Figure 8.1. Giemsa-stained blood smear demonstrating a tetrad of intraerythrocytic merozoites of Babesia microti.

QUESTION 27. A 56-year-old man, JFK airport employee (Long Island, NY), presents with fever to 39.5°C, malaise, fatigue, and myalgias for 1 week in September. Initial blood work demonstrates new onset of anemia (Hb 11.3 g/dL), mild leukopenia, and thrombocytopenia. Reticulocyte count is 6%, low-density lipoprotein (LDL) is elevated, and Coombs tests are negative. Blood smear results are shown in Figure 8.1.

    This infection was most likely transmitted by:

    A. Anopheles quadrimaculatus

    B. Aedes aegypti

    C. Culex pipiens

    D. Ixodes scapularis

    E. None of the above

ANSWERS

1. E. The patient developed candidemia in the setting of gastrointestinal perforation and prolonged intensive care unit stay. Candida blood isolates cannot be dismissed as contaminants, and in current practice all patients with candidemia should be treated. Blood cultures should be repeated until persistently negative, and treatment should continue for at least 2 weeks following the last positive blood isolate. Given the risk factors of the patient, his doctors elected to use fluconazole prophylaxis. Although not routinely recommended, this increases the risk of fluconazole-resistant Candida infections. For someone who develops candidemia during fluconazole administration, azole resistance should be assumed and other treatments used while the isolate is identified and susceptibility testing is performed. The options for this patient include amphotericin B or one of its lipid formulations or any of the echinocandins (caspofungin, micafungin, or anidulafungin). As the patient already has acute renal dysfunction, the best option for the patient is to start an echinocandin. Echinocandins are fungicidal against Candida spp. by disrupting fungal cell wall synthesis by inhibiting 1,3-β-d-glucan synthase. They are as effective as amphotericin B with a better safety profile (Mora-Duarte et al. N Engl J Med. 2002;347:2020–2029). Candida has a high tendency to form biofilms; thus, removal and replacement of all intravenous access is recommended routinely if feasible. An ophthalmologic examination is frequently recommended to exclude endophthalmitis. It is an infrequent complication but one that can require a different management (Rodríguez-Adrián et al. Medicine. 2003;82:187–202). We favor routine identification of Candida species and susceptibility testing of all invasive infections. Patients with fluconazole or voriconazole susceptible isolates can be safely switched to oral azole treatment after susceptibility testing results become available. New Candida treatment guidelines (Pappas et al. Clin Infect Dis. 2009;48:503–535) are available at www.idsociety.org.

    2. D. Not all yeasts isolated from blood are Candida spp. This patient is at increased risk of cryptococcosis given new diagnosis of AIDS and history of headaches. AIDS patients often present with more than one synchronous problem. Patient was also at risk of candidemia given central venous access placed under urgent conditions. Removing central access is reasonable given data, but patient needs antifungal therapy. Fluconazole is a reasonable initial treatment for candidemia but not for cryptococcosis, especially when there is concern for disseminated or central nervous system involvement; it is associated with treatment failures and emergence of resistance in that setting. Caspofungin and other echinocandins are not active against Cryptococcus neoformans, so they are not a good option if cryptococcosis is in the differential.

    Best empirical treatment in this case is amphotericin B. If cryptococcemia is confirmed by identification of the yeast or by determination of a serum cryptococcal antigen, the patient should undergo examination of his cerebrospinal fluid to exclude or confirm presence of cryptococcal meningitis. If cryptococcal meningitis is confirmed, flucytosine at 100 mg/kg/day can be added to the initial regimen for induction treatment for cryptococcal meningitis. (For further details, please see Perfect et al. Clin Infect Dis. 2010;50:291–322, available at www.idsociety.org.)

    3. C. Patient has pneumonia and septic shock due to Streptococcus pneumoniae. Although vancomycin should be used empirically for the treatment of pneumococcal meningitis until antimicrobial susceptibilities are back, vancomycin is not usually indicated for treatment of pneumococcal pneumonia or bacteremia. The combination of third-generation cephalosporins, such as ceftriaxone, and quinolones provides excellent empirical treatment for pneumonia for severely ill patients. Gentamicin adds little to the regimen chosen in the emergency room given your clinical impression; the patient is already in renal failure (gentamicin is not a pressor drug).

    4. D. Antacids containing magnesium or aluminum salts, including sucralfate, will bind quinolones efficiently and impede their absorption. Quinolones should be administered at least 2 hours apart from antacids (Davies, Maesen. Rev Infect Dis. 1989;11 Suppl 5:S1083–S1090).

    5. E. Although broad-spectrum antibiotic treatment is appropriate in a patient with evidence of cellulitis and sepsis, this patient has the classical presentation of clostridial myonecrosis (gas gangrene) caused by traumatic exposure to Clostridium sp. (most commonly C. perfringens).Features include soft tissue trauma followed in 1–4 days by the sudden onset of unrelenting pain at the wound site with evidence of gas in the underlying tissue. Optimal management includes rapid surgical debridement and antibacterial administration. Penicillin G in combination with clindamycin is considered the treatment of choice. Other agents with activity are considered second-line agents, including chloramphenicol, metronidazole, imipenem, and combination beta-lactam/beta-lactamase inhibitors. Hyperbaric oxygen could be considered but without delay to surgical intervention (Stevens et al. Clin Infect Dis. 2005;41:1373–1406, available at www.idsociety.org).

    6. B. The treatment of choice for enterococcal endocarditis is the combination of a cell-wall-active drug (ampicillin, penicillin, or vancomycin) and an aminoglycoside (gentamicin or streptomycin). When used alone, cell-wall–active drugs are bacteriostatic against enterococci. The combination, however, is bactericidal because of synergy between the two classes of drugs. Synergy is most commonly achieved when gentamicin is the antibiotic used, but about 10–25% of enterococci that are resistant to gentamicin are susceptible to streptomycin (when used with a cell-wall-active drug). Because the organism in this case is susceptible to ampicillin and does not produce a beta-lactamase, sulbactam, a beta-lactamase inhibitor, has no additional effect.

    Quinupristin/dalfopristin is a combination of two streptogramin antibiotics. It has bacteriostatic activity against gram-positive organisms including vancomycin-resistant (VRE) Enterococcus faecium (not active against E. faecalis) and methicillin-resistant Staphylococcus aureus (MRSA). It is used for treatment of VRE and MRSA but not for vancomycin- or ampicillin-susceptible enterococci or methicillin-sensitive staphylococci. Enterococci susceptible to ampicillin may be susceptible to imipenem, but ampicillin is preferred for treating these strains. Linezolid and daptomycin have good activity against enterococci, but the data on non-VRE enterococcal endocarditis are lacking.

    The reaction described is an example of the “red man” syndrome that occurs when vancomycin is administered rapidly or in high concentrations. It is not an allergy but is caused by the release of histamine from mast cells. By slowing the infusion rate and/or diluting the concentration of vancomycin, recurrence of this reaction can be avoided.

    Ciprofloxacin is active in vitro against this patient’s isolate but is less effective than ampicillin or vancomycin and is not considered first- or second-line therapy for enterococcal infections (Baddour et al. Circulation. 2005;111:e394–e433).

    7. D. The chest CT image describes a lung nodule with a halo sign. The presence of a halo sign is highly suggestive of invasive aspergillosis in patients with prolonged neutropenia during induction chemotherapy for acute leukemia or myeloablative allogeneic stem cell transplantation. Other angioinvasive molds and hematogenous seeding of the lung from septic emboli can have the same radiologic appearance. The presence of elevated circulating serum levels of galactomannan, a carbohydrate present in the cell wall of Aspergillus and Penicillium species, increases the certainty that the infection is indeed invasive aspergillosis to probable. Although a definitive diagnosis of invasive aspergillosis requires biopsy of the affected site and growth in culture of the mold, the clinical scenario, the presence of the halo sign, and an elevated galactomannan make a diagnosis of invasive aspergillosis likely.

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