Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Therapeutics > FUNGAL INFECTIONS > Flashcards

FUNGAL INFECTIONS Flashcards

1
Q

Oropharyngeal candidiasis (OPC, thrush)

A

infection of the oral mucosa with candida species

C. Albicans - most common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

esophageal candidiasis (EC)

A

infection of the esophagus with candida spp

C. Albicans- most common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Primary line of host defenses against superficial candida infection is

A

cell mediated immunity (mediated by CD4 T-cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clinical presentation of OPC

A
  • cottage-cheese like appearance, yellowish-white, soft plaques (or milk curds) overlying areas of erythema on the buccal mucosa, tongue, gums, and throat
  • symptoms range from none to painful mouth, burning tongue, metallic taste, dysphagia, and odynophagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clinical presentation of EC

A
  • dysphagia, odynophagia, and retrosternal chest pain are common
  • fever, few to numerous white or beige plaques of varying size
  • plaques can be hyperemic or edematous with ulceration in severe cases
  • Upper GI endoscopy with biopsy: the histologic presence of candida in lesions, culture warranted due to concern for drug resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Treatment of OPC - mild infection

A

Tropical regimens-treat for 7-14 days

  1. Clotrimazole 5x/day (hold in mouth for 15-20 minutes; do not swallow)
  2. Nystatin suspension- 5 mL swish and swallow QID
  3. miconazole mucoadhesive buccal tablet, apply to upper gum region daily
    - apply in morning after brushing teeth - hold in place for 30 seconds
    - eat and drink normally but avoid chewing gum
    - if falls off and swallowed in first 6 hours apply new tablet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment of OPC - systemic therapy needed for those with refractory OPC, those who cannot tolerate topical agents, patients with moderate to severe disease, and patients at high risk for disseminated systemic disease (neutropenia)

A
  1. fluconazole PO daily (preferred)
  2. Itraconazole solution daily - take on an empty stomach
  3. posaconazole suspension BID on day 1 and then once daily x 14 days (with food)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Treatment for fluconazole-refractory OPC

A
  • Treat for > 14 days (up to 28 days)*
    1. itraconazole solution daily
    2. posaconazole suspension BID x3 days then daily for 28 days
    3. amphotericin B deoxycholate suspension swish and swallow QID
    4. voriconazole BID (> 40 kg)
    5. Caspofungin IV daily (loading dose first)
    6. Micfungin IV daily
    7. Anidulafungin IV daily
    8. amphotericin B deoxycholate V
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Treatment for esophageal candidiasis

A
  • systemic treatment is always required*
  • Treat for 14-21 days
    1. fluconazole PO/IV daily
    2. Itraconazole solution PO daily
    3. Echinocandin
    4. Voriconazole PO/IV BID (> 40 kg)
    5. Posaconazole suspension PO BID or delayed-release tablets
    6. Amphotericin B deoxycholate IV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Treatment of fluconazole-refractory esophageal candidiasis

A
  1. itraconazole solution PO daily
  2. posaconazole suspension PO BID (with food)
  3. Voriconazole PO/IV (> 40 kg)
  4. amphotericin B deoxycholate or lipi-based formulation
  5. Enchinocandin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Histoplasmosis

A
  • infection caused by inhalation of dust-borne microconidia of the organisms.
  • endemic of the ohio and Mississippi river
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Histoplasmosis pathophysiology

A
  1. conidia become aerosolized when soil is disturbed -> inhaled and reach the bronchioles
  2. conidia germinate within 2-3 days releasing yeast forms that begin to multiply
  3. over the next 9-15 days organisms are phagocytized by macrophages but not killed (cell mediated immunity)
  4. infected macrophages migrate to lymph nodes and other sites to the body (liver, spleen) via the bloodstream (disseminated)
  5. over next 2-4 months tissue granulomas form with central caseation and necrosis (unless immunocompromised cannot make granulomas)
  6. these areas become encapsulated and calcified over several years with viable organisms trapped within necrotic tissue (unless immunocompromised)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

histoplasmosis diagnosis

A

standard of care: serologic testing - detect histoplasmosis antigen through blood, urine, BAL
-in patients with HIV/AIDs bone marrow biopsy and culture; antigen detection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Histoplasmosis treatment in immunocompetent host

A
  1. mild to moderate symptoms >4 weeks: itraconazole 200 mg TID x3 days then 200 mg QD or BID for 6-12 weeks
    - alternatives: posaconazole, fluconazole
  2. moderately severe-sevre disease: lipid amphotericin B IV daily x 1-2 weeks then itraconazole 200 mg TID x3 days followed by 200 mg BID for total of 12 weeks
    - amphotericin B deoxycholate if low risk of nephrotoxicity
    - methylprednisolone for the 1-2 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Histoplasmosis treatment in immunocompromised host

A
  • therapy needed for all patients*
    1. moderately severe-severe disseminated disease: lipid amphotericin B IV daily for 1-2weeks then itraconazole 200 mg TID x 3days followed by 200 mg BID for at least 12 months
  • obtain itraconazole concentration after 2 weeks (random conc >/= 1 mcg/mL
    2. less severe disease: itraconazole 200 mg TID x3 days followed by 200 mg BID x 12 months
  • alternative posaconazole, voriconazole, fluconazole (higher dose needed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Blastomycosis

A
  • caused by blastomyces dermatitides (broad based budding)
  • endemic in southeastern, south central, and midwest united states
  • pulmonary infection occurs secondary to inhalation of condida -> inflammatory response with neutrophilic recruitment to lungs -> dissemenation -> cell-mediated immunity -> formation of granulomas
  • accompanied with extrapulmonary manifestations: skin, bone/joints, genitourinary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pulmonary blastomycosis treatment in immunocompetent

A
  1. moderatly severe-severe disease: lipid amphotericin B IV daily or deoxycholate x 1-2 weeks or until improvement followed by itraconazole 200 mg PO TID x3 days then 200 mg PO BID for 6-12 months totals
  2. mild-moderate disease: itraconazole 200 mg PO TID x3 days, then 200 mg PO BID x6 months total
    - monitor serum concentrations of itraconazole after 2 weeks
18
Q

Treatment of disseminated pulmonary blastomycosis in immunocompetent

A
  1. moderately severe-severe: lipid amphotericin B x1-2 weeks or until improvement followed by itraconazole 200 mg TID x3 days followed by 200 mg PO BID for 6-12 months total
  2. mild-moderate disease: itraconazole 200 mg TID x 3 days then followed by 200 mg BID for 6 months total
19
Q

Extrapulmonary blastomycosis disease in immunocompetent

A
  1. CNS disease: lipid amphotericin B IV daily for 4-6 weeks followed by an oral azole as consolidation therapy
    - consolidation: fluconazole 800 mg PO; itraconazole 200 mg PO BID-TID; voriconazole 200-400 mg PO BID treat for >/= 12 months
  2. osteoarticular: treat for 12 months
  3. acute disease: lipi amphotericin B or amphotericin B IV x 1-2 weeks or until improvement, then suppressive therapy for 12 months
    - suppressive therapy: itraconazole 200 mg PO TID x3 days, then 200 mg PO BID for >12 months total
20
Q

Coccidioidomycosis

A
  • caused by coccidioides immitis

- endemic in the southwestern and wester US (California to texas)

21
Q

primary coccidioidomycosis (Valley fever)

A
  • non-specific symptoms: fever, cough, headache, sore throat, arthralgias, myalgias, and fatigue occur 1-4 weeks after exposure
  • diffuse macopapular rash appears in the first few days
  • primary pneumonia can be the first manifestation of disease - characterized by productive cough (blood-streaked); single or multiple soft or dense homogenous hilar or basal infiltrates on chest x-ray
22
Q

non-disseminated coccidioidomycosis treatment

A
  1. primary respiratory infection: fluconazole PO/IV or itraconazole PO and treat for 3-6 months
  2. symptomatic chronic cavity pneumonia: fluconazole or itraconazole
  3. diffuse pneumonia with bilateral or miliary infiltrates: amphotericin B (lipid or deocyholate) for several weeks, followed by an azole for 12 months total
23
Q

disseminated coccidioidomycosis treatment

A
  1. nonmeningeal disease: itraconazole or fluconazle or amphotericin B
  2. : meningeal disease: fluconazole IV/PO daily (not curative; life long suppressive therapy) - DOC
    - itraconazole
    - intrathecal amphotericin B with or without continuation of azole therapy
24
Q

Cryptococcosis

A
  • caused by cryptococcus neoformans and cryptococcus gatti
  • C. neoformans in immunocompromised host
  • C. gattii in immunocompetent host
  • encapsulated yeast found in soil and pigeon droppings
  • infection acquired by inhalation of the organism - resists phagocytosis due to capsule
  • cell-mediated immunity plays a major role in host defense against infection
  • disease may be localized in lungs or disseminate to other areas (CSF)
25
Q

cryptococcosis clinical presentation

A

-pulmonary: shortness of breath
-meningitis:
non-aids: HA, fever, N/V, mental status changes, nuchal rigidit
HIV/AIDs: fever malaise, headache

26
Q

Cryptococcosis diagnosis

A
  • meningitis - non-HIV: increased CSF opening pressure, CSF WBCs, CSF protein and decreased CSF glucose. Positive CSF cryptococcal antigen (blood and CSF)
  • reduced inflammatory response in HIV/AIDs with extremely high cryptococcal antigen titer
27
Q

Cryptococcal meningitis treatment in non-HIV infected, non-transplant host

A
  1. induction: amphotericin B deoxycholate + flucytosine in 4 divided doses for at least 2-4 weeks (may use lipid amphotericin B)
    - extended induction phase to 6 weeks if neurologic complications or flucytosine not given
  2. consolidation: fluconazole 400-800 mg PO daily x 8 weeks
  3. maintenance: fluconazole 200 mg PO daily x 6-12 months

-may use amphotericin B + flucytosine for 2 week induction phase in patients with low risk for therapeutic failure.

28
Q

cryptococcal meningitis treatment in HIV-infected patients

A
  1. induction: liposomal amphotericin B IV + flucytosine PO in 4 divided doses for >2 weeks
  2. consolidation: fluconazole 400 mg PO daily for >/= 8 weeks
  3. maintenance: fluconazole 200 mg PO daily to complete at least 1 year of azole therapy
    - may be stopped in patients with CD4 count >100 cells/mm3 who have undecteable viral load on ART for > 3 months and received at least 1 year of maintenance therapy
    - alternatives: amphotericin B (or lipid) for 4-6 weeks, amphotericin B deoxycholate + fluconazole for 2 weeks then fluconazole x 8 weeks, fluconazole + flucytosine for 6 weeks or fluconazole for 10-12 weeks
29
Q

cryptococcal meningitis treatment for organ transplant recipients

A
  1. induction: liposomal amphotericin B IV + flucytosine PO in 4 divided doses for >/= 2 weeks
  2. consolidation: fluconazole PO >/= 8 weeks
  3. maintenance: fluconazole PO >/= 6-12 months
30
Q

Candidiasis

A
  • caused by candida spps
  • C. albicans is a normal commensal of the skin, female genital tract, and entire GI tract of humans.
  • Most common cause of invasive fungal infections in humans
  • neutropenia (ANC < 500 cells/mm3) is the most common risk factor for candemia
31
Q

Candidiasis/candidemia pathophysiology and clinical presentation

A
  • candida usually acquired via GI tract or can enter blood stream via IV catheter (candida loves plastic)
  • intact skin is critical for prevention on invasive candidiasis
  • PMNs play a major role in patients host defense
32
Q

Candidemia treatment in nonneutropenic adults

A
  1. echinocandin (capsofungin-needs loading dose, micafungin, anidulafungin) recommeded as initial therapy
  2. fluconazole 800 mg loading dose then 400 mg IV or PO daily. alternative as initial therapy in selected patients who are not critically ill and who are unlikely to have fluconazole-resistant candida spps
  3. transition from echinocandin to fluconazole for pts who are clinically stable, have isolates susceptible to fluconazole and have negative repeat blood cultures after initiiation of therapy
    - alternatives lipid amphotericin B formulation, voriconazole
    - remove all IV catheters if possible
    - repeat blood cultures QD or QOD
    - treat for 14 days after first negative blood culture
33
Q

Candidemia treatment in neutropenic adults

A
  1. C. glabrata - echinocandin
  2. C. parapsilosis - fluconazole or lipid amphotericin B
  3. C. krusei - echinocandin, lipid amphotericin B or voriconazole
    - treat for 14 days after documented clearance of candida from blood, resolution of symptoms, and resolution of neutropenia
34
Q

Chronic disseminated (hepatosplenic) candidiasis

A
  1. lipi amphotericin B or an echinocandin for several weeks, followed by fluconazole (if patient is unlikely to have a fluconazole resistant isolate)
  2. continue therapy until documentation of lesion resolution on repeat imaging (several months)
  3. if debilitating persistent fevers, short-term (1-2 weeks) treatment with NSAID or corticosteroids
35
Q

Empiric treatment of suspected invasive candidiasis in ICU

A
  1. non-neutropenic adults: echinocandin (preferred) or fluconazole (no recent azole exposure and who are not colonized with azole resistant candida spps), liposomal amphotericin B
    - recommended duration for 2 weeks
  2. neutropenic adults: lipid anphotericin B, echinocandin, voriconazole, fluconazole, itraconazole (azoles should not be used in patients who have received azole for prophylaxis)
36
Q

prophylaxis of invasive candidiasis in the ICU

A
  1. fluconazole daily i high-risk patients in iCUs with a high rate of invasive candidiasis
  2. echinocandin as alternative
  3. daily bathing with chlorhexidine could be considered
37
Q

Intra-abdominal candidiasis treatment

A
  • consider empiric antifungal therapy for patients with clinical evidence of an intra-abdominal infection and significant risk factors for candidiasis (recent abdominal surgery, anastomotic leaks, or necrotizing pancreaatitis)
  • source control with appropriate drainage and debridement
  • treatment: echinocandin then transition to fluconazole if not used azoles and least likely for fluconazole resistant strains (alternatives lipid amphotericin B and voriconazole)
38
Q

Treatment of candida UTIs

A

-asymptomatic candiduria-treatment not recommended unless high risk of dissemination
-high risk patients: eutropenic patients, very low birth-weight infants, patients undergoing urologic procedure
neutropenic/low-birth-weight infants: echinocandidemia
urologic procedure: fluconazole for several days before and after procedure
1. symptomatic candida cystitis:
fluconazole-susceptible candida spps: fluconazole PO daily for 2 weeks
fluconazole-resistant: amphotericin B deoxycholate daily for 1-7 days, or amphotericin bladder irrigation for 5 days, or flucytosine for 7-10 days
-remove or replace indwelling bladder catheter.

39
Q

Aspergillosis

A
  • caused by: A. fumigatus*, A. flavus, A. niger, A. terreus
  • generally acquired by inhalation of airborne conidia that are small enough to reach alveoli or the paranasal sinuses
  • impaired host defenses are required for the development of invasive disease
  • phagocytes are the primary host defense system against invasive aspergillosis
  • prolonged neutropenia is the most important pre-disposing factor to the development of invasive aspergillosis
40
Q

Aspergillosis clinical presentation

A
  • characterized by vascular invasion leading to thrombosis, information, necrosis of tissue, and dissemination to other tissues and organs in the body
  • survival beyond 2-3 weeks is uncommon
  • classic signs/symptoms: pleuritic chest pain, fever, hemoptysis, friction rubs
  • hyphae invade the walls of bronchi and surrounding parenchyma resulting in an acute necrotixing, pyogenic pneumonitis
  • identification generally based on appearance of septate hyphae. the galactomannan is a cell wall polysaccharide specific to aspergillus spps that is detectable in serum and other bodily fluids
  • CT scan can see halo sign and crescent sign
41
Q

Treatment of Aspergillosis

A
  1. voriconazole (DOC)
    - alternative: lipid amphotericin B, isavuconazole, voriconazole + echinocandin in select patients
    - continue treatment for a minimum of 6-12 weeks
  2. salvage therapy: amphotericin B, caspofungin, micafungin, posaconcazole, itraconazole
42
Q

prophylaxis of aspergillosis

A
  • those who are neutropenic for a while
    1. poscaonazole
    2. alternative agents: voriconazole, itraconazole, micafungin, aerosolized amphotericin B

Therapeutics (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions