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microbio gram neg > Mycology 2: Oportunistic Pathogens > Flashcards

Mycology 2: Oportunistic Pathogens Flashcards

1
Q

What are the 4 main opportunistic fungi?

A

Cryptocococcus neoformans, Candida, Aspergillus, and Pneumocystis jiroveci.

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2
Q

Chronic Granulomatous Disease (CGD)

Mechanism and associated bugs

A

Mutations affecting NADPH oxidase, which normally causes oxidative burst in neutrophils and macrophages. Pxs have problems w/ Candida and Aspergillus.

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3
Q

Severe Combined Immunodeficiency

A

Lack of mature T and B cells. Often results in death early in life due to opportunistic infections

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4
Q

TNFa blockers
Use
2 examples

A

Monoclonal Abs against TNFa or receptors. Reduce fever, inflammation, and acute phase response. Used for autoimmune disorders and psoriasis. Examples include infliximab and etanercept.

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5
Q

Calcineurin Inhibitors
Mechanism
Use
2 examples

A

Suppress T cell activation. Used for transplant pxs. Examples include cyclosporine A and tacrolimus.

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6
Q

Mycophenolate Mofetil mechanism / use

A

Metabolic inhibitor that blocks T and B cell proliferation / function in transplant pxs.

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7
Q

What does HIV do? What does it not do?

A

Kills CD4 T cells. Damages CMI.

Does not damage innate immunity

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8
Q

Order of typical fungal infections in HIV pxs

A

1) Oral / esophageal candidiasis
2) Vaginal candidiasis
3) Oral candidiasis again
4) Pneumocystic pneumonia, Cryptococcal meningitis, Histo, Coccidiodomycosis
5) Aspergilliosis and resistant candidiasis

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9
Q

What are pxs w/ mono at risk of?

What viruses cause mono?

A

Epstein-Barr virus (EBV) suppresses immune function –> risk of oropharyngeal candidiasis.

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10
Q

How does diabetes increase risk of infection? (4 things)

A
  • Hyperglycemia fosters microbial growth and hinders phagocyte function.
  • Acidosis facilitates iron release from host transferrin → fungal use
  • Poor vasculature reduces access of WBCs and AB’s to infections
  • Peripheral neuropathy → undetected injuries / pathogen entry
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11
Q

3 varieties of Cryptococcus
Serotype
Location

A
  • C grubii – serotype A. Most common. (Serotype based on capsule)
  • C neoformans – serotype D. Common in Europe.
  • C gattii – serotypes B and C. Associated w/ eucalyptus trees. Mainly found in tropical regions.
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12
Q

Cryptococcus neoformans
Environment
Morphology

A
  • Ubiquitous in soil. Found in bird guano, especially pidgeons.
  • Monomorphic budding yeast
  • Natural environment – dry, low CO2, iron. Capsule is downregulated and yeast is easily aerosolized for inhalation.
  • Host environment – moist, high CO2, low iron. Capsule is upregulated. Yeast more easily resists host defense.
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13
Q

Cryptococcus neoformans virulence factors (3)

A

Polysaccharide capsule made of glucuronoxylomannan (GXM)
Thermotolerance - grows at 37 degrees
Melanin

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14
Q

Functions of cryptococcus capsule (3 things)

What is it made of?

A

Made of glucoronoxylomannan.

Antiphagocytic, depletes complement, and down regulates immune functions

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15
Q

What organism makes melanin? What is it’s function?

How is it made?

A

Cryptococcus
Antioxidative effects of melanin combat oxidative burst to inhibit host defense. Tough melanin coat also aids in resistance to heat, pH, UV, phagocytes, and antifungals.
• Phenols (NTs such as L dopa, dopamine, epi, and NE) → quinones via phenoloxidases or laccases → autopolymerize to melanins

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16
Q 
Cryptococcus neoformans infection
What is infecting route and morphology?
Population
What is the main disease
Pulmonary diseases (4)
Hematogenous diseases (4)
Diagnosis
Treatment
A
  • Infection occurs via inhalation of yeasts or sexual / asexual spores
  • Typically only occurs in immunocompromised pxs, especially HIV/AIDS pxs
  • Main disease is meningitis.
  • Initial pulmonary infection is usually asymptomatic. May cause diffuse interstitial pneumonia, pleural effusion and acute respiratory distress syndrome.
  • Spreads in blood → meningitis, encephalitis, skin, and prostate (reservoir site).
  • Encephalitis = infection w/in brain parenchyma.
  • Diagnosis - Cryptococcal antigen latex slide agglutination test (Ab against capsule) is most sensitive. India Ink has low sensitivity. Halo sign seen on imaging. Histology shows “soccer ball” appearance of encapsulated yeast.
  • Liposomal amphotericin B + 5-flucytosine for severe infection. May switch to fluconazole after improvement. Fluconazole used for less severe infection, prophylaxis, or suppression (may not be necessary in HIV pxs if on ART).
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17
Q

What is the leading cause of meningitis in pxs w/ AIDS?

A

Cryptococcus

18
Q

What virulence factor aids in CNS infection?

What bugs? (5)

A

CNS is common target for encapsulated pathogens.

Cryptococcus neoformans, Neisseria meningitides, Strep pneumoniae, Haemophilus influenzae type B, E coli K1

19
Q 
Candida albicans
Location of normal microbiota
Route / cause of infection
Morphology (normal microbiota, mucocutaneous disease, and disseminated disease; what aids transition?)
Virulence factors (4)
A

Normal microbiota in oropharynx, colon, vagina, and sometimes moist skin.
•Infection is usually endogenous, mainly in immunocompromised pxs or change in microbiota after AB’s.
•Morphology
• Normal microbiota – Budding yeast
• Localized mucocutaneous disease (skin, oropharynx, vagina) – germ tubes, pseudohyphae, and hyphae (all filamentous structures). Transition from yeast is aided by neutral pH, 37 degrees, and presence of serum. Occurs w/in minutes.
• Disseminated disease (rare), such as blood / kidneys – both yeast and filamentous forms
•Virulence factors – morphogenesis, adhesins, biofilm formation, hydrolytic enzymes

20
Q

Cutaneous candidiasis
Sxs
Location of Balantis candidiasis

A

Sxs - erythema, pain, itching

Balantis = head of penis / foreskin

21
Q

Oropharyngeal candidiasis (OPC, thrush)
Risk factors
Sxs
Diagnosis

A
  • Risk factors – HIV, young / old, diabetes, cancer, chemo, corticosteroids, infectious mononucleosis (EBV, CMV), AB’s, xerostomia (dry mouth), dentures (biofilms)
  • Sxs – white plaques w/ underlying erythema, pain, poor feeding, weight loss
  • Diagnosis – clinical from history, sxs, and appearance. May use KOH prep.
22
Q

What is the most common opportunistic infection in HIV pxs?

A

Oropharyngeal candidiasis. 90% of pxs have this at some point.

23
Q

Candida esophagitis
Population
Sxs (4)

A

Occurs w/ severe immunocompromise.

Sxs - odynophagia (painful swallowing), dysphagia (difficulty swallowing), weight loss, and malnutrition.

24
Q 
Vulvovaginal candidiasis
Lifetime incidence for women
Risk factors
Sxs (7)
Diagnosis
pH of vagina
A
  • 75% lifetime incidence.
  • Risk factors – AB’s, pregnancy, diabetes, corticosteroids, HIV
  • Sxs (non-specific) – erythema, itching, pain, thick cheesy vaginal discharge, external dysuria (painful urination at labia), dyspareunia (painful sex)
  • White plaques seen on speculum exam
  • Diagnosis requires pelvic exam and pelvic sampling. KOH. Culture of vaginal fluid or plaque.
  • Vaginal pH is normal (4.0).
25
Q 
Systemic / Disseminated Candidiasis
Overall incidence
Nosocomial incidence
Cause
Most common sites of spread
Prognosis
Diagnosis (6)
Treatment (less serious, more serious, very serious, immunocompetent)
A
  • Rare, even in HIV pxs
  • 3rd / 4th most common nosocomial blood stream infection. #1 fungal cause.
  • May be due to IV catheter or insertion of medical device w/ biofilm
  • Kidney is most common site of spread. May cause descending UTI. Other common sites include lung, brain, liver, and eye
  • High morbidity / mortality (worse than meningitis)
  • Diagnosis
  • Blood culture is definitive and is always considered to be significant. Presence of germ-tubes differentiates C albicans from other Candida species.
  • Beta-D-Glucan detection assay (cell wall protein). Not specific.
  • Detection of cell wall mannan (antigen), mannose / arabinitol (metabolites), or enolase / aspartyl proteinase (enzymes)
  • PCR for rDNA
  • Treatment
  • Topical antifungals / oral azoles (fluconazole) for less serious infections
  • IV azoles / echinocandins for moderately severe infections
  • IV echinocandins / amphotericin B for very serious infections
  • Immunocompetent px w/ transient compromise may not need any tx
26
Q

What is 2nd most common form of Candida?
Morphology
Population

A

C glabrata
Only yeast morphology
Mainly seen in elderly

27
Q

What 2 species of Candida are resistant to fluconazole?

A

C glabrata and C krusei

28
Q

What type of Candida affects neonates?

A

C parapsilosis

29
Q 
Aspergillus fumigatus
Environment
Morphology
Association
2 types of allergy
Type of toxin, what foods, sxs
A
  • Ubiquitous in environment
  • Only a mold form w/ asexual lifecycle including mycelia and conidia. 45 degree hyphae are colorless and actively grow in hosts. Conidia are pigmented and occur in low-nutrient environments.
  • Associated w/ neutropenia
  • Allergies - Farmer’s Lung and allergic bronchopulmonary aspergillosis (ABPA, severe)
  • Aflatoxin found in moldy foods such as grains our nuts. Rarely affects humans.
  • Toxin sxs - Acute sxs include hepatoxicity and liver failure. Chronic sxs include hepatocellular carcinoma.
30
Q

Aspergilloma
Disease process / examples
Tx

A

Fungus ball colonizing a pre-existing cavity, such as the lungs or sinuses.
Ex - emphysema, TB, alpha-1-antitrypsin deficiency.
Main tx is surgical excision. May also use anti-inflammatories.

31
Q

Invasive aspergillus
Example
Cause
What parts of the immune system kill aspergilli?

A
  • Invasive Pulmonary Aspergillosis (IPA)
  • Occurs w/ defects in innate immune defense (phagocytes).
  • Macrophages good at killing conidia. Neutrophils good at extracellular killing of conidia and hyphae
32
Q

Disseminated Aspergillus
Route of infection
Sxs
Prognosis if found before / after 10 days

A
  • Inhalation and spread through blood.
  • May not have any respiratory sxs due to being neutropenic (inflammation causes sxs). CNS is a target.
  • Mortality is 40% if diagnosed and treated w/in 10 days of infection. >90% mortality if not diagnosed before 10 days.
33
Q

Diagnosing Aspergillus (3)

A
  • Culture – from biopsy or BAL. Low sensitivity and specificity due to being so common in environment → contamination.
  • Serum / BAL assays – positive 1-2 weeks before culture
  • Aspergillus antigen assay – looks for galactomannan
  • Beta-D-glucan detection assay – not specific for Aspergillus.
  • CXR or CT - Halo sign appears earlier (hemorrhage around pulmonary infarction). Air crescent sign appears 1-3 weeks after halo (rim of cavitation)
34
Q

Treating Aspergillus (general tx, invasive / disseminated, transplant pxs, and prophylaxis)

A
  • General - azoles
  • Invasive / disseminated aspergillosis – voriconazole
  • Transplant pxs – voriconazole + echinocandin
  • Prophylaxis – Posaconazole
35
Q 
Pneumocystis jirovecii
2 different morphologies
Membrane composition
Cell wall composition
Antifungal resistance / susceptibility
Unique lab feature
Population
A
  • Trophozoites – unicellular. Outnumber cysts 10:1. Motile.
  • Cysts – larger w/ intracystic bodies. Highly refractive. May be generated by fusion of 2 haploid trophozoites followed by meiotic division. Non-motile.
  • Has cholesterol instead of ergosterol
  • Cell wall made of chitin / beta glucans
  • Resistant to amphotericin B and azoles
  • Susceptible to echinocandins and anti-parasitic drugs (used to be thought of as a parasite)
  • CanNOT be grown in vitro
  • Extreme opportunist, mainly affecting HIV pxs. Exposure is universal. 75% of HIV pxs have had PCP at least once. Causes 20% of AIDS deaths.
36
Q

Main disease caused by Pneumocystis jirovecii
Mechanism
Histology
Less common disease

A
  • Main disease is pneumonia after inhalation. PCP = pneumocystis pneumonia. Diffuse interstitial pneumonia w/ total lung involvement (beyond areas w/ fungus present).
  • Trophozoites attach to host pneumocytes and cause loss of cells lining alveoli.
  • Foamy red exudate fills alveoli → honeycomb appearance.
  • Fungemia / dissemination is possible w/ extreme immunocompromise.
37
Q

Diagnosis (3) / Treatment (3) for Pneumocystis

A
  • Diagnosis
  • Gold standard is seeing the organism on biopsy, BAL, or sputum
  • Beta-D-glucan assay – not specific
  • CXR / CT shows ground glass
  • Culture is NOT useful
  • Serology also NOT useful b/c everyone has been exposed.
  • Treatment
  • Amphotericin and azoles doesn’t work b/c there isn’t any ergosterol
  • TMP-Sulfa good for both active infection and prophylaxis.
  • Antiparasitic drugs – Pentamidine, dapsone, pyrimethamine, clindamycin, etc
  • Steroids to reduce inflammation
38
Q

What are the 2 most common yeasts to grow in blood?

A

Cryptococcus and Candida albicans?

39
Q

What is the most common germ-tube producer?

A

Candida albicans

40
Q

How is Candida albicans differentiated from other Candida? How are these other Candida spp differentiated from one another?

A

C albicans is the only one that grows germ tubes.

These other species are differentiated via carbohydrate / biochemical tests.

41
Q

Measuring the levels of what 2 normal components of blood aids in differentiating fungal infections from viral infections?

A

Low glucose and high protein

microbio gram neg (10 decks)

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