Micro Final - Fungus

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Hwp1

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GPI cell-wall adhesin of Candida albicans found only on germ tubes and true hyphae; mediates attachment to host epithelium by mimicking mammalian epithelial cell proteins that are substrates for an enzyme (transglutaminase) that forms cross-links.

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Virulence factors of Candida albicans

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Agglutinin-like cell-wall proteins
secreted aspartyl proteinases (SAPs)
Lipases and phosphatases
Efflux pumps, confering drug resistance

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This fungus is less susceptible to azoles and amphotericin B than C. albicans

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C. glabrata

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This fungus induces expression of adhesion genes in urine

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C. glabrata

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This fungus accounts for 15% of UTIs

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C. glabrata

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This genus of fungus accounts for 25% of UTIs

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Candida

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This fungus has recently been cultured from the oral cavity of HIV-infected patients and are most frequently implicated in cases of recurrent infection following antifungal drug treatment. Phenotypically, isolates are very similar to C. albicans in that isolates produce both germ-tubes and chlamydospores.

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Candida dubliniensis

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This fungus has unusual carbohydrate assimilation patterns and grows poorly or not at all at 42C.

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Candida dubliniensis

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Germ tubes

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Hyphal precursors. Identifying characteristic of Candida albicans. C. albicans is the only yeast that forms germ tubes within an hour of after incubation in serum at 37 degrees C. This is taken as presumptive identification of unknown yeasts as C. albicans in clinical laboratories. Biochemical tests are needed for definitive identification.

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These are diseases caused by C. albicans

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Diaper rash, thrush, vaginitis, mucositis, etc.

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This fungus grows predominantly in budding yeast form on usual lab culture media

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Candida albicans

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This fungus forms creamy white yeast colonies on most media

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Candida albicans

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This fungus forms vegetative hyphae beneath the agar surface on rich media at neutral pH at room temp

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Candida albicans

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This fungus grows in yeast, pseudohyphal and hyphal growth forms in host tissue

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Candida albicans

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This fungus grows mainly in hyphae and pseudohyphal forms when it invades host tissue

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Candida albicans

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These are four manifestations of oropharyngeal candidiasis

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Thrush (acute pseudomembranous): white patches on mucosa
erythematous: mild, reddening of mucosa
central papillary atrophy of dorsal tongue
angular cheilitis (invasion of epithelium at corners of mouth)

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This is the primary host defense against C. albicans

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Epidermis and epithelium

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Histatin

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Cationic peptide found in saliva. Harmful to C. albicans

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Defensins

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Cationic peptide found in epithelium. Harmful to C. albicans

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This is one way to test normal CMI response in people

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Skin test with C. albicans; it is present in the normal flora, thus immunocompetent people should be able to mount a cell-mediated response

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Antibodies to this fungal pathogen are not associated with protection

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Candida albicans

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Transglutaminase

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Mammalian epithelial cell enzyme that forms cross-links to create primary host defense barrier, cross-linking epithelial cell proteins. C albicans exploits this to attach hyphae to the mucosa

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ALS

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Agglutinin-like sequence. Permits attachment of C. albicans to mucosal epithelium and host proteins such as fibronectin

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SAP

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Secreted aspartyl proteinase. Hydrolytic enzyme of C. albicans

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Rapid germ-tube test

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Used to diagnoses C. albicans. Germ tube formation in serum within 1-2 hours. Diagnosis is only presumptive.

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Definitive dx of this fungal pathogen requires fermentation and assimilation of carbohydrates and other compounds

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C. albicans

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These are risk factors that predispose patients to candidiasis

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Xerostomia, antibiotics, poor oral hygeine, malnutrition or GI malabsorption, Fe, folic acid or vitamin deficiencies, carbohydrate-rich diets, heavy smoking, oral epithelial dysplasia, factors that alter the immune status of the host (age, HIV, DM, thyroid problems, pregnancy, cortisol

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Levels of this bacteria are reduced during candidiasis

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Lactobacillus

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These fungi are keratinophilc, having keratinases that allow them to use keratin as a substrate for growth

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Dermatophytes

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These fungal infections involve the dermis and subcutaneous tissue, and are rare in the US and other developed countries

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Subcutaneous mycoses

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This fungus causes dandruff and seborrheic dermatitis

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Malassezia

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This fungus causes Tinea nigra

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Cladosporium (Exophiala) weneckii

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10% NaOH mount

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Used for direct examination of clinical specimens of fungi

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Endothrix

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Fungal elements inside hair shaft

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Ectothrix

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Fungal elements around the hair shaft

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Griseofulvin

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Useful treatment for dermatophytes

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This is the most important acquired immune defense mechanism for inhibiting fungal infections

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CMI

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T/F: Fungi are NOT transmitted person-to-person in system mycoses

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True. Transmission requires spore formation, which is produced by hyphae which only grow in the environmental form

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Laboratory cultures of the mold forms of fungi causing this general type of infection are hazardous

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Systemic mycosis

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Less than 1% of infections with this fungal pathogen become progressive and require therapy

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Histoplasma capsulatum

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These are the primary fungal pathogens

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H. capsulatum
B. dermatitidis
C. immitis
C. posadasii
Paracocidiodes brasiliensis

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T/F: H. capsulatum produces a capsule

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False. Capsular appearance of the fungus is an artifact of staining.

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This fungal pathogen grows within macrophages; yeasts are able to survive in the phagocytic vacuole

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Histoplasma capsulatum

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This fungus produces macrocondidia with characteristic morphology (tuberculate) in its hyphal form

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Histoplasma capsulatum

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This disease is an opportunistic disease often mistake for TB, arising in pts with structural defects of the lung

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Chronic pulmonary histoplasmosis

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This fungus may infect epithelial cells, which may serve as a reservoir of infection

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Histoplasma capsulatum

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This fungus spends 2-3 days germinating in the bronchioles or alveoli before proliferating in macrophages, which migrate to the mediastinal lymph nodes, spleen and liver

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Histoplasma capsulatum

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This yeast proliferates for 9-15 days prior to the onset of CMI response

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Histoplasma capsulatum

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Native habitat of Histoplasma capsulatum

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Soil. Human-to-human transmission does NOT occur

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The Ohio River Valley and the central US (eg, Northern Texas) is a major endemic area of this fungal pathogen

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Histoplasma capsulatum

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Wright stain

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Reveals intracellular yeasts in macrophages infected with Histoplasma capsulatum

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This disease is particularly lethal to dogs

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Blastomycosis

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Cultures of this yeast appear cottony

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Blastomyces dermatitidis

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This fungus, in its yeast form, has single buds with a characteristic broad base

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Blastomyces dermatitidis

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Macrophages may carry this yeast to other organs in infections

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Blastomyces dermatitidis

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This fungus may produce influenza-like symptoms

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Blastomyces dermatitidis

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These two organisms are antigenetically cross reactive

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Histoplasma capsulatum and Blastomyces dermatitidis

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This fungus has an infection rate of 40%, with symptoms consistent with lower respiratory infection and/or systemic illness (chest pain, malaise, fever, chills, night sweats, anorexia, weakness, arthralgia).

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Coccidioides immitis

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Valley fever lasts for this long

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2-6 weeks

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A small number of cases of this disease progress to a chronic pulmonary form characterized by cavity formation

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Valley fever

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This fungus features barrel-shaped arthrocondidia which are easily fragmented and highly infectious

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Coccidioides immitis

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This fungus produces spherules in the host

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Coccidioides immitis

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This is the initial host response to Coccidioides immitis

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Macorphages and PMNs. However, the fungus is resistant to PMNs, thus not until CMI kicks in is the host protected

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This fungus grows in the lower sonoran life zone, and is endemic in certain areas of North, Central and South America, including Central Texas and other southwestern states

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Coccidioides immitis

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Lower sonoran life zone

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Arid climate, hot summer, low altitude, alkaline soil, sparse flora

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This fungus more commonly causes symptoms in men of dark-skinned races, particularly Filipinos

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Coccidioides immitis

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Disseminated infection of this fungal pathogen can cause anergy

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Coccidioides immitis

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Serological tests are useful for the monitoring of progress of this fungal disease

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Valley fever. IgM in first 3 weeks, IgG later on. Ab's disappear with resolution of disease, and persist with continued infection, thus they are a reliable indicatory of disease progress.

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This fungus causes pneumonitis with a "buckshot" appearance on chest radiograph with subsequent calcification in cases of heavy exposure.

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Histoplasma capsulatum

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Macrophages with intracellular yeasts is a hallmark of this disease

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Disseminated histoplasmosis

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An important attribute for virulence is this pathogen’s ability to grow within macrophages, surviving in the phagocytic vacuole.

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Histoplasma capsulatum

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This fungal pathogen can be tested for with a skin test similar to the skin test for TB

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Histoplasma capsulatum

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Skin test for this fungal pathogen becomes positive 1 – 4 weeks after the onset of primary symptoms and remains positive for life

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Histoplasma capsulatum

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This fungus transmits disease when spores are inhaled, germinate into pathogenic yeast phase cells in lung and produces an acute pulmonary infection that may be asymptomatic or may produce an influenza-like syndrome.

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Blastomyces dermatitidis

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This fungus causes infections that may resolve spontaneously, or it may disseminate throughout the body.

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Blastomyces dermatitidis

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This fungus exhibits tropism for skin and bone.

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Blastomyces dermatitidis

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Bad1

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Surface protein of Blastomyces dermatitidis required for virulence. "Blastomyces Adhesin." Bad1 promotes uptake of B. dermatitidis by macrophages, promoting dissemination. Homolgous to invasin gene of some gram negative bacteria.

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This fungus can survive in inactivated macrophages

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Blastomyces dermatitidis

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This fungal pathogen is prevalent near Mississippi and Ohio river basins and in the Carolinas. Wooded areas near waterways are a major risk factor.

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Blastomyces dermatitidis

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This fungal disease is endemic only in regions of the Western Hemisphere. In the United States, the endemic areas include southern Arizona, central California, Southern New Mexico, and west Texas.

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Coccidioidomycosis

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The environmental form of this bacteria is highly infectious and hazardous to laboratory workers.

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Coccidiodes immitis

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This fungus is characterized by a saprophytic growth phase and a parasitic growth phase

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Coccidiodes immitis

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This fungus is imaged as a spherule in the lung with endospores.

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Coccidiodes immitis

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T/F: About half of people exposed to Coccidiodies immitis will come down with Valley Fever

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True (40%)

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This fungal disease has a higher incidence of symptoms in dark-skinned races, particularly Filipinos men

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Coccidioidomycosis

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95% of acute episodes of this disease resolve spontaneously. Nevertheless, follow up for 1 to 2 years is recommended for early identification of chronic pulmonary and extrapulmonary forms.

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Coccidioidomycosis

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This pathogen causes what is considered an "AIDS-defining" illness

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Cryptococcus neoformans

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An unusually virulent form of this fungal pathogen broke out in the Pacific Northwest in 2000

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Cryptococcus neoformans

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This fungal pathogen was first identified from peach juice

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Cryptococcus neoformans

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These are major environment sources of C. neoformans

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Soil contaminated with pigeon droppings (neoformans, grubii); eucalyuptus trees and decaying wood (gattii)

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GXM serotypes B and C

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C. neoformans var. gattii

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GXM serotype A

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C. neoformans var. grubii

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GXM serotype D

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C. neoformans var. neoformans

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This is how capsule of C. neoformans is visualized

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India ink wet mount
Mucicarmine stain

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Melanin is an important virulence factor of this fungal pathogen

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Cryptococcus neoformans

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This pathogen uses dopamine as a substrate to generate melanin via phenol oxidase

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Cryptococcus neoformans

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This fungal pathogen is urease positive

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Cryptococcus neoformans

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This fungal pathogen can be inhaled either as a spore or as dessicated yeast forms

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Cryptococcus neoformans

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This is the most common disease caused by C. neoformans

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Chronic meningitis

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These are sequelae of disease caused by C. neorformans

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Eye lesions and blindness; lesions of skin and bone

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This fungus is ubiquitous and is associated with bird droppings and vegetation

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Cryptococcus neoformans

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Diagnosis of this fungus is by agglutination of latex beads coated with anti-capsular antibiotics

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Cryptococcus neoformans

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Flucytosine

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Treatment for C. neorformans, with amphotercin B

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These conditions are associated with invasive candidiasis

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Neutropenia
Chemotherapy-induced injury to gut wall
Central venous catheter
Hyperalmentation

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These two species of fungi account for 70-80% of yeast isolated from pts with invasive candidiasis

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C. glabrata and C. albicans

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Blood cultures for this fungal pathogen in this disease may be negative despite the presence of abscess in internal organs

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Candida in internal candidiasis

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This fungal disease is characterized by fever and sepsis

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Invasive candidiasis

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These two species of this genus of fungus grow in mycelial form only (they are monomorphic), and form aerial, septate hyphae with characteristic stalk-like conidiophores bearing brush-like conidiospores which are easily airborne

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A. fumigatus and A. flavus

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These are diseases caused by Aspergillus

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1.Hypersensitivity pneumonitis
2. Secondary colonization in lung cavities that can cause hemoptysis
3. Systemic aspergillosis (neutropenia is an imp risk factor)

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This fungus is ubiquitous but is not associated with the normal flora

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Aspergillus
C. neoformans

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Histological staining of this fungus reveals septate hyphae that branch at regular intervals and tend to be oriented in the same direction

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Aspergillus

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These fungi grow in hyphae form that is coenocytic

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Zygomycetes. Coenocytic means that they are without cytoplasmic compartmentalization

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These fungi cause rhinocerebral infections in patients with metabolic acidosis (eg, diabetics)

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Zygomycetes (Mucor)

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This fungal pathogen is of low virulence and seldom produces disease in hosts with normal T cell function

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Pneumocystis carinii

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Specific Abs to this fungal pathogen are present in all children by the age of four

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Pneumocystis carinii

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Human forms of this fungal pathogen cannot be cultured and cannot be grown in animals

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Pneumocystis carinii

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This fungal pathogen exists in specific human and animal forms (Special Forms, sf) that do not infect other species

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Pneumocystis carinii

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This fungal pathogen was initially believed to be a parasite

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Pneumocystis carinii

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This fungal pathogen has cyst- and trophozoite-morphology similar to Apicomplexa

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Pneumocystis carinii

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T/F: P. carinii is highly contagious

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True.

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Transmission of Cryptococcus neoformans

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Inhalation

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GXM

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Glucuronoxylomannan. Component of Cryptococcus neoformans capsule

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Phenol oxidase

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Enzyme of C. neoformans. Involved in quinone-producing pathway from a DOPA and other catecholamine precursors. Quinone spontaneously polymerizes to produce melanin. Catacholamines are rich in CNS, which may contribute to propensity of C. neoformans to cause CNS disease.

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This affords protection to C. neoformans from host cell oxygen- and nitrogen-derived anti- microbial products.

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Phenol oxidase

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Alpha mating type of this fungus is more virulent in animal models

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Cryptococcus neoformans

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Serotypes of C. neoformans are based on differences of this between subspecies

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GXM capsule

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This fungus has a capsule that has highly regulated production depending on moisture, CO2, iron.

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Cryptococcus neoformans

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Latex agglutination

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Used for detection of C. neoformans. Latex agglutination is caused by the capsule.

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This fungus produces urease--an important feature for diagnosis

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Cryptococcus neoformans

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This pathogen is the is the fourth most common cause of hospital blood stream infections, surpassing all Gram negative rods.

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Candida albicans

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Treatment of severe C. albicans infection

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Amphotericin B (binds ergosterol), azoles, caspofungin

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Neutropenia chemotherapy

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Major risk factor for aspergillus infection

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This pathogen is highly sporulating, with 1-100 spores per cubic meter of air indoors and outdoors

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Aspergillus

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This is the most prevalent airborne fungal pathogen

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Aspergillus

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The mortality rate of this disease is as high as 50-100% and definitive diagnosis by culture may take as long as 4 weeks.

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Invasive aspergillosis

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This genus plays essential ecological role in recycling carbon and energy

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Aspergillus

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Once in tissue in invasive form, this organism spreads rapidly, penetrating tissue barriers

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Aspergillus

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This fungus is susceptible to certain antiparasitic agents such as pentamidine, trimethoprim/sulfamethoxazole.

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Pneumocystis carinii

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This fungus is resistant to amphotericin B

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Pneumocystis carinii

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This fungus lacks ergosterol, featuring cholesterol and other sterols

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Pneumocystis carinii

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This fungus was long thought to be an animal parasite

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Pneumocystis carinii

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EF3

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Longation factor found only in fungi

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Fungi cell wall components (3)

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Chitin, glucan and mannoproteins

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This fungus produces cysts that are 5-8 microns in diameter. Sporozoites are released when cyst ruptures

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Pneumocystis carinii

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Visualization of Pneumocystis

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Gomori’s methenamine silver (GMS) and Giemsa stain

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This fungal pathogen is from an unknown source, and antibodies present in serum by 4 years old.

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Pneumocystis carinii

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These are the most common candidal infections in HIV-infected children, occurring in as many as 50-85% of patients.

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Oral thrush and diaper dermatitis

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HAART

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Highly active antiretroviral therapy

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Despite the severe immunosuppression that results from advanced HIV infection, there are relatively few cases of this disease in patients with HIV disease.

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Aspergillosis

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Exported repetitive protein

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Protein of M. tuberculosis that prevents fusion of phagosome with lysosome, allowing the bacteria to exist within reticuloendothelial cells (macrophages)

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Granulomatous lesions

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Central area of Langhans giant cells containing tubercule bacilli surrounded by a zone of epithelioid cells

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Tubercle

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Granuloma surrounded by fibrous tissue that has undergone central caseation necrosis. They heal by fibrosis and calcification

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This is the slowest-growing human bacterial pathogen

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With a doubling time of 14 days, M. leprae is the slowest-growing human bacterial pathogen

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Antibiotic therapy for this disease must be continued for many years (2-3 yrs) due to its slow growing time

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M. leprae

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These bacteria are obligate aerobes

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Mycobacteria

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These bacteria are acid-fast NON-motile

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Mycobacteria

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These are mostly facultative intracellular organisms

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Mycobacteria

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This species of bacteria cannot be cultured on artificial media

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M. leprae

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These bacteria have cell walls with a triple layer, and contain mycolic (fatty) acids

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Mycobacteria

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Ziehl-Neelsen stain

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Acid fast stain for mycobacteria

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Kinyoun

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Acid fast stain for mycobacteria

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These bacteria are acid-fast

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Mycobacteria
Nocardia

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Structure of mycolic acid

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Two long hydrophobic chains

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This genus of bacteria is a distant relative of mycobacteria

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Corynebacteria

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This genus of bacteria contains mycolic acids but are not acid fast because of the short chain length

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Corynebacteria

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These bacteria are only weakly acid fast

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Nocardia

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Cord factor

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Virulence factor of M. tuberculosis. It consists of two mycolic acids attached to the disaccharide, trehalose.

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This genus of bacteria has a high lipid content, accounting for 40-60% of its dry weight

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Mycobacteria

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Wax D

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Unusual lipid of mycobacteria.

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These are the elements of mycobacteria that are attacked in CMI response

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Lipids

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These confer resistance of mycobacteria to drying and chemicals

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Lipids

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This accounts for the slowness of Mycobacterial growth

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High lipid content, which decreases permeability

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Generation time of TB

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15-20 hours (compared to 1 hour for most bacterial pathogens)

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Freund's adjuvant

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Used to boost the immune system. The "complete" form includes mycobacterium lipids.

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Hansen's bacillus

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Another name for M. leprae

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This bacteria has a low temperature preference, and thus localizes to cooler body areas (skin, nose, mucous membranes of upper resp tract; superficial nerves)

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M. leprae

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This bacteria has as its natural hosts humans and armadillos

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M. leprae

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This bacteria can be adapted to grow in the foot pad of mice for experimental but not diagnostic studies

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M. leprae

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This organism has never been cultured in artificial media

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M. leprae

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T/F: Children are more susceptible to leprosy than adults

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True.

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Incubation period of leprosy

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Usually 2-5 years, but can be a few months to 30 years

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This disease has as its primary lesion a skin macule that is hypopigmented, erythematous or a raised and brown wheal-like papule (like a mosquito bite)

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Leprosy

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This disease primarily involves the skin and nerves

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Leprosy

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Cases of this disease with long duration show amyloidosis of the kidney, liver and spleen

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Leprosy

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Lepromatous leprosy

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Macrophage or histiocyte takes up bacilli ("Lepra cell"=macrophage w
leprae)
Large volume of bacilli (5x106 per gram of infected tissue)
Raised nodule or diffuse thickening of skin with ulceration possible
Polyclonal hyper IgG
Negative lepromin skin test (weakend CMI)
T-cell mobilization is weakened
Poor prognosis

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Tuberculoid leprosy

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Resembles TB (chronic granulomatous lesions, epithelioid and giant cells, but without caseation)
Few if any bacteria at center of lesion
Flat, red or hypopigmented lesions
Normal IgG leveles
Positive lepromin skin test--DTH is intact
Better prognosis than lepromatous leprosy

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ENL

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Erythema Nodosum Leprosum. Complication of leprosy resembling an immune-complex disease (hypersensitivity type III). Treat with immunosuppressants

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Phenolic glycolipid

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Component of M. leprae. Antibodies to phenolic glycolipid are diagnostic but not protective

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This disease may cause anergy, and thus poorer immune response, but can improve after treatment

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Lepromatous leprosy

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Clofazimine

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Treatment for lepromatous leprosy

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Dapsone

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Treatment for lepromatous leprosy. Sulfonamide-like action.

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NRAMP1

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Gene that regulates phagolysosomal environments in cells. Variant alleles of NRAMP1 are implicated in increased susceptibility to MTB

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Polymorphisms in vitamin D receptor genes are associated with protection against this disease

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TB

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IL-2

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Autocrine signal responsible for expanding T-cell populations, thus increasing the number of T-cells that express a specific T-cell receptor for a particular anigen (eg, MTB).

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IFN-gamma

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Activates macrophages harboring phagocytosed pathogens. Important in the dx of MTB. Mononuclear cells from pts with TB infection and/or disease produce IFN in response to TB-specific antigens (ESAT, CFP 10). Requires that the pt have normal T-cell immunity, though.

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TNF-alpha

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Induces phagosomal fusion with lysosomes, killing intracellular pathogens. Autocrine signalling--released by the macrophages themselves.

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Number of new active cases a year worldwide of TB

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6-8 million

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Number of deaths per year due to TB

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2-3 million

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Pathogenesis of TB

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Inhaled
Ingested by alveolar macrophages
Transient bacteremia occurs
Granuloma formation in lungs and possibly other sites (brain, liver, kidney)

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Infection vs. disease in tuberculosis

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Infection is identified by PPD skin test
Disease is identified by culture of MTB from lung or other sites, or by clinical picture

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90% of people infected by this bacteria remain latently infected, and 10% develop active disease

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Mycobacterium tuberculosis

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Clustered cases

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Used in the context of TB infection. Clustered cases are those that match TB "molecular fingerprints" of other cases, implying new infection rather than latent infection in an individual.

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These organisms can remain viable for weeks at 4 C

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Mycobacterium

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Mycobacterial immunity greatly relies on this

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CD4+ cells. Thus HIV renders pts very susceptible to mycobacterial infection

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This disease appears to increase productive HIV infection in mononuclear cells (via TNF)

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Tuberculosis

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MDR

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Multiple drug resistance [TB]. Rifampin and isonaizid resistance.

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T/F: Resistance in TB is encoded by plasmids

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False. Encoded by chromosomal DNA. No evidence of plasmids in TB

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Lowenstein Jensen

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Egg-based medium for growing MTB.

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ESAT

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TB specific antigen

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CFP 10

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TB specific antigen

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RIPE

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Standard tx for TB.
Rifampin
Isoniazid (INH)
Pyrazinamide
Ethambutol

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Mechanisms for RIPE drugs

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Rifampin: Cidal for intracellular
INH: Cidal for extracellular
Pyrazinamid: Targets intracellular
Ethambutol: Static, not cidal; helps prevent resistance

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Side effects for RIPE drugs

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Rifampin: Hepatitis, neuropathy, CNS, B6 deficiency
INH: Influenza, hepatitis, orange urine, drug interactions
Pyrazinamide: GI, heptatitis, rash, arthralgia, uric acid
Ethambutol: Optic neuritis, rash

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Duration of TB antibiotic therapy

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6 months. 2 months intensive. 4 months continuation phase.

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IRIS

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Immune restoration inflammatory syndrome. Paradoxical effect of combined TB and HIV therapy, which may occur with first 2 months of tx and last 10-40 days

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TB is monitored by culturing this

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Sputum

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PPD test

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Purified protein derivative. Reaction occurs at 2-10 weeks after initial infection.

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This bacteria is the most common NTM causing human infections

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Mycobacterium avium complex

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Clinical syndromes of this bacteria include cervical adenitis in children, TB-like pulmonary disease, disseminated infection in AIDS pts

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Mycobacterium avium complex

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Macrolide (clarithromycin, azithromycin)

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Tx for Mycobacterium avium infection

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Skin test studies have shown that 30-40% of adults worldwide are infected with this bacteria

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Mycobacterium avium complex

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This bacteria is a relatively common cause of false positive PPD tests

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Mycobacterium avium complex

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This bacteria can cause gastrointestinal TB

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Mycobacterium bovis

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Vaccine for TB

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Attenuated live M. bovis strain called Bacille Calmette Guerin (BCG). 80% effective against childhood TB, 50% against all other. Prevents leprosy, MAC infection (other mycobacterium). Duration of ~15 years with no known booster. Not very safe; complications include local swelling and drainage for several weeks, abscess with adenopathy (BCG-itis), osteomyelitis, disseminated BCG infection (in immunosuppressed pts).

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BCG vaccine

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Vaccine for TB. Live, Bacille Calmette Guerin

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This is used as an immunostimulant in topical treatment of bladder carcinoma

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TB vaccine