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IAHI Block 1 > 16 - Systemic and Opportunistic Mycoses > Flashcards

16 - Systemic and Opportunistic Mycoses Flashcards

1
Q

What are opportunistic pathogens?

A

They are unable to cause overt disease in healthy hosts, and need an opportunity to become pathogenic.
-opportunity includes defects in human immune system and defects in barrier function.

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2
Q

What are the important opportunistic fungal pathogens?

A

Candida, cryptococcus, Aspergillus, Mucor and Rhizopus, and pneumocystis

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3
Q

What infection is caused by Candida species?

A

Thrush.

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4
Q

What are the two types of diseases caused by candida? What is their morphology?

A

Mucocutaneous candidiasis and disseminated candidiasis.

They are yeasts (oval) that reproduce by budding. Most species form thred-like hyphae and sausage-life pseudohyphae.

On media colonies are discrete, circular, smooth, and white.

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5
Q

What is the most frequent species of candida? Describe how we get it?

A

C. albicans, which almost all humans are colonized with in the GI during first month of life.

Most infections are from hosts own colonizing organisms.

Increased susceptibility with immune and barrier defects. Third most common central-line associated blood infection.

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6
Q

What are the types of mucocutaneous candidiasis? What is the mortality?

A

Oropharyngeal (thursh), esophageal, diaper dermatitis, vulvovaginal, cutaneous, onychomycosis, and chronic mucocutaneous.

Low mortality but high morbidity.

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7
Q

What are types of disseminated candadiasis? What is the mortality?

A

Candidemia, hepatosplenic, meningitis, endocarditis, endopthalmic, renal.

Mortality can be >40%.

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8
Q

What are predisposing factors to mucocutaneous candida infection?

A

Antibiotics, barrier disruption, diabetes, T-cell dysfunction (cell mediated immunity).

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9
Q

What are predisposing factors to disseminated candida infection?

A

Antibiotics, intravascular devices, hyperalimentation, GI surgery, hemodialysis, extremes of age, severe neutropenia.

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10
Q

What is one way to diagnose candida in the lab? What are the advantages and disadvantages?

A

Histologic examination using OH prep, silver stain, or gram.

Advantages: no special media needed and you can identify the species

Limitations: growth from non-sterile body site often represents colonization, sensitivity 50% for disseminated candidiasis.

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11
Q

What is a second way to diagnose candida in the lab?

A

Serum molecular testing for 1,3-beta-D-glucan, PCR.

Sensitivity and specificity not perfect.

Does not distinguish candida species from other fungi.

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12
Q

What is the treatment for uncomplicated mucocutaneous infection, chronic nucocutaneous infection, and disseminated infection?

A
  1. Topical therapy: nystatin (can be oral or topical), clotrimazole (oral), miconazole (topical).
  2. Systemic therapy, anti-fungal resistance common
  3. Systemic anti-gunfal; usually need to remove catheters and long treatment is needed for high-risk hosts: echinocandins, azoles, amphotericin.
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13
Q

When is thrush normally seen?

A

In the first 6 mo of life, extremely common finding in untreated HIV infection (>90%), and seen with improper use of corticosteroids for asthma and denture use.

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14
Q

When is esophageal candidiases seen?

A

It’s a painful, cryptic infection.

Commonly seen with untreated HIV patients (~10&)

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15
Q

What is the appearance of diaper dermatitis?

A

Beefy, erythematous plaques with satellite lesions.

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16
Q

What are symptoms and risk factors associates with vulvovaginal candidiasis?

A

Pruritic or burning pain, usually with cheesy-white discharge.

75% incidence in post-pubertal women. No increased incidence in untreated HIV infection.

Risk increased with broad spectrum antibiotics, uncontrolled diabetes, pregnancy, or oral contraceptive use.

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17
Q

What is paronychia, onychomycosis?

A

Candida infection of the nails.

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18
Q

What is the result of chronic mucocutaneous candidiasis?

A

Heterogenous collection of clinical syndromes, frequently unique susceptibility to candida infections.

Leads to chronic malnutrition and failure-to-thrive.

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19
Q

What is candidemia associated with?

A

This is a type of disseminated candidiasis that occurs in the bloodstream, often a line-associated infection.

Global incidence of 400,000 cases/year.

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20
Q

What are the risks associated with candida endocarditis?

A

High mortality disease, requires anti-fungal treatment for life.

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21
Q

Which drug is appropriate empiric treatment for disseminated candidiasis?

A

Caspofungin

22
Q

What is the usual mode of transmission for cryptococcus species? What is the infection called?

A

Respiratory (inhalation).

Called cryptococcosis

23
Q

What is the morphology of cryptococcus?

A

Uninucleate, budding yeast that are round to oval.

Thick polysaccharide capsule appears as a halo, especially with india ink stains.

24
Q

What is the epidemiology of cryptococcus?

A

Worldwide, ubiquitous in the soil. Expore to pigeons.

Organism acquired for inhaltion aerosolized cells from environment.

25
Q

What are the two types of cryptococcus species? Describe the differences between the two.

A

C. neoformans: ubiquitous, infection risk with cell mediated immunodeficiency, esp. untreated HIV and chronic corticosteroid use.

C. gatti: more geographically limited to tropical and subtripical places and pacific NW. Infection is associated with immunoCOMPETENT hosts.

26
Q

What clinical syndromes are associated with cryptococcus?

A

Initial pulm infections that’s often asymptomatic or mild.

Dissemination to organs via bloodtream or lymphatics.

  • most common focal organ disease is cerebromeningeal.
  • less common is skin, prostate, bone.
27
Q

How would you diagnose cryptococcus?

A

Blood or CSF for india ink stain.

Culture looking for encapsulated budding yeast.

Capsular polysaccharide antigen testing available from serum and CSF.

28
Q

What is the treatment and risk of cryptococcal meningitis?

A

12% mortality with drug therapy, lethal without.

Amphotericin B + flucytosine for 2 weeks, followed by 8 weeks oral azole.

Lifelong suppresion may be required if immune defect cannot be reversed.

29
Q

What infection/disease is associated with aspergillus? What is the morphology?

A

Aspergillosis.

Moly with dichotomously branched (acute angle) and septate hyphae. Looks like a dandelion that you blow on.

30
Q

What is the epidemiology of aspergillus?

A

True saphrophyte: organism that lives on dead or decaying matter.

Foudn in soil, site, water, storage tanks, food compost, decaying vegetation, fire proofing materials, bedding, pillows, ventillation.

Spores are widespread and are readily inhaled.

31
Q

What clinical syndromes are related to invasive aspergillosis?

A

Invasive disease: in the immunocomp - prolonged neutropenia and phagocyte disfunction. Lower resp tract , sinuses, skin entry. Angioinvasive with dissemination to CNS and CV system.

32
Q

What are the clinical syndromes associated with aspergillosis with saprophytic involvement?

A

Immunocompetent host with underlying lung disease or chronic otitis media.

Pulmonary aspergilloma.

Aspergillus otomycosis.

33
Q

What allergic conditions are associated with aspergillosis?

A

Allergic aspergillus sinusitis.

Allergic bronchopulmonary aspergillosis.

34
Q

How would you diagnose aspergillus in the lab?

A

10% KOH or silver stains of tissue or bronchoalveolar lavage specimans.

Culture on special fungal media with lactophenol cotton blue prep for morphology.

Galactomannan (imperfect sensitivity)

Aspergillus specific IgE and eosinophilia for allergic disease.

35
Q

What is the 1st and 2nd line treatment for disseminated aspergillus? How is aspergilloma treated?

A

1st line: voriconazole
2nd line: amphotericin
70% mortality

Aspergilloma: resection, no antifungal therapy.

36
Q

What is aspergilloma?

A

Localized aspergillus infection associated with anatomically protected site, for example pulmonary sequestration.

37
Q

A 3 yo boy with recently diagnosed leukemia develops a fever and is found to have pulmonary noduleson CT. A funal infection is suspected. What clinical sample is most likely to yield the organism?

A

Lung tissue.

Tissue is the issue (pulmonary nodules) so you need to sample this to diagnose.

38
Q

What is mucormycosis?

A

An infection caused by members of the order mucorales such as mucor and rhizopus species.

39
Q

What is the morphology of mucormycosis? What is the mortality related to this illness? What are risk factors?

A

Gray to brown wooly colonies. Sparsely septate or aseptate hyphae with right angle branching. Ribbon-like. Spores in sporganium and rootlike structures called rhizoids.

70-100% mortality. Get infection from inhalation, ingestion, of wound contamination.

Risk: immunocompri., bruns, diabetes mellitus.

40
Q

Clinical syndromes associated with mucormycosis?

A

Rhinocerebran - associated with diabetic ketoacidosis

Pulmonary-neutropenic patients

Cuteaneous- burns

Disseminated infections: from angioinvasion

41
Q

How is mucormycosis diagnosed? How is it treated?

A

Tissue for histologic examination and culture.

Debridement and correct immunodeficiency.

Amphotericin B for first line therapy, posaconazole alternative.

42
Q

A 2 year old boy with leukemia develops neutopenic fever. On nasal endoscopy, a black exophytic mass is found in the right middle turbinate. Which treatment modality decreases mortality from this infection?

A

Surgical debridement.

Neutropenia indicates that this is mucormycosis.

43
Q

What disease/infection is associated with pneumocystis jirovecii? What are the two morphological forms?

A

Pneumocystic pneumonia (PCP) in immunocomprimised patients.

Cysts (5-8 micrometers) with 8 intracystic bodies.
Trophozoites (1-5 micrometers)

44
Q

What is the epidemiology of pneumocystis jirovecii? What are risk factors for it?

A

85% of healthy children are seropositive (their immune system can protect them against it).

Risk factors: deficient cell-mediated immunity (CD4 <200), HIV, transplant, oncology patients, congenital immunodeficiency syndromes.

45
Q

What are the clinical sympatoms of pneumocystis jirovecii? What is the mortality when treated and untreated?

A

Insidious or rapid onset pneumonia.

Frothy pulmonary edema with cellular infiltrate.

Progressive dyspnea and hypoxia.

Mortality when treated: 4-50%, nearly 100% when untreated.

46
Q

How is pneumocystis jirovecii diagnose? How is it treated?

A

Micro identification in sputum, bronchoalveolar lavage, or lung tissue looking for thick walled cysts.

PCR of respiratory tract secretions - sensitive and specific.

TMP-SMX first line prophylaxis most important. Or use TMP-SMX after infected.

47
Q

What is a risk factor associated with pneumocystic pneumonia (PCP)?

A

Medication non-compliance

48
Q

Why is Candida auris a notable pathogen?

A

High rates of anti-fungal resistance, its ability to be transmitted from person-to-person

Propensity for disseminated disease.

Unrecognized colonization leading to hospital ward outbreaks.

49
Q

Which defects in natural barriers to infection are associated with candida, aspergillus, and rhizopus/mucor?

A

Candida: decreased normal flora, indwelling catheters, dentures.

Aspergillus: burns or underlying lung disease

Rhizopus/mucor: burns, diabetes

50
Q

Which species are associated with defects in neutrophil number or function (ie chemotherapy)?

A

Candida, aspergillus, rhizopus/mucor.

51
Q

Which species are associated with defects in cell-mediated immunity (CMI) such as HIV, lymphoma, SCID, chemo with steroids, or transplant immunosuppression?

A

Candida, cryptococcus, pneumocytis jiroveci, histoplasma capsulatum.

IAHI Block 1 (19 decks)

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