Opportunistic Fungal Infections Notes

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Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Opportunistic Fungal Infections essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Opportunistic Fungal Infections:

Aspergillus fumigatus

Pneumocystis jirovecii (Pneumocystis pneumonia)

Sporothrix schenckii

Candida

Cryptococcus neoformans

Mucormycosis

NOTES NOTES OPPORTUNISTIC FUNGAL INFECTIONS GENERALLY, WHAT ARE THEY? PATHOLOGY & CAUSES ▪ Range of infections caused by fungi; take advantage of weakened immunity (e.g. HIV/ AIDS, malignancy, immunosuppression), altered microbiota, breached integumentary barriers ▪ Present in environment worldwide → immunocompetent, healthy individuals can be exposed without resulting in disease RISK FACTORS ▪ Immunosuppression (e.g. HIV/AIDS, neutropenia, chemotherapy, hematologic malignancies, transplant recipients) SIGNS & SYMPTOMS ▪ Primary local cutaneous, pulmonary infection to dissemination to various internal organs DIAGNOSIS LAB RESULTS ▪ Direct microscopy with staining, culture, tissue biopsy, bronchoalveolar lavage (sputum sample if pulmonary in origin), polymerase chain reaction (PCR) TREATMENT MEDICATIONS ▪ Antifungals ASPERGILLUS FUMIGATUS osms.it/aspergillus-fumigatus PATHOLOGY & CAUSES ▪ Saprophytic fungi species responsible for majority of invasive, chronic aspergillosis ▪ Found in soil, compost ▪ Asexual reproduction → production of green pigmented asexual conidia (spores) → aerosolized → individuals inhale everyday → macrophages attempt to clear conidia → secondary inflammation after conidia germinate into hyphal forms → neutrophil recruitment → activation of 460 OSMOSIS.ORG cellular immunity to kill hyphae ▪ Histopathologically, invasive aspergillosis characterized by progression across tissue planes ▫ Hallmark: vascular invasion → infarction + tissue necrosis ▪ Characteristics of Aspergillus as successful opportunistic pathogen ▫ Ability to grow at 37ºC/98.6°F ▫ Small conidial (2.5–3 micrometers) → buoyant in air for prolonged periods of time → inhaled deeply into lung alveoli
Chapter 84 Opportunistic Fungal Infections ▪ Aspergillus hyphae angioinvasive ▫ Thrombose arteries → hemorrhagic infarcts → abscesses ▪ Suspect in immunocompromised individuals with respiratory distress, fever (despite broad-spectrum antibiotics) ▪ Second most common cause of invasive fungal infections in neutropenic individuals (after Candida species) ▪ Specifically affects pulmonary, sinus, central nervous system (CNS) Diseases ▪ Necrotizing otitis externa ▫ More common in advanced HIV cases ▪ Acute pulmonary aspergillosis ▫ Inhaled conidia ▫ Most common cause of death in persons with chronic granulomatous disease (CGD) ▫ Can spread locally to involve pleura, chest wall, vertebrae → dissemination to other organs Figure 84.1 Bronchial washing stained with Grocott methenamine silver stain from and individual with pulmonary aspergillosis. The hyphae are uniform, narrow and branch at acute angles. ▪ Cerebral aspergillosis ▫ Occurs in approx. 40% of individuals with invasive aspergillosis ▫ Hematogenous dissemination from extracranial focus (e.g. lung)/direct extension from sinus ▫ Most common brain abscess in stem cell transplant individuals ▪ Pulmonary aspergilloma ▫ Nonsaphrophytic (noninvasive) ▫ Colonization of pre-existing cavities (e.g. tuberculosis, sarcoidosis, bullous emphysema, bronchiectasis) ▫ Occurs in 15–25% of persons with cavitating lung disease from tuberculosis ▫ Lesion impinges on major vessel/airway → massive hemorrhage → hemoptysis ▫ “Fungus ball” ▪ Allergic bronchopulmonary aspergillosis ▫ Exposure to allergens of A. fumigatus → saprophytical growth → colonization of bronchial lumen → persistent bronchial inflammation → IgE-mediated allergic response in airways → hypersensitivity lung disease → bronchial obstruction ▫ Affects those with asthma (1–2%)/cystic fibrosis (1–15%) RISK FACTORS ▪ Decreased immunity ▫ Malignancy, chemotherapy, transplant (esp. from HLA-mismatched donor), HIV/AIDS, immunosuppressant therapy, neutropenia, prolonged high dose corticosteroid use ▪ Prior pulmonary damage/disease ▪ ↑ age ▪ History of tuberculosis, histoplasmosis, sarcoidosis, bronchiectasis ▪ Cystic fibrosis, asthma (allergic bronchopulmonary aspergillosis) COMPLICATIONS ▪ Hemorrhage → massive hemoptysis ▪ Widespread bronchiectasis + fibrosis → respiratory failure, death SIGNS & SYMPTOMS ▪ Acute pulmonary aspergillosis ▫ Unremitting fever in high-risk cases (most common), dry cough, chest pain, dyspnea (more common in persons with diffuse disease), ↑ erythrocyte sedimentation rate (ESR) OSMOSIS.ORG 461
▪ Invasive sinusitis ▫ Ear/facial pain, discharge, swelling; nasal septum/turbinate pallor; epistaxis; orbital swelling, headache; localized areas of frank crusting, ulceration, blackened necrotic areas ▪ Cerebral infection ▫ Headache, nausea, vomiting; altered mental status, confusion, cranial nerve palsies, hemiparesis ▪ Pulmonary aspergilloma ▫ May be asymptomatic; persistent, productive chronic cough, hemoptysis, weight loss ▪ Allergic bronchopulmonary aspergillosis ▫ Manifestations due to immune system response to A. fumigatus antigens; asthma-like symptoms (e.g. wheezing), eosinophilia ▪ Invasive aspergillosis ▫ Acute onset of fever, cough, respiratory distress, diffuse bilateral pulmonary infiltrates DIAGNOSIS DIAGNOSTIC IMAGING CT scan ▪ Increased sensitivity for radiological diagnosis ▪ Halo sign ▫ Neutropenic individuals (hemorrhagic nodule due to angioinvasion); rim of ground glass opacity surrounding nodule ▪ Air crescent sign ▫ Can develop from halo sign; cavitation → sloughed lung tissue encircled with rim of air MRI ▪ Target sign ▫ Nodule with lower central signal, higher contrast-enhancing signal on periphery; late stage disease ▪ For diagnosis of cerebral aspergillosis; multiple lesions in basal ganglia 462 OSMOSIS.ORG X-ray ▪ Unilateral infiltrates (interstitial, alveolar, mixed), cavitary lesions, multiple nondefined 1–3cm.0.39–1.18in peripheral nodules coalesce into larger masses LAB RESULTS Tissue biopsy ▪ Not utilized frequently due to invasive nature; ↑ risk of bleeding or secondary infection in immunosuppressed individuals Cultures ▪ Respiratory tract, sputum cultures commonly negative; rarely diagnosed by blood Bronchoalveolar lavage ▪ Approx. 40% diagnostic yield Serology ▪ Useful for diagnosis of aspergilloma, allergic bronchopulmonary aspergillosis in immunocompetent individual; not useful in immunocompromised Galactomannan antigen testing ▪ Enzyme immunosorbent assay recognizes side chains of galactomannan molecule ▫ Positive: invasive disease ▫ High false-positive rate in neutropenic cases Allergic bronchopulmonary aspergillosis ▪ Eosinophilia, ↑ serum IgE Figure 84.2 A tissue section containing Aspergillus hyphae and fruiting heads.
Chapter 84 Opportunistic Fungal Infections TREATMENT MEDICATIONS ▪ Invasive aspergillosis ▫ Voriconazole (preferred over amphotericin B)/caspofungin; azoleresistance developing ▪ Local pulmonary aspergilloma ▫ Percutaneous intracavitary instillation of antifungals ▪ Allergic bronchopulmonary aspergillosis ▫ Corticosteroids (attenuate immune system response) ▫ Antifungal therapy: itraconazole (decrease fungal burden, antigen load) ▫ Preventative long term antifungal therapy in immunocompromised individuals SURGERY ▪ Local pulmonary aspergilloma ▫ Surgical removal (e.g. lobectomy in massive hemoptysis) CANDIDA osms.it/candida PATHOLOGY & CAUSES ▪ Oval, budding yeast; forms hyphae, pseudohyphae ▪ Nonpathological colonization of humans → overgrowth leads to pathology ▪ Most common cause of invasive fungal infections in immunocompromised individuals (e.g. neutropenic cases) ▫ C. albicans species most common cause of candidiasis ▫ Increasing proportion of fungal infections caused by nonalbicans Candida species (e.g. C. tropicalis, C. parapsilosis, C. kruseim, C. glabrata) Chronic mucocutaneous candidiasis ▪ Persistent infection of mucous membranes, skin, nails ▪ More commonly affects those with defective T-cell mediated immunity Vulvovaginal candidiasis (VVC) ▪ Originates from spread from GI tract, sexual transmission ▪ Occurs in 75% of healthy individuals who are biologically female ▫ 80–90% caused by C. albicans ▫ 10–20% of those with VVC have severe, recurrent infections; usually from nonalbicans species Candida esophagitis ▪ Most common in severely immunocompromised individuals (e.g. HIV individuals) ▪ May occur in absence of thrush ▪ In individuals with AIDS, can occur simultaneously with cytomegalovirus, herpes simplex infection (HSV) Disseminated/invasive candidiasis ▪ Rare in immunocompetent individuals ▪ Development of invasive disease due to interaction between Candida species virulence factors, colonization burden, host immunological status ▪ Candidemia ▫ Isolation of Candida from blood culture ▪ Candida species exhibit tissue tropism → deep organ involvement (e.g. liver, spleen, brain, bone) in absence of prolonged candidemia OSMOSIS.ORG 463
RISK FACTORS ▪ Antibiotic therapy, diabetes mellitus (poorly controlled), immunocompromised state (e.g. immunosuppressive therapy, neutropenia, hematologic malignancy, chemotherapy, transplant), chronic granulomatous disease, Job syndrome, impaired cell-mediated immunity, pregnancy, contraceptive use (hormonal/intravaginal, intrauterine devices) COMPLICATIONS ▪ ▪ ▪ ▪ hypertension, flank mass, pyelonephritis, acute urinary obstruction from fungal mycetoma → hydronephrosis CNS: altered mental status, characteristic symptoms of meningitis Optic: chorioretinal infections, lens abscess Hepatosplenic: right upper quadrant pain; nausea, vomiting; hepatosplenomegaly Other: endocarditis (may be from central vascular catheters), bone/joint infections ▪ Meningoencephalitis ▫ Obstructive hydrocephalus, calcifications, thrombosis ▪ Renal system ▫ Pyelonephritis ▪ Abscesses in multiple organs ▪ Sepsis, septic shock SIGNS & SYMPTOMS Mucocutaneous growth (most common) ▪ Mouth, oropharynx ▫ AKA thrush ▫ Thick, pearly white, curd-like plaques on oral mucosa ▫ Painful → dysphagia/odynophagia ▫ Otherwise unexplained → suspect HIV infection ▪ Vagina ▫ Thick, cottage-cheese-like, white vaginal discharge ▫ Painless, pruritic ▫ Dysuria possible ▪ Cutaneous candidiasis ▫ Erythematous pruritic patches + satellite lesions ▫ Individuals who are obese, diabetic ▫ Skin folds, underneath breasts ▪ GI tract ▫ May be asymptomatic ▫ Esophagus → odynophagia Disseminated/invasive candidiasis ▪ Candidemia: nonspecific (hard to distinguish from bacteremia); most commonly manifests as persistent fever despite antibiotic therapy ▪ Renal system: candiduria, rising creatinine, 464 OSMOSIS.ORG Figure 84.3 Oral candidiasis on the tongue of a child who had recently taken oral antibiotics. DIAGNOSIS LAB RESULTS ▪ Microscopic examination ▫ KOH preparation; visualization of hyphae, pseudohyphae, blastospores ▪ Invasive candidiasis ▫ Blood/tissue culture ▪ PCR ▪ Esophagitis ▫ Tissue biopsy (definitive)
Chapter 84 Opportunistic Fungal Infections OTHER DIAGNOSTICS ▪ Clinical presentation, history TREATMENT MEDICATIONS ▪ Oropharyngeal candidiasis ▫ Oral nystatin suspension; clotrimazole troches (dissolves in mouth) ▪ Candida dermatitis ▫ Topical nystatin/miconazole ▪ Vulvovaginal candidiasis ▫ Local miconazole/clotrimazole creams; oral fluconazole ▪ Invasive, systemic candidiasis ▫ Echinocandins; voriconazole, caspofungin (preferred over amphotericin/fluconazole) ▪ Individuals with HIV ▫ Prophylactic antifungals (e.g. oral nystatin, fluconazole) OTHER INTERVENTIONS ▪ Candida dermatitis ▫ Keep skin dry ▪ Invasive, systemic candidiasis ▫ Immediate removal of all central lines, catheters (Candida can develop rapid biofilms) CRYPTOCOCCUS NEOFORMANS osms.it/cryptococcus-neoformans PATHOLOGY & CAUSES ▪ Heavily encapsulated, nondimorphic, yeastlike fungus, urease positive ▪ Virulence factors ▫ Grows well in 37ºC/98.6°F environment ▫ Produces polysaccharide capsule, melanin (neurotropism) ▪ Most common cause of fungal meningitis in immunocompromised adults ▪ Found in bird droppings, soil → inhalation of airborne fungi → evident/nonevident pulmonary infection → spreads lymphohematogenously (can affect any organ) → meninges ▪ CNS infection associated with high mortality COMPLICATIONS ▪ Increased intracranial pressure → herniation → death ▪ May be due to buildup of cryptococcal polysaccharide at arachnoid villi → disruption in cerebrospinal fluid (CSF) reabsorption RISK FACTORS ▪ Impaired cell-mediated immunity, highdose corticosteroid treatment, hematologic malignancies (e.g. leukemia, lymphoma) ▪ HIV/AIDS (most common immunocompromising state): < 100 cells/ mm3 CD4+ count Figure 84.4 A histology photomicrograph of the lung. OSMOSIS.ORG 465
SIGNS & SYMPTOMS ▪ Pulmonary manifestations ▫ Asymptomatic in 1/3 of immunocompetent individuals; fever, cough, pleuritic chest pain, dyspnea, weight loss, hemoptysis ▪ Neurologic manifestations (most common) ▫ Acute/insidious; headache, fever, vomiting, nuchal rigidity, mental status changes/seizures, cryptococcal abscesses (e.g. cryptococcomas, not common) ▪ Skin manifestations (10–15%) ▫ Result of direct hematogenous spread/ extension from bone lesion; single/ multiple pustules/papules → ulcer/ abscess ▪ Bone infection (5–10%) ▫ Pain, swelling; joint involvement; often found incidentally DIAGNOSIS DIAGNOSTIC IMAGING Chest X-ray ▪ Focal/diffuse interstitial infiltrates, hilar lymphadenopathy LAB RESULTS ▪ CSF ▫ Lymphocytic pleocytosis; ↓ glucose; ↑ protein, opening pressure; results may be unchanged in individuals with AIDS ▪ Direct microscopic analysis of CSF/other body secretions ▫ India ink: capsule visualized with clear halo ▫ Mucicarmine: visualization of red inner capsule ▫ Visualize budding ▪ Culture ▫ Sabouraud glucose agar, incubation up to two weeks ▪ Cryptococcal capsular antigen (serum, CSF, urine, bronchoalveolar lavage) ▫ Most reliable nonculture-based method 466 OSMOSIS.ORG ▪ Latex agglutination test ▫ Detects polysaccharide capsular antigen, ↑ specificity Figure 84.5 Bronchial washings from an immunocompromised individual with pulmonary cryptococcosis. The cryptococcus spores have a characteristically thick capsule. TREATMENT MEDICATIONS ▪ Amphotericin B, flucytosine ▪ Prevention in HIV cases with CD4+ cell counts < 100 cells/mm3—fluconazole OTHER INTERVENTIONS ▪ ↑ intracranial pressure complication treatment ▫ Repeat CSF drainage (most important factor in reducing mortality)
Chapter 84 Opportunistic Fungal Infections MUCORMYCOSIS osms.it/mucormycosis PATHOLOGY & CAUSES ▪ Several genera of family Mucoraceae causing rapidly progressive, invasive mucormycosis in various body systems ▪ Subphylum Mucoromycotina, order Mucorales ▫ Most human infections from members of family Mucoraceae ▫ Six genera: Rhizopus, Mucor, Actinomucor, Rhizomucor, Apophysomyces ▪ Present in decomposing organic matter (e.g. spoiled food items, soil) ▪ Forms broad, aseptate hyphae branching at right angles by sexual reproduction with formation of zygospores ▪ Inhalation of spores → sinuses, lungs primary location of infection ▪ Immunocompetent host → lung macrophages ingest, kill spores → neutrophils kill hyphae ▪ Immunosuppressed individuals → macrophages fail to stop spore germination ▪ Severe neutropenia/diabetic ketoacidotic individuals → abnormal neutrophil function → increased risk of invasive infection ▪ Angioinvasive mold → results in thrombosis, infarction, necrosis of surrounding tissues Diseases ▪ Rhinocerebral mucormycosis ▫ Necrotic lesion in paranasal sinus → orbit, face, palate, brain ▫ Most common in diabetic ketoacidosis ▫ Progresses rapidly ▪ Pulmonary mucormycosis ▫ Most common in severe neutropenic individuals ▪ Gastrointestinal mucormycosis ▫ Rare, occurs in severely malnourished children ▫ Can affect all segments of GI tract (esp. stomach, small/large intestine, esophagus) ▪ Cutaneous mucormycosis ▫ Due to traumatic implantation of spores from soil (e.g. site of surgical incisions, burn wounds) ▫ Extensive necrotic infection → necrotizing cellulitis ▫ Most common in immunocompetent individuals ▪ Disseminated mucormycosis (involves CNS) ▫ Most common in severe neutropenic individuals following pulmonary infection ▫ Brain (most commonly affected), metastatic necrotic lesions can occur in any organ RISK FACTORS ▪ DM ▪ Diabetic ketoacidosis state ▫ ↑ risk for rhinocerebral mucormycosis ▪ Leukemia, neutropenia, chemotherapy ▫ ↑ risk of rhinocerebral, pulmonary, disseminated disease ▪ Severe malnutrition ▫ GI mucormycosis ▪ Deferoxamine treatment for iron overload state ▪ Recipient of bone marrow transplant ▪ Prolonged use of corticosteroids/other immunosuppressive therapies ▪ Prolonged use of broad-spectrum antibiotics ▪ IV drug use COMPLICATIONS ▪ Cavernous sinus thrombosis, cranial nerve palsies (e.g. proptosis, ptosis, dilation, fixation of pupil), vision loss, OSMOSIS.ORG 467
brain abscess, necrosis of frontal lobes, GI tract perforation, perirenal abscess, renal infarction SIGNS & SYMPTOMS ▪ Typical course: rapid onset of necrotic lesion → fulminant course requiring aggressive therapy ▪ Rhinocerebral ▫ Black, necrotic lesion on nasal/palatine mucosa; nasal/sinus congestion, pain; epistaxis; fever; edema, induration, necrosis of perinasal, periorbital tissue ▪ Pulmonary ▫ Nonspecific, pneumonia-like; may involve pleuritic chest pain, cough, fever, hemoptysis ▪ GI ▫ Abdominal pain, bleeding (e.g. hematemesis) ▪ Cutaneous ▫ Painful edema, erythema → raised, indurated lesions with black, necrotic center ▪ Disseminated ▫ Altered mental status (e.g. lethargy, obtunded state, confused) DIAGNOSIS DIAGNOSTIC IMAGING CT scan, MRI ▪ Thoracic: nodular lesions, cavitations ▪ Head: extension of infection in sinuses → affecting brain tissue LAB RESULTS ▪ Histopathological identification ▫ Distinct hyphae; broad irregularly branched with rare septations 468 OSMOSIS.ORG Figure 84.6 Bronchial washings stained with Papanicolaou stain from an individual with pulmonary mucormycosis. The mucor hyphae contain no septa, are of variable width and branch at a wide angle. TREATMENT MEDICATIONS ▪ Aggressive antifungal therapy ▫ Amphotericin B SURGERY ▪ Infected necrotic tissue ▫ Extensive surgical debridement OTHER INTERVENTIONS ▪ Adjunctive therapy ▫ Hyperbaric oxygen, immune modulation, white blood cell infusion
Chapter 84 Opportunistic Fungal Infections PNEUMOCYSTIS JIROVECII (PNEUMOCYSTIS PNEUMONIA) osms.it/pneumocystis-jirovecii PATHOLOGY & CAUSES ▪ Opportunistic yeast-like fungi (originally classified as protozoan) responsible for pneumocystis pneumonia ▪ Formerly known as Pneumocystis carinii ▪ Airborne transmission route; human-tohuman route occurs early in life ▪ Immunocompetent individuals may act as asymptomatic reservoirs ▪ 5–7 micrometer cysts contain up to eight pleomorphic intracystic sporozoites → become excysted → form trophozoites ▪ Reside in alveoli ▪ Disease: pneumocystis pneumonia ▫ Occurs exclusively in immunocompromised individuals ▫ Remains localized in lungs ▫ Clinical manifestations due to inflammatory reaction in alveoli lumen/ septum ▫ Fatal if left untreated RISK FACTORS ▪ Defects in cell-mediated immunity, HIV/ AIDS, severe combined immunodeficiency syndrome, hematological malignancies, transplant recipients, hyper IgM syndrome SIGNS & SYMPTOMS ▪ Most infections asymptomatic in immunocompetent individuals ▪ Abrupt onset of tachypnea, fever, cough ▪ Respiratory distress DIAGNOSIS DIAGNOSTIC IMAGING Chest X-ray/CT scan ▪ Diffuse, bilateral ground glass opacities ▪ First appearing in perihilar area → progresses peripherally, apical regions spared LAB RESULTS ▪ Microscopic examination with silver stain ▫ Disc-shaped yeast ▪ Open lung biopsy ▪ Bronchoalveolar lavage ▪ PCR of sputum/lavage samples ▪ ↓ PaO2 (reflects severity of disease) ▪ Unchanged WBC count TREATMENT Figure 84.7 A foamy alveolar cast in a bronchial washing taken from an individual with Pneumocystis pneumonia. MEDICATIONS ▪ Trimethoprim-sulfamethoxazole ▪ Alternatives ▫ Pentamide, dapsone + trimethoprim, atovaquone OSMOSIS.ORG 469
▪ Prophylactic trimethoprimsulfamethoxazole/pentamide ▫ Individuals with HIV, < 200 CD4+ cells/ mm3 OTHER INTERVENTIONS ▪ Respiratory support Figure 84.8 A bronchial wash stained with Grocott’s methenamine silver highlighting Pneumocystis spores. SPOROTHRIX SCHENCKII osms.it/sporothrix-schenckii PATHOLOGY & CAUSES ▪ Chronic subcutaneous thermally dimorphic fungus → sporotrichosis ▪ Found in soil, decomposing vegetation, plant materials (e.g. moss, hay, wood, rose bushes) ▪ Found worldwide, mostly in temperate/ tropical regions (16–22ºC/60.8–71.6°F) ▪ Outside human body grows as filamentous mold; in tissue grows as small budding yeast cells Diseases ▪ Lymphocutaneous sporotrichosis ▫ Follows traumatic inoculation of skin/ subcutaneous tissue (e.g. minor insult from thorns or splinters) → incubation 1–4 weeks → papule develops at site of inoculation → ulceration of primary lesion → nonpurulent, odorless drainage → similar lesions occur along lymphatic channel proximal to primary lesion ▪ Pulmonary sporotrichosis ▫ Following inhalation of Sporothrix conidia ▫ May progress to disseminated disease 470 OSMOSIS.ORG ▪ Osteoarticular sporotrichosis ▫ Most commonly affected joints: knee, elbow, wrist, ankle ▫ Chronic infection with progressive decreased range of motion, pain, swelling ▪ Meningeal sporotrichosis ▫ Rare, mostly in individuals with cellular immune defects (e.g. lymphoma, AIDS) ▫ Chronic course ▪ Disseminated cutaneous sporotrichosis ▫ Rare (< 1%) ▫ Numerous small papules/vesicles → necrotic, ulcerated nodules on trunk, limbs ▫ Follows lymphatic spread RISK FACTORS ▪ Lymphocutaneous ▫ Exposure due to skin trauma (e.g. living in homes with dirt floors) ▫ Individual with outdoor preoccupation ▫ Contact with cats ▪ Pulmonary ▫ Chronic obstructive pulmonary disease (COPD) ▪ Excessive alcohol use
Chapter 84 Opportunistic Fungal Infections SIGNS & SYMPTOMS ▪ Lymphocutaneous sporotrichosis ▫ Primary papule → ulcerated lesion; similar lesions visualized along lymphatic channel proximally; chronic, fixed cutaneous lesion ▪ Pulmonary ▫ Fever, night sweats, weight loss, fatigue; dyspnea, cough; purulent sputum; hemoptysis ▪ Osteoarticular sporotrichosis; progressive decreased range of motion, pain, swelling in joints ▪ Meningeal sporotrichosis ▫ Chronic (weeks to months) fever, headache DIAGNOSIS DIAGNOSTIC IMAGING Chest X-ray ▪ Unilateral/bilateral upper lobe cavities ▪ Variable amount of fibrosis ▪ Scattered nodular lesions LAB RESULTS ▪ Culture (most sensitive) ▫ Tissue biopsy, sputum, body fluid ▫ Sabouraud’s agar at room temperature ▫ Characteristic arrangement of conidia on hyphae ▪ Direct microscopy ▫ Typical oval/cigar-shaped cells ▫ Asteroid bodies of S. Schenckii ▪ CSF analysis ▫ Lymphocytic pleocytosis, ↑ protein, ↓ glucose OTHER DIAGNOSTICS ▪ Clinical examination, history Figure 84.10 Sporothrix fungi forming conidia. Figure 84.9 Partially healed skin lesions of sporotrichosis in a typical lymphcutaneous distribution. TREATMENT MEDICATIONS ▪ Localized: itraconazole ▪ Severe: amphotericin B OSMOSIS.ORG 471

Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Opportunistic Fungal Infections essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Opportunistic Fungal Infections:

Aspergillus fumigatus

Pneumocystis jirovecii (Pneumocystis pneumonia)

Sporothrix schenckii

Candida

Cryptococcus neoformans

Mucormycosis