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IV-18. The answer is A. (Chap. 124) Patients with infective endocarditis on antibiotic therapy can be expected to demonstrate clinical improvement within 5 to 7 days. Blood cultures frequently remain positive for 3 to 5 days for Staphylococcus aureus treated with β-lactam antibiotics and 7 to 9 days with vancomycin. Neither rifampin nor gentamicin has been shown to provide clinical benefit in the scenario described in this question. Vancomycin peak and trough levels have not been shown to improve drug efficacy in infective endocarditis. It is too early in therapy to consider this case representative of vancomycin failure. The efficacy of daptomycin or linezolid because an alternative to vancomycin for left-sided MRSA endocarditis has not been established.

IV-19. The answer is B. (Chap. 125) Bullae (Latin for bubbles) are skin lesions that are greater than 5 mm and fluid filled. They may be regular or irregularly shaped and filled with serous or seropurulent fluid. Clostridium spp., including perfringens, may cause bullae through myonecrosis. Staphylococcus causes scalded skin syndrome through elaboration of the exfoliatin toxin from phage group II, particularly in neonates. Streptococcus pyogenes, the causative agent of impetigo, may cause bullae initially that progress to crusted lesions. MRSA may also cause impetigo. The halophilic Vibrio, including V. vulnificus, may cause an aggressive fasciitis with bullae formation. Patients with cirrhosis exposed to Gulf of Mexico or Atlantic waters (or ingestion of raw seafood from those waters) are at greatest risk. Infection with the dimorphic fungus, Sporothrix schenckii, presents with discrete crusted lesions resembling ringworm. Lesions may progress to ulcerate. Patients often have a history of working with soil or roses.

IV-20. The answer is D. (Chap. 125) This patient has necrotizing fasciitis and myonecrosis. His computed tomography scan shows edema and inflammation of the left chest wall. Necrotizing fasciitis and myonecrosis may also be caused by infection with mixed aerobes and anaerobes, Staphylococcus aureus including, methicillin-resistant S. aureus, and Clostridium spp. Treatment involves prompt surgical evaluation and empiric therapy for the causative agents. Mycobacterium tuberculosis would most commonly cause cavitary lung lesions. Coxsackie virus causes vesicular lesions during acute infection. There may be myalgias and elevated muscle enzymes but not frank myonecrosis. Rickettsia akari is the causative agent of rickettsialpox. It occurs after a mite bite with a papule with central vesicle that evolves to form a painless black eschar. Rickettsialpox has been recently described in Ohio, Arizona, and Utah. Varicella-zoster virus causes chickenpox with acute infection and zoster with reactivation. The lesions are crusting vesicles, not fasciitis or myonecrosis.

IV-21. The answer is C. (Chap. 126) Although Staphylococcus aureus (methicillin-resistant S. aureus and methicillin-sensitive S. aureus) is the most common bacteria causing osteomyelitis, the infection may also be caused by gram-negative organisms (Pseudomonas aeruginosa, Escherichia coli),

coagulase-negative staphylococci, enterococci, and propionibacteria. Mycobacterium tuberculosis is an important cause of vertebral osteomyelitis in countries with fewer medical resources and high prevalence (along with brucellosis). Prosthetic joint implants and stabilization devices are commonly sources of osteomyelitis, often seeded from bacteremia or after trauma. MRSA osteomyelitis is a growing problem in hospitals throughout the developed world, particularly after surgery. The reason for the higher morbidity and cost may be related to virulence factors or less effective or timely treatment. Patients with diabetes are at very high risk of osteomyelitis of the foot and require a high index of suspicion.

IV-22. The answer is A. (Chap. 126) The therapy for osteomyelitis is challenging because of the multiplicity of potential causative organisms, the diagnostic difficulty, and the prolonged necessary therapy. Early surgical intervention may be beneficial diagnostically and therapeutically. In this case, the Gram stain is polymicrobial, and the putrid smell is very specific for anaerobic organisms. The diagnosis of acute osteomyelitis is also very likely based on the positive probe to bone test and wide ulcer. Broad-spectrum antibiotics are indicated. Vancomycin and linezolid cover methicillin-resistant Staphylococcus aureus (MRSA) and streptococcal isolates but would miss gram-negative rods and anaerobic bacteria. Metronidazole covers only anaerobes, missing gram-positive organisms that are key in the initiation of diabetic foot infections. Clindamycin covers gram-positive organisms and anaerobes but misses gram-negative rods. Ampicillin–sulbactam is broad-spectrum antibiotic and covers all three classes of organism except MRSA. If the patient has a history of MRSA or MRSA risk factors, then the addition of vancomycin or linezolid is a strong consideration. Recent studies have also suggested that daptomycin may be a promising therapy for MRSA osteomyelitis.

IV-23. The answer is A. (Chap. 127) Primary (spontaneous) bacterial peritonitis (PBP) occurs when the peritoneal cavity becomes infected without an apparent source of contamination. PBP occurs most often in patients with cirrhosis, usually with preexisting ascites. The bacterial likely invade the peritoneal fluid because of poor hepatic filtration in cirrhosis. Although fever is present in up to 80% of cases, abdominal pain, acute onset, and peritoneal signs are often absent. Patients may present with nonspecific findings such as malaise or worsening encephalopathy. A neutrophil count in peritoneal fluid of greater than 250/μL is diagnostic; there is no % neutrophil differential threshold. Diagnosis is often difficult because peritoneal culture findings are often negative. Blood cultures may reveal the causative organism. The most common organisms are enteric gram-negative bacilli, but gram-positive cocci are often found. Anaerobes are not common (in contrast to secondary bacterial peritonitis), and empiric antibiotics targeting them are not necessary if PBP is suspected. Third-generation cephalosporins or piperacillin–tazobactam are reasonable initial empiric therapy. Diagnosis requires exclusion of a primary intraabdominal source of peritonitis.

IV-24. The answer is D. (Chap. 127) This patient has continuous ambulatory peritoneal dialysis (CAPD)–associated peritonitis. Unlike primary or secondary bacterial peritonitis, this infection is usually caused by skin organisms, most commonly Staphylococcus spp. The organisms migrate into the peritoneal fluid via the device. There may not be a tunnel or exit-site infection. Peritonitis is the most common reason for discontinuing CAPD. Y-connectors and diligent technique decrease the risk of CAPD. In contrast to PBP and similar to spontaneous bacterial peritonitis (SBP), the onset of symptoms is usually acute with diffuse pain and peritoneal signs. The dialysate will be cloudy with greater than 100 WBC/μL and greater than 50% neutrophils. Dialysate should be placed in blood culture media and

often is often positive with one organism. Finding more than one organism in culture should prompt an evaluation for SBP. Empirical intraperitoneal coverage for CAPD peritonitis should be directed against staphylococcal species based on local epidemiology. If the patient is severely ill, intravenous antibiotics should be added. If the patient does not respond within 4 days, catheter removal should be considered.

IV-25. The answer is D. (Chap. 127) The computed tomography scan shows a large complex liver abscess in the right lobe. Liver abscesses may arise from hematogenous spread, biliary disease (most common currently), pylephlebitis, or contiguous infection in the peritoneal cavity. Fever is the only common physical finding in liver abscess. Up to 50% of patients may not have symptoms or signs to direct attention to the liver. Nonspecific symptoms are common, and liver abscess is an important cause of fever of unexplained origin in elderly patients. The only reliably abnormal serum studies are elevated alkaline phosphatase or WBC in 70% of patients. Liver abscess may be suggested by an elevated hemidiaphragm on chest radiograph. The most common causative organisms in presumed biliary disease are gram-negative bacilli. Anaerobes are not common unless pelvic or other enteric sources are suspected. Fungal liver abscesses occur after fungemia in immunocompromised patients receiving chemotherapy, often presenting symptomatically with neutrophil reconstitution. Drainage, usually percutaneous, is the mainstay of therapy and is useful initially diagnostically (Figure IV-25B).

FIGURE IV-25B

IV-26. The answer is C. (Chap. 127) It is important to distinguish between primary (spontaneous) and secondary peritonitis. Primary peritonitis is a result of long-standing ascites, usually as a result of cirrhosis. The pathogenesis is poorly understood but may involve bacteremic spread or translocation across the gut wall of usually only a single species of pathogenic bacteria. Secondary peritonitis is caused by rupture of a hollow viscous or irritation of the peritoneum caused by a contiguous abscess or pyogenic infection. It typically presents with peritoneal signs and in most cases represents a surgical emergency. Secondary peritonitis in a patient with cirrhosis is difficult to distinguish on clinical grounds from primary (spontaneous) peritonitis. It is often overlooked because classic peritoneal signs

are almost always lacking, and it is uniformly fatal in the absence of surgery. Suspicion for this diagnosis should occur when ascites shows a protein greater than 1 g/dL, lactate dehydrogenase (LDH) greater than serum LDH, glucose level below 50 mg/dL, or a polymicrobial Gram stain. When this diagnosis is suspected, abdominal radiography is indicated to rule out free air, and prompt surgical consultation is warranted. Unlike with primary (spontaneous) bacterial peritonitis, in cases of secondary peritonitis, antibiotics should include anaerobic coverage and often antifungal agents. This patient requires intravenous fluid because he has hypotension and tachycardia caused by sepsis. Drotrecogin alfa has been shown to reduce mortality in patients with sepsis, but it is not indicated in patients with thrombocytopenia, cirrhosis, and ascites.

IV-27. The answer is B. (Chap. 128) Acute infectious diarrhea remains a leading cause of death worldwide, especially among children younger than 5 years of age. The major categories of acute diarrheal illness include noninflammatory, inflammatory, and penetrating diarrhea. Vibrio cholerae causes diarrhea through production of an enterotoxin, which is characteristic of noninflammatory diarrhea. After ingestion of a large volume (10⁵–10⁶) of organisms, V. cholerae attaches to the brush border of the small intestinal enterocytes and produces cholera toxin. The primary clinical characteristic of diarrheal illness caused by toxin production is profuse watery diarrhea that is not bloody. Fecal leukocytes are typically not present in noninflammatory diarrhea. However, a mild increase in fecal lactoferrin can be seen because this test is more sensitive for the presence of mild inflammation. Other pathogens that are common causes of noninflammatory diarrhea are enterotoxigenic Escherichia coli, Bacillus cereus, Staphylococcus aureus, and viral diarrhea, among others. The site of inflammation in inflammatory diarrhea is typically the colon or distal small bowel. In inflammatory diarrhea, there is invasion of leukocytes into the wall of the intestines. The prototypical pathogen of inflammatory diarrhea is Shigella dysenteriae. Bloody stools are common, and the stool contains large quantities of fecal leukocytes and fecal lactoferrin. Other pathogens that cause inflammatory diarrhea are most Salmonella species, Campylobacter jejuni, eneterohemorrhagic Escherichia coli, and Clostridium difficile.

Penetrating diarrhea is caused by either Salmonella typhi or Yersinia enterocolitica . The site of inflammation in penetrating diarrhea is the distal small bowel. In penetrating diarrhea, these organisms penetrate the intestinal wall and multiply within Peyer’s patches and intestinal lymph nodes before disseminating into the bloodstream. Clinically, penetrating diarrhea presents as enteric fever with fever, relative bradycardia, abdominal pain, leukopenia, and splenomegaly.

IV-28 and IV-29. The answers are B and D, respectively. (Chap. 128) Traveler’s diarrhea is common among individuals traveling to Asia, Africa, and Central and South America, affecting 25% to 50% of travelers to these areas. Most traveler’s diarrhea begins within 3 to 5 days after arrival and is self-limited, lasting 1 to 5 days. Most individuals acquire traveler’s diarrhea after consuming contaminated food or water. Although some organisms have a geographic association, enterotoxigenic and enteroaggregative Escherichia coli are found worldwide and are the most common causes of traveler’s diarrhea. In Asia, Campylobacter jejuni is also common. This presentation would be uncommon for Shigella spp. because it most frequently causes bloody diarrhea. Norovirus is associated with a more profuse diarrhea. It has been the causative organism in large outbreaks on cruise ships. Giardia lamblia is a parasite that is responsible for 5% or less of traveler’s diarrhea.

The approach to treatment of traveler’s diarrhea should be tailored to the severity of the patient’s symptoms. In general, most cases are self-limited. As long as an individual is able to maintain adequate

fluid intake, no specific therapy may be required if there are no more than one or two unformed stools daily without distressing abdominal symptoms, bloody stools, or fever. In this scenario, the patient is not having a large number of stools, but in the presence of distressing abdominal symptoms, use of bismuth subsalicylate or loperamide is recommended. If loperamide is used, an initial dose of 4 mg is given followed by 2 mg after passage of each unformed stool. Antibacterial therapy is only recommended if there is evidence of inflammatory diarrhea (bloody stools or fever) or there are more than two unformed stools daily. The antibacterial agent of choice is usually a fluoroquinolone. Ciprofloxacin given as a single dose of 750 mg or 500 mg three times daily for 3 days is typically effective. In Thailand, Campylobacter jejuni is a common agent and has a high degree of fluoroquinolone resistance. For travelers to Thailand who require antibiotics, azithromycin is recommended with an initial dose of 10 mg/kg on the first day followed by 5 mg/kg on days 2 and 3 if diarrhea persists.

IV-30. The answer is C. (Chap. 128) Acute bacterial food poisoning occurring 1 to 6 hours after ingestion of contaminated food is most commonly caused by infection with Staphylococcus aureus or Bacillus cereus. S. aureus is associated with ingestion of ham, poultry, potato or egg salad, mayonnaise, or cream pastries that have been allowed to remain at room temperature after cooking. B. cereus is classically associated with contaminated fried rice. The symptoms of bacterial food poisoning begin abruptly with nausea, vomiting, abdominal cramping, and diarrhea. However, fever is not a common finding and should cause one to consider other etiologies of vomiting and diarrhea.

IV-31. The answer is C. (Chap. 128) The patient most likely has food poisoning caused by contamination of the fried rice with Bacillus cereus. This toxin-mediated disease occurs when heat-resistant spores germinate after boiling. Frying before serving may not destroy the preformed toxin. The emetic form of illness occurs within 6 hours of eating and is self-limited. No therapy is necessary unless the patient develops severe dehydration. This patient currently has no symptoms consistent with volume depletion; therefore, she does not need intravenous fluids at present. Sarcoidosis does not predispose patients to infectious diseases.

IV-32. The answer is E. (Chap. 129) Although frequent nonbloody diarrheal illness is commonly associated with Clostridium difficile infection, other presentations are well described, including fever in 28% of cases, abdominal pain, and leukocytosis. Adynamic ileus is often seen with C. difficile infection, and leukocytosis in this condition should be a clue that C. difficile is at play. Recurrent infection after therapy has been described in 15% to 30% of cases.

IV-33. The answer is D. (Chap. 129) Clostridium difficile infection is diagnosed by the following means: diarrhea of three or more stools per day for 2 or more days with no other cause plus (1) demonstration of toxin A or B in the stool, (2) polymerase chain reaction for toxin-producing C. difficile of the stool, or (3) demonstration of pseudomembranes on colonoscopy. Although many tests are available, none has adequate sensitivity to definitively rule out C. difficile infection. Thus, empiric therapy is appropriate in a patient (such as patient C) with a high likelihood of C. difficile infection.

IV-34. The answer is C. (Chap. 129) The patient has evidence of recurrent Clostridium difficile infection, which occurs in up to 30% of treated patients. Because there is no evidence that she has severe infection and this is her first recurrence, the recommended therapy is to retreat with oral metronidazole. Vancomycin is reserved for patients with severe infection either initially or with

recurrence. Fecal transplantation, intravenous immunoglobulin, and oral nitazoxanide are all potential therapies for patients with multiple recurrences.

IV-35. The answer is E. (Chap. 129) Clindamycin, ampicillin, and cephalosporins (including ceftriaxone) were the first antibiotics associated with Clostridium difficile–associated disease and still are. More recently, broad-spectrum fluoroquinolones, including moxifloxacin and ciprofloxacin, have been associated with outbreaks of C. difficile, including outbreaks in some locations of a more virulent strain that has caused severe disease among elderly outpatients. For unclear reasons, β-lactams other than the later generation cephalosporins appear to carry a lesser risk of disease. Penicillin–β-lactamase combination antibiotics appear to have lower risk of C. difficile–associated disease than the other agents mentioned. Cases have even been reported associated with metronidazole and vancomycin administration. Nevertheless, all patients initiating antibiotics should be warned to seek care if they develop diarrhea that is severe or persists for more than 1 day because all antibiotics carry some risk for C. difficile–associated disease.

IV-36. The answer is A. (Chap. 130) Common causes of urethral discomfort and discharge in men include Chlamydia trachomatis, Neisseria gonorrhoeae, Mycoplasma genitalium, Ureaplasma urealyticum, Trichomonas vaginalis, and herpes simplex virus. Gardnerella spp. is the usual cause of bacterial vaginosis in women and is not a pathogen in men.

IV-37. The answer is C. (Chap. 130) The patient has symptoms consistent with the urethral syndrome characterized by “internal” dysuria with urgency and frequency and pyuria but no uropathogens at counts of 10²/mL or greater in urine. This is most commonly caused by infection with Chlamydia trachomatis or Neisseria gonorrhoeae and can be readily confirmed by nucleic acid amplification testing for these pathogens in the urine. “External” dysuria includes pain in the vulva during urination, often without frequency or urgency. This is found in vulvovaginal candidiasis and herpes simplex infection, which can be visualized on physical examination. Cervical culture would not be useful with her urinary symptoms. Elevated vaginal pH above 5.0 is commonly present in trichomonal vaginitis. Clue cells on vaginal secretion microscopy suggest bacterial vaginosis.

IV-38. The answer is B. (Chap. 130) Bacterial vaginosis is associated with Gardnerella vaginalis and various anaerobic or noncultured bacteria. It generally has malodorous discharge that is white or gray. There is no external irritation, and pH of vaginal fluid is usually above 4.5; a fishy odor is present with 10% KOH preparation; and microscopy shows clue cells, few leukocytes, and many mixed microbiota. Normal vaginal findings are described in patient D with pH below 4.5 and lactobacilli seen on microscopic examination. A high pH above 5 with external irritation is often found in vulvovaginal candidiasis, but the presence of motile trichomonads is diagnostic for trichomonal vaginitis.

IV-39. The answer is E. (Chap. 130) In a study of patients with mucopurulent cervicitis seen at a sexually transmitted disease clinic in the 1980s, more than one-third of cervical samples failed to reveal any etiology. In a recent similar study in Baltimore using nucleic acid amplification testing, more than half of the cases were not microbiologically identified. Chlamydia trachomatis is the most frequently diagnosed organism followed by Neisseria gonorrhoeae. Because of the difficulty in making a microbiologic diagnosis, empiric therapy for C. trachomatis and, in areas were N. gonorrhoeae is highly endemic, gonococcus is indicated.

IV-40. The answer is C. (Chap. 130) The presence of right upper quadrant tenderness in conjunction with classic findings of pelvic inflammatory disease is highly suggestive of Fitz-Hugh-Curtis syndrome or perihepatitis caused by inflammation of the liver capsule caused by either Neisseria gonorrhoeae or Chlamydia trachomatis infection. Although this condition may be easily visualized by laproscopic examination, the resolution of right upper quadrant symptoms with therapy of pelvic inflammatory disease is the more common proof of the diagnosis. The presence of normal liver function testing is reassuring that hepatitis is not present, making hepatitis C virus infection unlikely.

IV-41. The answer is A. (Chap. 130) The most common causes of genital ulceration are herpes simplex virus, syphilis, and chancroid. Gonorrhea typically manifests as a urethritis, not genital ulcers. Syphilitic ulcers (primary chancre) are firm, shallow single ulcers that are not pustular and are generally not painful. Despite these usual findings, rapid plasma reagin testing is indicated in all cases of genital ulceration given the disparate presentations of Treponema pallidum. Herpes simplex virus ulcers are quite painful but are vesicular rather than pustular. In primary infection, they may be bilateral, but with reactivation, they are generally unilateral. Haemophilus ducreyi, the agent responsible for chancroid, causes multiple ulcers, often starting as pustules, that are soft, friable, and exquisitely tender, as present in this case. Primary infection with HIV usually causes an acute febrile illness, not focal ulcers. The presence of genital ulcers increases the likelihood of acquisition and transmission of HIV.

IV-42. The answer is F. (Chap. 130) HIV is the leading cause of death in some developing countries. Efforts to decrease transmission include screening and treatment of sexually associated infections. All of the listed conditions have been linked with higher acquisition of HIV based on epidemiologic studies and high biologic plausibility. Up to 50% of women of reproductive age in developing countries have bacterial vaginosis. All of the bacterial infections are curable, and treatment can decrease the frequency of genital herpes recurrences. This highlights an additional reason that primary care doctors should screen for each of these infections in female patients with detailed historic questions, genitourinary and rectal examinations, and evidence-based routine screening for these infections based on age and risk category.

IV-43. The answer is B. (Chap. 131) Nosocomial infections have reservoirs and sources just as do community-acquired pathogens. In hospitalized patients, cross-contamination (i.e., indirect spread of organisms from one patient to the next) accounts for many nosocomial infections. Although hand hygiene is uniformly recommended for health care practitioners, adherence to hand washing is low often because of time pressure, inconvenience, and skin damage. Because of improved adherence, alcohol-based hand rubs are now recommended for all heath care workers except when hands are visibly soiled or after care of a patient with Clostridium difficile infection, whose spores may not be killed by alcohol and thus require thorough hand wash with soap and water.

IV-44. The answer is E. (Chap. 132) Ultimately, solid organ transplant patients are at highest risk for infection because of T-cell immunodeficiency from antirejection medicines. As a result, they are also at risk for reactivation of many of the viruses from the herpes virus family, most notably cytomegalovirus, varicella-zoster virus, and Epstein-Barr virus. However, immediately after transplant, these deficits have not yet developed in full. Neutropenia is not common after solid organ transplantation as in bone marrow transplantation. In fact, patients are most at risk of infections typical for all hospitalized

patients, including wound infections, urinary tract infection, pneumonia, Clostridium difficile infection, and line-associated infection. Therefore, a standard evaluation of a febrile patient in the first weeks after a solid organ transplant should include a detailed physical examination, blood and urine cultures, urinalysis, chest radiography, and C. difficile stool antigen or toxin studies if warranted, in addition to a transplant-specific evaluation.

IV-45. The answer is E. (Chap. 132) The patient presents with symptoms suggestive of infection in the middle period after transplantation (1–4 months). In patients with prior cytomegalovirus (CMV) exposure or receipt of CMV-positive organ transplant, this is a period of time when CMV infection is most common. The patient presented here has classic signs of CMV disease with generalized symptoms in addition to dysfunction of her transplanted organ (kidney). Often bone marrow suppression is present, demonstrated here by lymphopenia. Because CMV infection is linked with graft dysfunction and rejection, prophylaxis is frequently used, including valganciclovir. Trimethoprim–sulfamethoxazole is used for Pneumocystis jiroveci prophylaxis, acyclovir generally is used for varicellazoster virus prophylaxis, itraconazole may be considered in patients considered at risk for histoplasmosis reactivation, and isoniazid is used for individuals with recent purified protein derivative conversion or positive chest imaging and no prior treatment.

IV-46. The answer is E. (Chap. 132) Toxoplasma gondii commonly achieves latency in cysts during acute infection. Reactivation in the central nervous system in AIDS patients is well known. However, Toxoplasma cysts also reside in the heart. Thus, transplanting a Toxoplasma-positive heart into a Toxoplasma-negative recipient may cause reactivation in the months after transplant. Serologic screening of cardiac donors and recipients for T. gondii is important. To account for this possibility, prophylactic doses of trimethoprim–sulfamethoxazole, which is also effective prophylaxis against Pneumocystis and Nocardia spp., is standard after cardiac transplantation. Cardiac transplant recipients, similar to all other solid organ transplant recipients, are at risk of developing infections related to impaired cellular immunity, particularly more than 1 month to 1 year post-transplant. Wound infections or mediastinitis from skin organisms may complicate the early transplant (<1 month) period.

IV-47. The answer is C. (Chaps. 132 and 204) During the first week after hematopoietic stem cell transplantation, the highest risk of infection comes from aerobic nosocomially acquired bacteria. However, after about 7 days, the risk of fungal infection rises, particularly with prolonged neutropenia. The patient presented here presents with symptoms and signs of a respiratory illness after prolonged neutropenia; fungal infection is high on the differential diagnosis list. The computed tomography scan with nodules and associated halo sign is suggestive of Aspergillus infection. The halo sign often occurs in Aspergillus infection in the context of an increasing neutrophil count after a prolonged nadir. The serum galactomannan antigen test detects galactomannan, a major component of the Aspergillus cell wall that is released during growth of hyphae. The presence of this compound suggests invasion and growth of the mold. This noninvasive test is receiving wider acceptance in the diagnosis of invasive Aspergillus spp. in immunocompromised hosts. Additionally, galactomannan assays in bronchoalveolar lavage fluid may aid diagnosis of invasive Aspergillus in immunocompromised hosts (American Journal of Respiratory and Critical Care Medicine 177: 27-34, 2008). In the absence of purulent sputum, sputum cultures are unlikely to be helpful. Aspergillus is seldom cultured from the sputum in cases of invasive aspergillosis. Examination of buffy coat is useful for the diagnosis of histoplasmosis, but the focal nodules with halo sign and absence of other systemic symptoms makes histoplasmosis less

Date: 2016-04-22; view: 1226