eyes, Ears, Bone, Thyroid,
Gut
IV. Pneumocystis Jerovici
o ERA OF AIDS o Life Cycle :
 Most important Opportunistic fungal pathogen  Sexual
 Disease almost Diagnostic for AIDS  Asexual
 Primary Indicator of AIDS  Human Infection : Free trophic forms
 Uninucleated Sporocyst or
o Discovered = 1909  Thick Walled Cyst – 8 ovoid- fusiform intracystic bodies  Ruptures
 Found in Healthy humans Trophozoites  Asexual reproduction (Fission) or  Sexual
 Thought : Developmental Stage of Trypanosomes Reproduction  Encystation
 1988 – Reclassified as Yeast – Molecular Evidence
 1999 – Name change to Pneumocystis jerovici
o Pneumocystis carinii - Protozoan????

 Recent rRNA Nucleotide Analysis  FUNGUS
 Pneumocystis jerovici
 Ascomycetes
 Resemble like a protozoan
o Worldwide: Symptoms occur

 Mild respiratory during Childhood.
 Respiratory Infection
o HALL MARK
 Interstitial pneumonitis( PCP )  Pneumocystis Pneumonia  Plasma Cell o Morphology
Infiltrates  See image below
 Most common presentation
o CXR: Ground glass Appearance

 Interstitial infiltrates
o Occurrence:
 Primarily Aids
 Hospitalized Infants  Premature & Malnourished o Pneumocystis carinii  found in rats
 Elderly o Pneumocystis jerovici in  human species
 Cancer & Organ Transplant Recipients - Under Immunosuppressive Drugs
o Pathogenesis
o Predisposing Factors:  P. jiroveci is extracellular pathogen  Lining of Alveoli
 Corticosteroid Therapy  In AIDS patients – Alveolar infiltrates  Plasma Cells  Interstitial Plasma
 Transplant Recipients Cell Pneumonias
 Antineoplastic Therapy  Plasma cells Absent in AIDS related Pneumocystis pneumonia
 Transplant Recipients  Blockade of oxygen exchange interface, results in Cyanosis
 DEATH  Respiratory Failure
o Note:
 If Retroviral Treatment Is Delayed  Major Cause Of Death In Aids Patients.
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o Laboratory Diagnosis
 Clinical specimens :
 bronchoalveolar lavage – ( bal ) = 90-100% sensitive
 Sputum, trans-bronchial aspirate,
 Brush biopsy, open biopsy
 Microscopic examination presence of cysts or trophozoites
 Culture  not possible
 Serologic test
 direct fluorescent method with monoclonal ab
 rapid and emerging method
 Serology – epidemiological study –establish prevalence of infection.
o Immunity – Pneumocystis
 In the absence of Immunosuppression does not cause disease.
 CMI- plays a dominant role in resistance to Infection.
 Infection not seen until CD4 counts drop to <400/microliters.
 Infection: CD4 Count < 200/ul – High Risk
o Treatment
 Acute Cases – Trimethoprim - Sulfamethoxazole
 Pentamidine, Isothionate  very effective compounds
 Aerosolized pentamidine  particularly for AIDS patients
 Trimethoprim-Dapsone
 Clindamycin-Primaquine
 Atovaquone
 Trimetrexate
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ASPERGILLUS SPECIES
V. Aspergillus Species
o Aspergillosis
 Constellation: Several Diseases
 Inhalation of Spores
 Not Dimorphic
 Distribution – Ubiquitous  Soil, food, compost, Agricultural building, Air
vents, Offices
 Growing problem to AIDS patients
 Exposure
 Mild Allergies  Serious diseases
 Can infect  All body tissues
o Three clinical pulmonary diseases :

 Hypersensitivity Aspergillosis or Pneumonitis
 Allergic Bronchopulmonary Disease – Spore Inhalation
 Asthma or Other allergic symptoms – Atopic Persons – Elevated IgE
 Range : Mild – No damage  Chronic - Recurrent Episodes 
Permanent Damage
 10-20% : Asthmatics react : A.fumigatus
 Allergic Alveolitis
 Develop :Heavy & repeated exposure to larger number of spores
 Maltsters Lung
 Form of Allergic Alveolitis caused by Aspergillus claveus – from barley
o Non-Invasive Aspergillomas
 Ball-like Masses of Hyphae/Mycelium - Enclosed Dense Fibrous CT
 Form in Cavities resulting from previous PTB
 Asymptomatic – Coughing of blood tinged sputum (Hemoptysis)
 at times Invasion of BV
 Fungus ball, see photo on the next page
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Non-Pulmonary Aspergilloma
o Paranasal Sinuses, Ear Canal Aspergilloma

 Paranasal Granulomas  A. flavus, A.fumigatus
 May invade paranasal sinuses spread Bone  Orbit of eye  Brain
 Otomycosis – Fungus balls: External Auditory canal
o Eyelids, Eye sockets, Conjunctiva Aspergilloma
o Cutaneous Aspergillosis: Skin trauma

 Dissemination : Lungs to skin
 Immunocompromised patients
 Raised, red papules  Necrotic
o Systemic Aspergillosis  Involves major Organ Systems  AIDS

 Seen IV Drug Users
 Abscesses – Brain, heart, kidneys, bones & GIT.
 Systemic Involvement – often Fatal especially when brain is involved
o Mycotoxicoses  Acquired – Contaminated food
o Endocarditis
 A rare complication of Aspergillosis
 Risk factor: Open heart surgeries
 Poor prognosis
 Clinical History & Radiographic finding  Confirmed by Laboratory
Techniques
 KOH & GMS Smears:
 Tissue Specimens:
 Directional Branching of septate
 hyphae & Distinctive conidia
 Confirmation Difficult
 Repeated specimens
o Acute Invasive Pulmonary Aspergillosis
 Hard to isolate
 More Serious Disease  Mild Pneumonia - Fever, cough, pain.
 Pulmonary Necrosis  Significant Respiratory impairment
 Predisposing Factor - Neutropenia
 Aspergillus fumigatus- Most common
 High Mortality – BM recipients
 Lung sole site in 70 % of patients
 Fungus invades blood vessels:
 Thrombosis
 Septic emboli
 Spread : Kidney & Heart
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o Treatment and Prevention:

 Hypersensitivity  Anti-Histamines & Desensitization to allergens
 Invasive Disease
 Surgical removal of Aspergillomas & surrounding tissues
 High Dose IV Amphotericin B + Other antifungal
 Maintenance
 Prevent Relapse in Immunocompromised
 Itraconazole
PENICILLIUM SPECIES
VI. Penicillium Species
Pencillium marneffi
o Dimorphic Invasive Fungus

 Only species of Penicillium - Pathogenic & Dimorphic
 Pulmonary Disease - Inhalation : Conidia
o 3rd Most Common Disease

 AIDS in S.E. Asia – Emerge
 Early Indicator – Particular part of that World E.g. Thailand , China
o Behind PTB & Cryptococcosis
o Serious Disseminated Infectio
o Skin Lesions
 Papular in AIDS
 Molluscum contagiosum-like lesions
 Hematogenous Dissemination
o Infection
 Mononuclear phagocytic System
 Mimics:
 Tuberculosis
 Leishmaniasis
 Histoplasmosis
 Cryptococcosis
o Isolated – Bamboo Rats & Occasionally – Soil
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o Morphology :  Microscopy
 Dimorphic fungi  Elliptical Fission Yeast – Inside Phagocytes ( Buffy Coat BM, lesions, LN )
 Mold form  at 25ᴼ c – sporulates  Internal cross-walls, no budding cells
 Yeast cells  Diagnostic
 at 37ᴼ c
 intracellular resembles histoplasmosis  Culture – SBA
 elongated & more pleomorphic, no budding with transverse septum  Blue-green to Yellowish colonies
 Production: Soluble Red Pigment
o Clinical Manifestations :
 Fever  Immunoblot methods
 Cough  PCR
 Cxr – pulmonary infiltrates  Nucleic Acid Based Testing – Confirm identification
 Lymphadenopathy
 Organomegaly o Treatment & Prevention
 Blood  leukopenia & thrombocytopenia  Amphotericin B with or without flucytosine  Treatment of choice
 Amphotericin x 2 weeks followed by Itraconazole x 10 weeks
 Prevention of Relapse in AIDS  Lifelong treatment - Itraconazole
ZYGOMYCOSIS
VII. Zygomycosis
o Mucormycosis or Phycomycosis
o Saprophytic Mold Fungi
o Opportunistic Fungal infection
 Various Fungal Genera
 Division:
 Zygomycota
 Mucor
 Rhizopus – Food spoilage – Black bread Mold
 Rhizomucor
 Absidia
o Worldwide Distribution – Soil, decaying Organic matter

o Lesions : Face & Head Area  Spread Everywhere  Lungs , Skin , GIT
o Pathogenesis Of Zygomycosis
 IDEAL SPECIMEN :
 INFECTION
 Blood, Tissues, skin lesions, Lymph node, Bone marrow,
 Broncho-alveolar lavage  Nasal mucosa  Nasal turbinate Paranasal sinuses  Orbit  Brain
 Use of Special Stains
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o Predisposing Factors:  Microscopy

 Uncontrolled diabetes mellitus  KOH & GMS Stained Tissue
 pH of Blood & tissue fluids  Very large or Broad Thick-walled Nonseptated Hyphae (Ribbon-like)
 Enhance invasion with Wide Irregular Branching ( 90ᴼAngle ) often Fractured or Twisted
 Leukemia  Large prolific Sporangia
 Lymphoma
 Clinical Diagnosis
o Prognosis:  E.g. Rhinocerebral Mycosis – Clinical Observation – Mouth , Nose Then
 Leading to  Fatal Outcome use Laboratory techniques - Confirm
 Improvement  Anti-fungal treatment.
 Spread to lungs  Disseminated infection o Microscopic Appearance
 Majority – Microscopy
o Clinical Conditions - Disseminated Form:  Broad aseptate mycelium numerous asexual spores inside sporangium –
 Rhinocerebral Zygomycosis - Inhalation of Spores develops at end of the aerial hyphae
 Infection : Paranasal Sinuses
 Spread Mouth  Nose = Macroscopic Cotton-like Growth
 Blood Vessel Invasion  Fibrous Clots  Tissue necrosis
 Brain Involvement  Fast & fatal = Brain Abscesses
 Manifestation:
 Extensive Cellulitis & Tissue destruction.
 Risks Factors:
 Diabetes mellitus
 Leukemia
 Lymphomas
 Pulmonary Zygomycosis
 Deep Inhalation of Spores ( Moldy Foods )  Bronchioles & Alveoli 
Necrosis  Lung cavitation
 Gastrointestinal Zygomycosis
 Ingestion of fungal elements  Necrotic Ulcers GIT
 Cutaneous Zygomycosis
 Skin trauma – Introduction of Fungal elements E.g. Burns & Needle
Puncture
 Lesions : Pustular  Ulcers  Abscesses  Necrotic Patches of Skin
o Laboratory Diagnosis:
 Clinical history – Important
 Clinical Specimens: Skin Scrapings , Lung Aspirates & biopsies
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OTHER OPPORTUNISTIC MYCOSES

o Treatment & Prevention
 Surgical removal  Infected Tissues VIII. Other Opportunistic Mycoses
 Medications : o Advances in Medicine have resulted in increase in fungal infections
 Oral: Nystatin , Amphotericin B, Gentian violet o Devastating systemic infections have been caused by species of
 Enteritis: Ketoconazole  Fusarium
 Vaginitis: Nystatin, Amphotericin B Suppositories  Paecilomyces
 Systemic: Amphotericin B + 5 flucytosine  Bipolaris
 Curvilaria
 Alternaria
o Early Diagnosis
 Highly essential for effective cure #JourneytoVNECK
 Treatment  Effective if commenced Early in the infection
 High doses of I V Amphotericin B – 8-10 WEEKS  DOC – ALL ZYGOMYCOSIS
 Surgical interventions +
AMDG
 Control of Diabetes - Basic requirement for better clinical outcome Gloria in Excelsis Deo
“Brace yourself, winter is coming.”

That is, Prelims is coming.
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Opportunistic Mycoses - DR Santos

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MICROBIOLOGY: OPPORTUNISTIC MYCOSES

Reference: Dr. Camilo Santos’ Lecture

INTRODUCTION o Population at Risks: ( Predisposing Factors )

o Conditions: Weakened Immune Function:

o Classical Opportunists o Transmission of Opportunistic Fungi

II. Candida Species

o Dominant Opportunistic Mycoses

o CLINICAL INFECTION  Localized  Severe Systemic Infection o MORPHOLOGY :

 Surface Virulence Molecules  Receptors, Adhesins, Pyrogens, &

o TRANSMISSION: Member = Normal flora

 Vulvovaginitis or Vaginal thrush

 Candidal Blood-borne Infection – Candidemias

o Principal Targets of Systemic Infection:

 Chorioretinitis, Endophthalmitis, & Traumatic Keratitis

 Confirmatory Test - C. albicans

III. Cryptococcus Species

 India Ink Smears

 Filobasidiella neoformans – Sexual form of Cryptococcus

o Four Serotypes - A,B,C,D o Pathogenesis:

 Dissemination - Few cases: Skin, Bones, Viscera

 Carbohydrate Assimilation Testing

o Pneumocystis carinii - Protozoan????

o Worldwide: Symptoms occur

o CXR: Ground glass Appearance

o Three clinical pulmonary diseases :

o Paranasal Sinuses, Ear Canal Aspergilloma

o Eyelids, Eye sockets, Conjunctiva Aspergilloma

o Cutaneous Aspergillosis: Skin trauma

o Systemic Aspergillosis  Involves major Organ Systems  AIDS

o Mycotoxicoses  Acquired – Contaminated food

o Treatment and Prevention:

VI. Penicillium Species

o Dimorphic Invasive Fungus

o 3rd Most Common Disease

o Behind PTB & Cryptococcosis

o Serious Disseminated Infectio

o Isolated – Bamboo Rats & Occasionally – Soil

o Worldwide Distribution – Soil, decaying Organic matter

o Predisposing Factors:  Microscopy

 Lesions : Pustular  Ulcers  Abscesses  Necrotic Patches of Skin

OTHER OPPORTUNISTIC MYCOSES

“Brace yourself, winter is coming.”

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