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micro unit 4 > opportinistic mycoses > Flashcards

opportinistic mycoses Flashcards

1
Q

where is cryptococcus neoformans found

A

worldwide, environmental. esp in bird droppings - pigeons

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2
Q

what does cryptococcus neoformans look like

A

oval budding yeast, narrow-based bud. it also has a polysaccharide capsule.

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3
Q

is cryptococcus neoformans dimoprhic?

A

no

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4
Q

is cryptococcus neoformans contagious?

A

no human to human transmission

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5
Q

how is cryptococcus neoformans transmitted?

A

by inhalation. this may be asymp or lead to pneumonia.

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6
Q

what is a risk for hematogenous dissemination of cryptococcus neoformans

A

AIDS or immunosuppression

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7
Q

what doe disseminated infection of cryptococcus neoformans look like?

A

leads to meningitis with skin nodules. fever and stiff neck may be underwhelming or absent due to low inflammation

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8
Q

common history of cryptococcus neoformans systemic infection

A

transplant, HIV, cancer, or steroid use.

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9
Q

labs for cryptococcus neoformans

A

CSF with india stain to observe the yeast with the wide capsule. culture from the CSF or mucoid colonies on the agar. serologic test for CRAG cryptococcal antigen. routine blood work may be normal.

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10
Q

what stains to see cryptococcus neoformans

A

india stain, PAS, methenamine silver, mucicarmine.

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11
Q

treatment for the cryptococcus neoformans infection

A

amphotericin B and flucytosine.

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12
Q

treatment of cryptococcus neoformans in AIDS patients

A

use fluconazole for long term suppression. for pneumonia or prostate infection use fluconazole or itraconazole for 6-12 months.

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13
Q

aspergillus fumagatus characteristics?

A

only a mold, not thermally dimorphic. has septae with V-shaped branches. walls are nearly parallel.

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14
Q

what do the conidia of aspergillus fumigates look like?

A

radiating chains.

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15
Q

how do we contract aspergillus fumagatus

A

they are widespread and found on decaying vegetations. the infection is inhalation. but they can colonies abraded skin, burns, cornea, ear and sinuses.

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16
Q

what virulence factors does aspergillus fumigatus have

A

gliotoxin (immunosuppressive), toxic metabolites and proteases.

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17
Q

what are the four presentation of aspergillus fumigatus infections?

A

allergic bronchopulmonary aspergillus, aspergilloma, chronic necrotizing pulmonary aspergillosis, and invasive aspergilosis.

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18
Q

allergic bronchopulmonary aspergillosis

A

HSR to infection of the bronchus by aspergillus. exacerbates asthma and cystic fibrosis.

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19
Q

aspergilloma

A

fungus balls form at the site of a cavitary lesion left by past TB or pulmonary mycosis or CF. risk of pulmonary hemorrhage.

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20
Q

Chronic necrotizing pulmonary aspergillosis.

A

hyphae invade the lung tissue causing pneumonia with hemoptysis and granulomase. rare, hard to diagnose

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21
Q

what is the mortality of CNPA? why

A

10-100% hard to diagnose.

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22
Q

invasive aspergillosis

A

rapidly progressive invasion of the blood vessels. leads to infarction, hemorrhage, necrosis. is a common cause of death of the immunosuppressed.

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23
Q

ABPA symptoms.

A

coughing up brownish mucous plugs that contain hyphea. the person is allergic to aspergillus, underlying asthma or CF, blood in sputum, fever/wheezing/pulmonary infiltrates that are not responsive to antibiotics. CXR shows clusters of mucous-clogged bronchi.

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24
Q

what is grape-cluster or hand in mitten syndrome?

A

this is the pulmonary infiltrates caused by ABPA on CXR. they are mucous-clogged bronchi

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25
Q

aspergilloma symptoms.

A

cough, fever, dangerous hemoptysis. the fungus ball is visible of the CXR as a ball with an air-crescent sign. it will change position when the patient moves.

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26
Q

is aspergilloma an isolated finding?

A

can be. or it can be a complication of the CNPA or invasive asperillosis.

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27
Q

CNPA symptoms

A

fever, cough, night sweats, weight loss, history of ineffective treatment for TB. subacute pneumonia that is unresponsive to antibiotics. history of alcoholism collagen-vascular disease, chronic granuloma disease, COPD, long term steroids, hard to diagnose, need sample from the lung aspirate.

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28
Q

invasive aspergillosis

A

history of profound immunosuppression or COPD and longterm steroids. will present with fever, cough, pleuritic chest pain, worsening hypoxemia. will show halo-sign on CT>

29
Q

characteristic asperilloma sign

A

air-crescent sign

30
Q

characteristic invasive aspergillus sign

A

halo-sign.

31
Q

labs for aspergillus fumagatus

A

biopsy shows hyphae at acute angles. cultures will have radiating chains of conidia. invasive disease will have high levels of glactomannan antigen. ABPA high levels of IgE, eosinophilia, hyphae in mucous.

32
Q

treatment for ABPA

A

oral steroids and itraconizole consider sinus surgery and omalizumab.

33
Q

treatment for aspergilloma

A

remove surgically and use itraconzaole.

34
Q

treatment for CNPA or invasive

A

amphoterin B but may not work. Alt: voriconazole, caspofungin, immune reconstitution, surgical resection.

35
Q

mucor/rhizopus characteristic

A

mucor, rhiopus or absidia. widespread environmental. they are not thermally dimorphic.

36
Q

how are mucor/rhizopus transmitted?

A

airborne asexual spores. invade patients with low immunity.

37
Q

common patients to get mucor/rhizopus

A

diabetes, burns, leukemia.

38
Q

what happens to patients with mucor/rhizopus

A

it proliferates in the walls of blood vessels, particularly in the lungs, GI, and paranasal sinuses. they cause infection and necrosis downstream.

39
Q

what is common in diabetics with mucor/rhizopus

A

they will get infection that blocks the blood supply to the brain. rhinocerebral mucormycosis.

40
Q

how do we diagnose mucor/rhizopus

A

look for the symptoms at the infected site. brian, eyes, lungs, skin, GI, CNS. there is failure die to impaired blood flow.

41
Q

common history of someone with mucor/rhizopus

A

diabetes, burns, leukemia, IV steroids, TNF-alpha blockers, iron overload.

42
Q

what is mucor/rhizopus not associated with?

A

AIDS.

43
Q

what is mucor/rhizopus highly associated with?

A

diabetes.

44
Q

labs for mucor/rhizopus

A

biopsy shows non septate hyphae with broad irregular walls. the hyphae are at right angles. cultures difficult but will have sporangium in the spores.

45
Q

treatment for mucor/rhizopus

A

frequently fatal. if caught early then treat with amphotericin B and surgical removal of necrotic tissue. also can use posaconazole.

46
Q

fusarium spp characteristics

A

pathogen of plants/crops. different species cause different diseases.

47
Q

mycotoxicity (fusarium)

A

some species express mycotoxins that are fatal. can be in contaminated wheat.

48
Q

what is common for immunocompromised patients with fusarium

A

develop infection under the fingernails or in the cornea. treat with ampho B, voriconazole, posaconizole.

49
Q

who is most commonly to get disseminated infection with fusarium

A

someone with neutropenia.

50
Q

what common infections does fusarium solani give?

A

corneal and disseminated.

51
Q

which immunodeficiencies are risks for fusarium

A

neutropenia and T-cell deficiency. ESP hematopoetic stem cell transplants.

52
Q

what are the virulence factors for fusarium

A

immunosuppressive mycotoxins, proteases, collagenases, and the ability to adhere to prosthetic material

53
Q

how is fusarium transmitted?

A

it is environmentally ubiquitous. airborne is the main pathogenesis. however aspiration of inhaled water is also a cause.

54
Q

local infections of fusarium

A

burns or use of contaminated contact lens solution. locally invasive can also follow solid organ transplant.

55
Q

systems commonly affected by fusarium

A

eye, skin, sinus, fungemia, pneumonia.

56
Q

fusarium of the eye.

A

may progress from corneal infection or be seeded from a blood infection.

57
Q

fusarium of the sinus

A

may be due to allergic sinusitis in immunocompetent or invasive sinusitis in immunocompromised.

58
Q

fusarium of the skin

A

localized at wound sites in the immunocompetent. in immunocompromised they can spread anywhere and have preference for the toes. they give a more gangrenous appearance.

59
Q

fusarium fungemia

A

more common for fusarium than for aspergillus. may be seen in immunocompetent with central venous catheters but more commonly seen due to dissemination

60
Q

fusarium disseminated

A

combination of skin lesions and culture is diagnostic. neutropenic or profoundly t cell depleted patient. 75% mortality.

61
Q

how do we diagnose fusarium

A

must take samples from several sites due its commonality. a single positive is rarely true. it is a banana-shaped macroconidia with a foot-cell at the base. the hyphae closely resemble aspergillus but also may contain yeast form. PCR is available.

62
Q

treatment for fusarium

A

it is anti fungal resistant! localized infections need surgical removal with topical care of natamycin or vorconazaole.

63
Q

how to treat disseminated fusarium

A

need amphotericin B and also immune reconstitution that can be done quickly. prognosis is poor.

64
Q

prevention of fusarium

A

high-risk patients need to be kept in HEPA-filtered rooms with positive pressure. also require filtered water supply and scrub showers. pre-op should include screening for infection.

65
Q

what kind of resistance does fusarium have

A

innate resistance!

66
Q

what kind of resistance does candidia have?

A

acquired

67
Q

what is the highest risk for rhizopus infection for someone predisposed but not exposed?

A

diabetes!

68
Q

what is the highest risk for a deadly cryptococcal infection?

A

HIV

micro unit 4 (6 decks)

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