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85 Cards in this Set

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What are three pathology stains that are routinely used to identify fungal organisms in tissue?
Mayer's Mucicarmine (Cryptococcus)
Gomori's Methenamine silver (GMS) - standard for all fungal species
Periodic acid Schiff with distase - stains organisms magenta
What are three genera of dermatophytes?
Epidermophyton
Microsporum
Trichophton
What is the habitat of the dermatophytes and how does it affect the presentation of clinical disease?
Dermatophyte infections may be acquired from soil, animals (wild and domestic), and humans.
What is the preferred food substrate of dermatophytes and how does it affect the presentation of clinical disease?
Dermatophytes are fungi that utilize keratin as a food substrate. Infections are frequently found on skin and hair.
What is the preferred food substrate of Candida albicans and how does it affect the presentation of clinical disease?
Glucose. Clinical patterns of infection include mucocutaneous and systemic.
substrate of Malassezia furfur and how does it affect the presentation of clinical disease?
Lipophilic - sebaceous lipids are food source. Skin and scalp.
What are the ecological habitats of localized cutaneous infections and how do they typically gain access to the body?
The localized cutaneous fungal infections constitute a group of mycoses usually caused by soil saphrophytes that are introduced into the skin via traumatic inoculation.
What is meant by a sporotrichoid infection and what is the clinical differential diagnosis?
Soil saprophyte, with a dimorphic form, especially associated with sphagmum peat moss. Clinical disease most often is lymphocutaneous - ulder followed by localized lymphangitis and lymphadenitis. Adults - extremities, Kids - face. The fixed cutaneous form is characterized by an ulceration that becomes verucous.
What is a dematiaceous fungus and what are three localized fungal infection that can be produced by a dematiaceous species?
A dematiaceous fungus is dark in color. Dematiaceous fungi include: Chromomycosis/Chromoblastomycosis (Fonsecaea pedrosoi), Phacohyphomycosis (Exophiala jeanselmei), Eumycotic Mycetoma (Madurella mycetomatis, madurella grisea)
Name the only localized cutaneous infection produced by an organism that is classified as an algae and how do people aquire this infection?
Protohecosis is produced by Prototheca species and usually appears after cleaning aquariums
What are three clinical diseases that are the result of fungal hypersensitivity rxns?
Allergic rhinitis, Bronchial asthma, Alveolitis
What is a mycotoxicoses? What is an example of human mycotoxicoses and how does it produce disease in humans?
Accidental or intentional result of toxic fungi or fungal products. "Turkey X" disease resulted from Aspergillus flavus contamination. Claviceps purpurea infects rye and produces and alpha adrenergic blockade -> vasoconstriction -> erythema, necrosis, gangrene and death.
What are dimorphic fungi? What are the classic five fungal infections produced by dimorphic fungi?
Dimorphic fungi can transition between yeast and hyphal forms. The classic dimorphic fungi are: Sporotrichosis, North American blastomycosis, Coccidioidomycosis, Paracoccidioidomycosis, and Histoplasmosis
Compare the ecological niches of blastomycosis, coccidiodomycosis, paracoccidiodomycosis and histoplasmosis and how does this affect the distribution of infection?
Blastomycosis - soil (high humidity, low pH); Coccidioidomycosis - soil; Paracoccidioidomycosis - soil where coffee is grown; Histoplasmosis - soil with high nitrogen, starling or bat excreta
Blastomycosis - east/central US; Coccidioidomycosis - US, central, south america; Paracoccidioidomycosis - coffee distribution; Histoplasmosis - Ohio-Mississippi Valley
List four types of patients that are particularly susceptible to disease from opportunistic fungi and be able to explain why are they suceptible?
- immunocompromised host
- diabetic ketoacidosis
- cancer patient
- malnourished patients
Why are diabetics in ketoacidosis prone to develop mucormycosis?
Mucormycosis is thermotolerant, thrives in high concentrations of glucose and in the presence of ketones and prefer an acidic pH.
Describe the pathogenesis of candidiasis and explain how the various symptoms reflect the habitat of the fungus?
Cutaneous infection - very red inflammatory lesions, pustule, plaque
Mucocutaneous, GI, Oral, UTI, Genital, Endocarditis, Septicemia
Describe the pathogenesis of pneumocystosis and the methods used for its diagnosis and treatment.
Natural habitat is a lung -> dyspnea, fever and a nonproductive cough with variable tachypnea, tachycardia and cyanosis. Difuse, bilateral infiltrates on chest xray. Stain (biopsy, sputum, etc.) with methenamine silver. Lacks ergosterol, so ergosterol synthesis inhibitors are no good. Trimethoprim-sulfamethoxazole (inhibits folic acid synthesis) is treatment of choice.
What does Amphotericin B do?
It binds to ergosterol in fungal cell membranes -> leakage of cellular contents -> death.
How is amphotericin B administered? Where does it go?
Infused as a suspension (IV). It does NOT reach the CNS.
What's the bad part of amphotericin B?
VERY TOXIC. Premedicate with acetaminophen/diphenhydramine or give hydrocortisone concurrently.
What do you use amphotericin B for?
Severe, rapidly progressing fungal infections.
What is the mechanism of action for ketoconazole, itraconazole and fluconazole?
Inhibit 14alpha-demethylase which synthesizes ergosterol.
What is the drug of choice for reaching the CSF?
Fluconazole
What is Mayer's mucicarmine good for?
Highlighting capsules of Cryptococcus
What is Gomori's Methenamine Silves (GMS) good for?
Standard stain. Not good for small yeast.
What does periodic acid schiff with diastase do?
Stains orgainisms magenta.
What are dermatophytes?
Fungi that utilize keratin as a food substrate?
What kind of infection are the tineas?
Dermatophye infections
What is the most common cause of tinea capitis?
Trichophyton tonsurans
Who gets tinea capitis?
kids
What is the most common cause of tinea corporis, tinea pedis and tinea cruris?
Trichophyton rubrum
How do you treat dermatophytoses?
Topicals: ketoconazole, miconazole, clotrimazole, econazole, butenafine, naftifine, terbinafine.
Oral: griseofulvin, fulconazole, itraconazole, terbinafine.
How do you treat candidiasis?
Topical: gentian violet, imidazoles, ciclopirox olamine, naftidine and terbinafine
Systemic: fluconazole
What does tinea versicolor like?
sebaceous lipids of skin and scalp
What does the KOH of malassezia furfur look like?
spagetti and meatballs
What is the buzzword for Sporotrichosis?
sphagmum peat moss
What is the lymphocutaneous form of Sporotrichosis?
ulcer followed by localized lymphangitis and lymphadenitis (usually hands)
What shape is Sporotrichosis?
cigar shaped
What is the morphology of blastomycosis?
thick walled yeast with broad based budding
What is the characteristic shape of coccidioidomycosis?
barrel shaped arthrospores that alternate with cells that lose their cytoplasm
What should you do if you suspect coccidioidomycosis?
Alert the laboratory!
Where do you get histoplasmosis?
Spelunking in the Ohio-Mississippi Valley. Bird (starling) or bat poo.
What do pigeons give you?
Cryptocococcis
What kind of fungal infection do especially diabetics get?
Mucormycosis (Rhinocerebral)
Ketoconazole and Itraconazole are inhibitors or inducers of CP450 of steroid biosynthesis?
Inhibitors
What are some adverse reactions of Ketoconazole and Itraconazole?
Gynecomastia, decreased libido, menstrual irregularities, teratogenic
Who shouldn't take Fluconazole?
Pregnant women
How do you treat fungal meningitis (cryptococcis)?
Fluconazole
What is the drug of choice for candidiasis (mucocuatenous, oral, esophageal) histo, blasto and coccidio in immunocompetent patients w/o severe illness?
Itraconazole
How does Caspofungin work?
Inhibits the synthesis of Beta (1,3) D-glucan
What are the pertinent pharmokinetics of Caspofungin?
Administered IV; renal and hepatic elimination; inducer of cytochrome P450
How do you treat invasive aspergillosis?
Caspofungin
What do you use Flucytosine for?
Flucytosin reaches the CNS. Use in combination with Amphotericin to treat deep-seated cryptococcosis and candidiasis. Fungal meningitis.
How does Griseofulvin work?
It inhibits mitosis by binding to microtubules.
How does Terbinafine work and what do you use it for?
It interferes with ergosterol synthesis. It is used for the systemic treatment of superficial (hair, skin, nail) mycoses
Name a topical antifungal.
Clotrimazole
Identify known human prion diseases.
Creutzfeld-Jacob Dz (CJD), new variant CJD, Gerstmann-Strassler-scheinker syndrome, Fatal familial insomnia, Kuru
Identify known animal prion diseases.
Chronic wasting disease, Bovine spongiform encephalopathy, Scrapie, Transmissible mink encephalopathy.
What is seen on microscopic examination of a CJD brain?
Non-inflammatory lesions, microscopic sponge with tiny holes.
What is the evidence supporting the infectious protein hypothesis?
Resistant to inactivation by UV light. Resistant to DNase and RNase. Protease resistant protein which is infectious. All vertebrates encodes prion protein (PrP) PrPc - normal, PrPSc - infectious form. Prp is expressed in many tissues, especially neurons. Mice w/o PrP can't be inoculation with PrPSc.
How can an infectious protein "replicate?"
PrPSc has the ability to catalyze the conversion of normal PrP to pathologic PrPSc, which converts more and more. Accumulated PrPSc leads to the death of neurons and spongiform encephalopathy.
What is the conformational difference between PrPSc and PrPC?
PrPSc has b-sheet conformation, PrPC has a-helical conformation.
Which prion disease is acquired sproadically?
CJD. Somatic mutation, possibly.
Which prion diseases are acquired hereditarily?
CJD, GSS, FFI
Which prion diseases are infectious?
CJD. Kuru, vCJD (from BSE?) - could be Iatrogenic.
Can an animal prion (cow or elk) infect a human?
There is a barrier, but it is not absolute, so cross-species infectivity does occur.
What is the structure of a retrovirus viron? What enzymes are packaged with the genome?
Two copies of RNA genome plus three essential genes: gag, pol and env. Env - glycoprotiens that determine host range; Gag - proteins form the capsid which encloses viral RNA genome; matrix, capsid, nucleocapsid and protease proteins; pol - reverse transcriptase, integrase and ribonuclease.(Rous Sarcoma virus (RSV) also has src, which is a tyrosine kinase -> sarcomagenesis.)
What is the structure of the HIV virus, from inside to out?
Two copies of genome, bound by nucleocapsis within core formed by p24 capsid. Matrix protein and then host derived viral envelope with transmembrane (gp41) and surface (gp120) proteins.
What is the retrovirus infectious cycle?
Retroviruses bind receptors, penetrate and uncoat. Genome is transcribed by reverse transcriptase to produce linear dsDNA with long terminal repeat sequences (promoter/enhancer elements). DNA -> nucleus. Integrated proviral DNA is transcribed by host RNA polymerase -> mRNA and viral RNA genomes. Budding from plasma membrane.
Where does viral DNA insert and what do we call it?
It inserts at random sites in host chromosomes and one integrated, we call it proviral DNA.
What are general simmilaries and differences between the retrovirus replicative cycle and the replicative cycles of +stranded RNA viruses and DNA viruses?
??
What are the most important retroviruses that infect humans?
HTLV-1 causes t-cell leukemias/lymphoma and tropical spastic paralysis, transforms lymphocytes; HIV 1&2 -> AIDS (kills CD4 cells/Thelper); All of these viruses are called Lentiviruses
What are the types of human disease caused by retroviruses?
HTLV-1: Adult T-cell leukemia, tropic spastic paraparesis; ATL: lymphoproliferative disorder, malignancy; HAM/TSP: chronic, progressive paralytic dz of CNS
What are some good retrovirus targets for drug therapy and why are they good?
Target viral enzymes b/c of specificity. Targets: reverse transcriptase, integrase (fnx of transcriptase), virally encoded protease, viral envelope function and viral budding.
What do retrovirus oncogenes do?
Transform fibroblasts and hematopoietic cells and cause tumors, sarcomas, endotheliomas, and neurolymphomatosis. Broadly, the fall into four categories: Growth factors, growth factor receptors, signal transducers, and transcription factors. The viral oncogene causes cancer, but the cellular protooncogene does not.
Why does the viral oncogene cause cancer while the cellular protooncogene does not?
Mechanisms of activation, mutations, point of insertion
Describe the molecular features of HIV.
Inside -> Out: 2 copies of single stranded RNA genome, with protease, integrase, P6 and P9 proteins. Core is surrounded by P24. Envelope includes P17. gp41 transmembrane glycoproteins and gp120 outer membrane glycoproteins.
Describe the replication cycle of HIV.
1. Cell entry. 2. Reverse tramscription and integration. 3. Virus production. 4. Viral maturation
Descrive the dynamics of HIV infection.
Virus in plasma > CD4 cell -> productively infected and latently infected cells. Generation time is 2.6 days. 10^10 virons produced each day.
Describe the drugs used in HAART and the reasons for using more than one drug to treat HIV infections.
Maximally supressive therapy requires combo of at least 3 drugs. NRTIs, NNRTIs, PIs, Entry Inhibitors.
Describ the clinical progression of HIV-infected patients and the relevance of CD4+ cell numbers in disease progression.
Markers of dz progression: CD4 count and Plasma HIV RNA level. As CD4 count goes down: Thrush, TB, PCP, Histo, Coccidio, Crypto, CMV, Myvo avium
What are the most important diseases caused by adenoviruses?
Acute respriatory illnes, pneumonia. Diarrhea in children. Obesity?? Persistent infections of the tonsils, adenoids and other lymphoid tissues.
What are the implications of the large number of serotypes of adenoviruses?
49 serotypes. Hexons contain family-reactive derminants that cross-react with similar Ag in all mastadenoviruses.
Compare adenoviruses with other human pathogenic DNA viruses in terms of viron structure and mechanism of spread.
Adenoviruses are naked, icosahedral, virons with linear, dsDNA and associated packaging proteins Replication and capsid formation occurs in nucleus. Survive well in lower GI tract, throat and feces.