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49 Cards in this Set
- Front
- Back
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What is the treatment for candidemia? |
1. ABx: Caspofungin or micafungin - is appropriate initial therapy, but not for those with meningitis, UTI ro endopthalmitis because of poor organ penetration --> amphotericin In patients with suspcetible strains, can step down to azole if known to be susceptible Treatment duration - 14 dafter clearance of organism from bloodstream 2. Removal of catheter - parapsilosis is always catheter related, in NTP patients may be related to gut translocation, but if candidemia persistes should remove catheter |
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What is treatment for different strains of canddia? |
In patients with candida glabrata - susceptibility testing should be done before switching to azole Parapsilosis - may have reduced susptibility to echinocandins and should be treated with azoles |
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Do you treat candida UTI? |
Only treat if symptomatic and asymptomatic if patient has neutorpenia |
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What is ABPA? how is it diagnosed? What are the clinical symptoms? |
Aspergillus is a ubiquitous environmental mold, ABPA is caused by colonization of the larger airways Cardinal symptoms: asthma, fleeting pulmonary infiltrates on chest imaging, peripheral eosinophilia, elevated IgE elevels and serum aspergillus precipitating antibodies, and cutaneous reactivity to Aspergillus antigens |
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What is the treatment of ABPA? |
Itraconazole or voriconazole In addition to standard therapy, acute or recurrent exacerbations should include steoids to control acute inflammation and limit lung damage |
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What is an aspergilloma? What are the symptoms? |
Colonization of a previous pulmonary cavity/cyst with aspergillosis - Symptoms are like Tb, cough, hemoptysis, dyspnea, weigh tloss fever, fatigue - Radiographic images show a round mass w/in a pulmonary cavity/cyst |
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How is aspergilloma diagnosed? How is it treated? |
Sputum cultures are usually positive Surgical resection: indicated for hemoptysis and is considered defnitive therapy For those who are not considered candidates for surgical resection, can treat with itraconazole, voriconazole or posaconazole |
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What is the diagnostic test for invasive aspergillus? |
Galactomannan antigen immunoassay is increasingly used for diagnosis - a polysaccharide contained in the cell wall of aspergillus, presence in serum or body fluids suggests invasive infection - Sensitivity of the assay is impaired by antifungal therapy, can also use BD glucan but this is not sensitive |
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Who is at risk for mucormycosis? |
Immunocompromise from HSCT, organ transplant, cancer chemotherapy Patients with uncotnrolled diabetes or ketoacidosis have a unique susceptibility Patients treated with deferoxamine for iron overload states are also at risk Patient siwth severe burns or trauma can contract mucormyosis through contamination of wounds |
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What are the sites of involvement of mucor? |
Lungs, GI tract skin Most common: rhinocerebral - phyiscal exam shows a black exchar Pulmonary mucormyosis w/ thrombosis and infarction is most frequently in patients w/ heme malignancies Cutaneous involvement: in burn victims |
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How is mucor diagnosed? |
TIssue biopsy: broad irregular and ribbon like aspetate hyphae that have right angle branching Bcx are usually negative |
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What is the treatment for mucormycosis? |
Liposomal ampho B, high dose ampho B Alteratives are posaconazole and isavuconazonium |
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What is the organ invovlement of crypto in non-immunosuppressed patients? In immunosuppressed patients? |
Crypto is inahled and causes initial pulmonary infection, but patients with cell mediated immunity do not get infection - In those with symptoms - treat lung infection with 6-12 months of fluconazole in patients midl to moderate symptoms due to concern for progressive or disseminated disease in the event of immunosuppression - Alternatives include itra and amphoB/flucytosine In immunosuppressed patients, CNS is most common organ manifestation - HA, change in MS and HA, visual abnormalities and CN palsies can occur - Can also dissmeinate to skin, prostate, bone, eye and urinary tract. Skin lesions include ulcers, plaques, cellulities, puples, nodules |
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How is cryptococcus diagnosed?
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Serum crypto antigen CSF crypto antigen Diagnosis is confirmed by culture In patients w/ HIV, there is a latex agglutaintion assay for cryptococcal antigen that is highly sensitive and specific for the diagnosis of meningits, but is less useful in patients w/o HIV |
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What is the treatment of cryptococcal meningitis? |
1. In patients with AIDs: Induction with amphotericin and flucytosine for 2 weeks, consolidation w/ fluc for 8 weeks, and maintenance w/ oral fluconazole for >1 year 2. In patients with transplant: Only difference is maintencance can be 6 months to 1 year 3. In patients without HIV/AIDs or transplant: Induction with ampho/flucytosine for >4 weeks, consolidation with oral fluc for 8 weeks, maintenance with oral fluc for 6-12 months |
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What are the clinical manifestations of blasto? What is the epi?
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- Lung involvement, followed by bone, skin joints and prostate - Skin lesions: papules, nodules, verrucous lesions,d raining lesions |
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What should be done to work up disseminated blasto?
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GU infection can be asymptomatic or associated with symptoms of prostatism Ucx should be obtained because prostatitis can be a nidus for infection - There is no orole for serologic assays - Biopsy histo shows yeast w/ budding forms |
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What is the treatment for blasto?
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2. CNS: Lipid formulation of ampho followed by fluconazole: alternatives: itra and voriconazole |
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What are the pulmonary forms of histo? Epi?
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Can cause: fibrosing or granulomatous mediastinitis, bronchilithiasis, pulmonary nodules |
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What is the treatment of histo?
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Moderate to severe pulmonary: lipid ampho followed by itra Acute progressive disseminated: lipid formulation of ampho B followed by itraconazole |
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What is the epi of coccidio?
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- Infection is highest when dry and when soil is disturbed, in summer monthes; |
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What are the clinical manifestations of coccidio? What are the most common causes of dissemination?
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- Valley fever: subacute w/ respiratory symptoms, fever and erythema nodosum; arthralgia of multiple joints (desert rheumatism) - Disseminates to skin/bones, joints and meninges |
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How is coccidio diagnosed?
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- More helpful than chronic coccidiodal meningitis because cultures of the CSF are frequently negative |
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What is the treatment of coccidio?
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Pulmonary in immunosuppressed - higher risk for dissemination - itraconazole/fluconazole For sever coccidiodal PNA or disseminated disease: lipid formulation of ampho B followed by itra or fluc Coccidiomeningitis: Fluconazole; alternatives include ampho B, itra or vori |
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What is sporotrichosis?
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Acquired through landscaping or gradening Papule appears days to weeks later, ulcerates, similar lesions occur along lymphatic channels proximal to the inoculation site; |
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Where can sporotrichosis disseminate? What is the treatment?
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Dx w/ culture Treat w/ itraocnazole |
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What is the risk of active tb in patient who inhales mycobacterium? |
5% in the first year, 5% in lifetime after that - RFs for activation: immunocompromise - HIV, malignancy, diabetes, CKD, injection drug use, tobacco, malnutrition or those receiving immunosuppressive therapy |
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What is the criteria for a positive skin test? |
Measures delayed hypersensitivity A TST: positive after 2-12 weeks of infection, measuring transverse diameter of induration NOT erythema 5mm - close exposure to someone w/ tb, HIV, fibrotic changes on CXR c/w old tb, transplant or on immunosuppressives 10mm - health care workers, injection drug use, homelessness, jail/prisons, <5 year arrival from high prevalence countries 15 mm - all other people |
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What creates false neg for tb skin test? |
False negative - overwhelming activ etb, immunosuppressed, old/young False positive - infection w/ atypical mycobacterium, patients w/ BCG vaccine |
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What is the criteria for a positive IGRA? What are the advantages? |
Measure T cell mediated IFN-gamma release in response to Mtb antigens; - Similar sensitivity to skin test but more specific Advantages: only one visit, availability of test results within 1 day, lack of booster response w/ subsequent results, fewer false positive results |
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What is the location of primary pulmonary tb? |
Primary pulmonary tb: may present w/ mid to lower zone unilateral infiltrates, hilar LAD, pleural effusions Reactivation tb classically presents w/ apical posterior fibrocaviatry disease of the upper lobes or superior segments of the lower lobes CXR can be normal, CT more sensitive |
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How is active tb confrimed? |
Confirmation of active disease requires growth of M. tb from culture or detection by nucleic acid based testing Sputum samples are sent for AFB staining followed by culture in liquid medium, which allow fro faster growth and detection (approximately 2 weeks) - Nucleic acid amplification testing of sputum can expedite - PPV is 95%, but is expensive; is positive in 65% of patients with neg stains on smear but eventually positive in culture |
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How is pleural fluid infection w/ tb diagnosed? |
Definitive diagnosis if biopsy: caseating granulomas on pleural biopsy Adenosine deaminase levels in pleural fluid may also be helpful in the evaluation of suspected pleural tb |
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How is tb meningitis diagnosd? |
LP with lymhpocyte predominance, high protein low glucose NAAT of CSF is high specific but has 50% sensitivity and neg test does not rule in out Send for AFB stain and cx Same tests should be run on pericardial fluid as in pleural fluid and CSF |
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What is the treatment for latent TB? |
1. 9 months of isoniazid 2. 3 months of isniazid and rifapentine OR 3. 4 months of rifampin 1st option for patients w/ HIV taking HAART 2nd option can be used in HIV cofinection but not rec in patietns w/ riampin or isoniazid resistant straitns, ro patients who are pregnant/plan to become pregnant |
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How should pregnant patients do for latent TB? |
Isoniazid is recommended for treatment of LTBI, or if the patient has been recently exposed or if she has HIV - If not, defer treatemtn until after delivery - Can start isoniazid to breastfeeding |
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What is the treatment for active tb? |
Initiation: RIPE: rifampin, isoniazid, pyrmidazine, ethambutol - administered for 2 months, followed by 4-7 month sof rifampin and isoniazid - Longer course of continuation phase recommneded for patients w/ cavitary pulmonary disease AND positive sputum cx after completing initial therapy, patients who did not recieve pyrazinamide as part of initial therapy, or those who are receiving once weekly rifapetine/iso whose sputum cx are positive after 2 months |
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What is the treatment duration for tb meningitis? how does treatment differ? |
6 months at least, with up to 9-12 months of treatment Adjunctive steroids are recommnede,d as well as for patients w/ concern for pericarditis |
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What are the AEs of isoniazid? |
Rash, liver enzyme elevation Hepatitis Peripheral neuropathy Lupus like syndrome Hepatitis risk increases w/ etoh consumption, pyroxidine can prevent peripheral neuropathy, Adjust for kidney injury |
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What are the Ses of pyrazinamide? |
Hepatitis Rash Hyperuricemia Stomach upset Adjust for kidney injury |
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What are the AEs of rifampin and rifabutin? |
Rifampin: hepatitis, rash, GI upset --> use in caution in patients on PIs and NNRTs Rifapentine is similar to rifampin Rifabutin: Rash, trhombocytopenia, hepatitis, severe arthralgias, leukopenia, uveitis: dose adjust for PIs and NNRTs Monitor for decreased antiretrovirla activity and rifabutin toxicity |
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What are the AEs of ethambutol? |
Optic neuritis, rash Patients should have baseline and periodic tests of visual acuityand color vision Adjust for kidney injury |
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When is patient considered no longer infections? |
Adequate treatment for tb greater than 2 weeks, improvement of symptoms, and 3 consective sputum smears collected at 8-24 hour intervals (including one early mornning collection) that is negative |
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What is the BCG vaccine and when should it be used? |
Mycobacterium bovis - given in endemic countries to prevent dissemination but does not prevent primary infection or reactivation of pulmonary tb; can be given in US in patients who may be at risk for exposure, health care workers traveling to areas with high prevalence Live attenuated - contraindicated in pregnatn or immunosuppressed patients |
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What is the epi of MAC? What are the symptoms? |
Middle aged, men, adult, smokers with underlying lung disease - Another group is lady windemere's - nonsmoking postmenopausal women with pectus excavatum, MVP, scoliosis and joint abnormalities\ - SYmptoms are of chronic cough, puurlent sputum without constitutional sy pmtoms - In patients with CD4 counts < 50, clinical presentation often consists of fever, night sweats, weight loss, GI symptoms |
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What is the treatment of MAC? |
Ethambutol Clarithromycin/azitrho Rifampin/rifabutin |
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What are the RFS for infection in M kansaii? What is the clinical manifestation? |
COPD, cancer, HIV, etoh abuse, drug associated immunosuppresstion Presents just like tb |
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What is the treatment of M kansaii? |
Isoniazid, rifampin, ethambutol |
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What are the other rapid nontb myobacterium and what are their clincial mainfestation? |
Mycobacterium absecessus - most common cause of RGM associated pulmonary infection even in patients without underlying lung disease Lymphadenitis - M. abscessus and M fortium All are seen inmmunosuppressed patients and apepar to be increasing in incidence as a cause of localized skin and soft tissue infections - usually after trauma, surgery (often associated w/ implanted prostehtic material), catheter insertion, or cosmetic procedures such as pedicures, tattoos and body piercing - source is nonsterile water |
