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MSII Micro Unit 4 > Opportunistic Mycoses > Flashcards

Opportunistic Mycoses Flashcards

1
Q

major human opportunistic mycoses

A
  • candidiasis
  • cryptococcosis
  • aspergilliosis
  • murcormycosis
  • fusariosis
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2
Q

themes in opportunistic mycoses

A
  • diseases and severity are widely varied
  • depends on the patients’ pre-existing conditions
  • most important predisposition is prolonged neutropenia
  • optimal treatment addresses both the infection and the underlying problem
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3
Q

ways to get prolonged neutropenia? and why is prolonged neutropenia bad?

A
  • most important predisposition for opportunistic mycoses
  • infections
  • aplastic anemia
  • arsenic poisoning
  • cancer
  • chemo
  • radiation
  • medications
  • hereditary disorders
  • vitamin deficiency
  • autoimmunity
  • hemodialysis
  • splenic sequestration
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4
Q

cryptococcosis organisms

A
  • neoformans and gattii form 5 serotypes
  • A and D are neoformans and most common
  • B and C are gattii
  • cause cryptococcosis, especially cryptococcal meningitis
  • neoformans is environmental, found worldwide in soil contaminated with bird droppings, especially pigeons
  • gatti found in litter under eucalyptus trees, cause less severe disease but prefers immunocompetent hosts (west coast)
  • oval yeasts with narrow based buds and wide polysaccharide capsule
  • pathogenic strains grow at 37 degrees
  • not thermally dimorphic, moldlike sexually reproducing form has a different trigger
  • no human to human transmission except organ transplant or needle sticks (which cause local cutaneous disease)
  • meningitis rare before 1946, now we have more immunocompromised patients living on steroids and chemo
  • disseminated disease was fatal before Amphotericin B in 1968
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5
Q

pathogenesis of cryptococcosis

A
  • transmitted by inhalation, pigeon droppings may be contagious for years
  • lung infection may be asymptomatic or lead to pneumonia
  • can be intracellular infection in alveolar macrophages
  • immunocompetent hosts restrict infection to lungs and raises Helper T cells; they have skin test conversion and antibodies to capsule
  • in people with deficient CMI, esp AIDS, dissemination leads to meningitis with skin nodules
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6
Q

inflammatory response to C neoformans

A
  • very blunted inflammatory response
  • can have granuloma formation
  • organ damage is by tissue distortion from growing yeast
  • blunted response complicates diagnosis and means that presentation is late in disease
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7
Q

virulence factors of cryptococcosis

A
  • capsule is most important
  • melanin in cell wall is antiphagocytic
  • phospholipase B for invading tissue
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8
Q

cryptococcosis diagnosis on exam: Hx

A
  • steroid use
  • malignant disease
  • transplantation
  • HIV infection
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9
Q

cryptococcosis diagnosis on exam: skin

A

-take biopsies of nodules, can grow yeast

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10
Q

cryptococcosis diagnosis on exam: pulmonary

A
  • range from asymptomatic to ARDS

- cough and chest pain common

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11
Q

cryptococcosis diagnosis on exam: cryptococcus and HIV

A
  • fever
  • cough
  • headache
  • weight loss
  • positive cultures from blood, CSF, urine
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12
Q

cryptococcosis diagnosis on exam: CNS

A
  • subacute meningitis or meningoencephalitis
  • antifungal therapy required for survival
  • CT and MRI
  • meningitis: headache, AMS, N/V
  • fever and stiff neck less common (arise from IF)
  • may also be sensory issues with eyes or ears
  • if not acute pyogenic, may wait for CT/MRI before LP
  • cryptococcomas: granulomas in brain cause focal neuro deficits
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13
Q

additional areas for cryptococcosis infection?

A
  • prostate
  • eyes
  • medullary cavity of bones
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14
Q

cryptococcosis diagnosis on lab: CSF

A

-stain with India Ink to observe yeast with wide capsule

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15
Q

cryptococcosis diagnosis on lab: biopsies

A

-stain with methenamine silver, periodic acid-schiff, mucicarmine

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16
Q

cryptococcosis diagnosis on lab: culture

A
  • at 37 degrees from CSF, blood, urine, sputum
  • look for mucoid colonies on Sabouraud again
  • will produce melanin in culture on special media
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17
Q

cryptococcosis diagnosis on lab: serology

A
  • crag for soluble cryptococcal antigen in blood and CSF
  • one of the only useful serologic tests for microbes
  • routine bloodwork may be normal
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18
Q

cryptococcosis treatment: meningitis

A
  • Amphotericin B (liposomal if kidney problems) plus flucytosine for 2 weeks followed by 10 more weeks of fluconazole
  • in AIDS patients, use fluconazole for long term suppression, clearance may not be an option
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19
Q

cryptococcosis treatment: prostate

A

-fluconazole

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20
Q

cryptococcosis treatment: pulmonary

A
  • in immunocompetent patients may not neat treatment

- can use 6-12 mo of fluconazole or itraconazole

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21
Q

cryptococcosis treatment: skin, bones, other

A

-Amphotericin B

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22
Q

how often do you have to check the CSF for crypto progress of treatment?

A
  • weekly
  • glucose and cell count will return to normal but protein anomalies may persist for years
  • do not discontinue therapy until cultures consistently fail
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23
Q

Aspergillosis organism

A
  • fumigatus (most common), niger, flavus, clavatus
  • ubiquitous environmental molds
  • only mold, not dimorphic, therefore can’t get into blood easily
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24
Q

Shape of aspergillus?

A
  • septate hyphae with V shaped branches
  • walls are nearly parallel
  • conidia form radiating chains
25
Q

what four syndromes does aspergillus cause?

A
  1. allergic bronchopulmonary aspergillosis (ABPA)
  2. Aspergilloma or colonizing aspergilliosis (fungus ball in lung)
  3. chronic necrotizing pulmonary aspergillosis (CNPA)
  4. invasive aspergillosis
    * which one of these syndromes the patient gets depends on immune status
26
Q

pathogenesis of aspergillosis

A
  • widespread on decaying vegetation worldwide
  • infectious conidia are airborned
  • conidia colonize abraded skin, burns, cornea, ear, sinuses, lung
  • healthy macrophage and neutrophil response eradicates fungus
  • some aspergillus produce toxic metabolites that inhibit macrophage responses (like steroids)
27
Q

allergic bronchopulmonary aspergillosis (ABPA)

A
  • hypersensitivity reaction to infection of bronchi
  • found in 1-10% of asthmatics, 7% of CF patients
  • presents as an exacerbation of current condition
28
Q

aspergilloma

A
  • fungus ball forms when aspergillus invades already formed cavitary lesions of TB or CF
  • associated with hemoptysis, may be life threatening
29
Q

chronic necrotizing pulmonary aspergillosis (CNPA)

A
  • in immunocompromised
  • can invade lungs
  • cause pneumonia with hemoptysis and granulomas
  • may find hyphae in granulomas
  • rare
  • hard to diagnose
  • often found at autopsy
  • 10-100% mortality
30
Q

invasive aspergillosis

A
  • rapidly progressive invasion of blood vessels in severely immunocompromised patients
  • involves infarction, hemorrhage, necrosis, often fatal
  • relatively common in severely immunosuppressed patients (5-20%)
31
Q

virulence factors of aspergillus

A
  • gliotoxin- immunosuppressive
  • toxic metabolites interfere with phagocytosis and opsonization
  • proteases may be involved in tissue invastion
32
Q

diagnosis of ABPA

A
  • positive skin test for aspergillus allergy with asthma or CF
  • coughing up brownish bronchial plugs containing hyphae
  • fever
  • wheezing
  • pulmonary infiltrates
  • unresponsive to antibiotics
  • hemoptysis
  • uncontrolled asthma
  • purulent sinus drainage
  • Xray or CT may show grape cluster or hand in mitten mucous clogged bronchi
33
Q

diagnosis of aspergilloma

A
  • fungus ball is visible on Xray or CT (mass in a cavity)
  • changes position when patient sits up/ lies down
  • does not invade tissue but may cause dangerous hemoptysis
  • cough and fever
  • may appear as a complication of chronic necrotizing pulmonary aspergillosis (CNPA) or invasive aspergillosis
34
Q

diagnosis of CNPA

A
  • subacute pneumonia that is unresponsive to antibiotics
  • underlying disease of alcoholism, collagen vascular disease, chronic granulomatous disease or COPD with long term corticosteroid therapy
  • needly biopsy, aspirate fluid if present for histo and culture
35
Q

diagnosis of invasive aspergillosis

A
  • history of profound immunosuppression or COPD with long term steroid therapy
  • fever, cough, dyspnea, pleuritic chest pain, neutropenia, sometimes hemoptysis, worsening hypoexemia
  • CXR is abnormal but variable
  • CT may show a halo sign: ground glass infiltrate surrounding a nodular density
  • represents a hemorrhage, invasive aspergillosis most common cause
  • bronchoscopy, needle biopsy, or open lung biopsy for culture and histology
36
Q

diagnosis of aspergillus on lab

A
  • culture from sputum, needly biopsy, or bronchoalveolar lavage fluid
  • visualize with silver stains, colonies with radiating chains of conidia
37
Q

invasive aspergillus on lab

A
  • septate hyphae branching at acute angles invading tissue
  • acute IF infiltrate
  • tissue necrosis
  • blood vessel invasion
  • high serum levels of glactomannan antigen
38
Q

ABPA on lab

A
  • high levels of aspergillus specific IgE
  • eosinophilia
  • mucus with degenerating eosinophils and hyphae
39
Q

treatment for ABPA

A
  • oral corticosteroids!-because need to dampen IgE
  • itraconazole
  • consider sinus surgery and/or omalizumab (anitbody to IgE that breaks up the chain to activate mast cells
40
Q

treatment for aspergilloma

A
  • remove surgically if hemoptysis

- oral itraconazole

41
Q

treatment for invasive aspergillus or CNPA

A
  • vorionazole and/or ampho B (liposomal if kidney probs)
  • alternative is capsofungin, might not works
  • decrease immunosuppression if possible
  • surgical resection of diseased area may be considered
42
Q

mucormycosis organism

A
  • RHIZOPUS
  • very rare (500/year in US)
  • life threatening (50-85%) mortality
  • sinus infections, invade brain
  • may also affect other organs
  • widespread environmental
  • not dimorphic
  • underlying risk factor include diabetes, neutropenia
  • must treat underlying disease, add Amph B, aggressive surgery
43
Q

pathogenesis of mucor

A
  • transmitted by airborne asexual spores
  • ubiquitous worldwide
  • cause disease only in vulnerable patients
  • usually inhaled, can also be ingested or introduced by trauma
  • invade tissues of patients with reduced immunity- diabetes, burns, leukemia, IV steroids, TNF a blockers, Fe overload
  • neutrophils are main defense
  • not highly associated with AIDS (CMI might not be critical)
  • proliferate in walls of blood vessels, particularly:
    1. paranasal sinuses, invading brain (50-70% mort, even when cured requires disfiguring surgery),
    2. lungs (harder to dx, higher mort),
    3. gut (of extremely malnourished)- harder to dx, higher mort
    4. skin, 15% mort
    5. disseminated, nearly 100% mort
  • cause infarction and necrosis of tissue downstream from blocked vessel
  • symptoms are at affected site
44
Q

rhinocerebral diagnosis of mucor

A
  • unilateral retro-orbital headache, facial pain, numbness, fever
  • progresses to diplopia and visual loss
  • reduced consciousness
  • black pus
  • necrotic eschars
  • CT may be useful for detecting sinusitis invading the brain
45
Q

wound infections in mucor

A

-unresponsive to antibiotics

46
Q

Lung and GI mucor

A
  • not specific presentations
  • bronchoalveolar lavage or biopsy may be useful
  • CT scan of lung for cavitation with and air crescent is highly suggestive of fungal infection
  • CT of gut may show mass
47
Q

cutaneous presentation of mucor

A

-cellulitis progression to dermal necrosis and black eschar formation

48
Q

mucor lab diagnosis

A
  • neutropenia, diabetic acidosis, iron overload
  • no useful antigen tests or CSF findings
  • biopsy- H&E or fungal stains show NONSEPTATE HYPHAE with broad irregular walls and branches AT RIGHT ANGLES, vascular invasion and necrosis, neutrophil infiltration
  • culture- colonies with spores contained in sporangium, difficult to culutre
49
Q

treatment for mucor

A
  • send to tertiary care facility
  • change any pre-existing bandages/ splints (could be contaminated)
  • if diagnosed early, treat underlyinf problem plus liposomal amphotericin B and aggressive surgical removal of necrotic tissue may helps
  • alternative posaconazole
  • repeated, disfiguring surgery required for survival
50
Q

Fusarium mycology

A
  • fusarium species are environmentally ubiquitous
  • identified microscopically by banana shaped macroconidia
  • primarily pathogens of plants, including important crops
  • F. solani is most common causing infection (50%), random other species contribute other 50%
51
Q

virulence factors of fusarium

A
  • immunosuppressive mycotoxins
  • collagenases and proteases
  • ability to adhere to prosthetic material
52
Q

three presentations of fusarium pathogenesis

A
  • mycotoxicosis
  • immunocompetent local infection
  • immunosuppressed opportunistic infection
53
Q

mycotoxicosis of fusarium

A
  • trichothecene mycotoxins- alimentary toxic aleukia (nasty hemorrhagic syndrome from ingesting/ contact)
  • widespread bleeding and immunosuppression with secondary sepsis
  • often fatal
  • 1940s USSR outbreaks in wheat
  • yellow rain
54
Q

immunocompetent local infection with fusarium

A
  • skin-burns
  • cornea (contaminated contact solution)
  • allergic sinusitis like ABPA
  • colonization of prosthetics and catheters
  • treated with amphotericin B, voriconazole, posaconazole
55
Q

immunosuppressed opportunistic infection with fusarium

A
  • prolonged neutropenia
  • long term steroids
  • bone marrow transplants
  • profound T cell recipients (HSCT recipientst)
56
Q

disseminated fusarium

A
  • usually invades from sinus or at wound site
  • presents as a fungemia with skin lesions
  • may also seed eye, lung, cause local sx there
  • grows from inside out
  • often lethal
57
Q

fusarium diagnosis

A
  • grows easily on fungal medial but environmentally ubiquitous
  • need multiple samples and sites to differentiate from lab contamination
  • histology may be helpful, but can only differentiate from aspergillus if yeast form is present with acute branching hyphae
  • PCR based tests and fungal metabolism tests available
58
Q

fusarium treatment

A
  • clinical trial data to compare efficacy of drugs and dosages
  • more resistant to antifungals than others
  • surgical excision of localized infections
  • try ampho B with natamycin or voriconazole
  • prognosis in disseminated disease is poor
59
Q

fusarium prevention

A
  • high risk patients should be kept in HEPA filtered POSITIVE pressure rooms
  • filtered water supplies and scrubbed down showers
  • pre-op workup for HSCT must include screening for fusarial infection, which may appear trivial before immunosuppression

MSII Micro Unit 4 (6 decks)

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