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TABLE 1.
Diagnosis
Adult patients \vith enteroviral meningitis usual] y present with
the sudden onset offever, headache, nuchal rigidity, ami photophobia. The duration of illness is usually less than 1 week,
and many patients report improvement after ctiagnostic lumbar puncture. Patients with mumps meningitis usually report
fever, vomiting, and headache. Salivary gland enlargement
occurs in only 50% of these patients. Patients with the syndrome ofbenign recurrent lymphocytic meningitis characteristically develop approximately 1O episodes of meningitis lasting 2 to 5 days followed by spontaneous recovery.
CSF finctings in patients with viral meningitis are shown
in Table l. Viral cultures of CSF are insensitive for ctiagnosis
and are not routinely recommended. Nucleic acid an1plification tests, such as polymerase chain reaction (PCR), are both
sensitive (86% to 100%) and specific (92% to 100%) for diagnosing enteroviral meningitis. PCR has also been useful for
ctiagnosing HSV-induced meningitis and for associating HSV-2
CSF Parameter
Viral Meningitisa
Opening pressure
<;250mm Hp
Bacteria! Meningitis
200-500 mm H20 b
X 106/L)
106/L)<
Leukocyte count
50-1000/J.JL (50-1000
Leukocyte differential
Lymphocytesd
Neutrophils
Glucose
Protein
Gram stain
Negative
Positive in 60 %-90 % 19
Culture
Negative
Positive in 70%-85%9
1000-5000/J.JL (1 000-5000
'
dMay have neutrophil predominance early in infection, but lymphocyte predominance occurs after the first 6 to 48 hours.
'The CSF:plasma glucose ratio is 50.40 in most patients.
'The likelihood of a positive Gram stain correlates with number of bacteria in the CSF.
9The yield of positive results is significantly reduced by prior admi nistration of an timicrobial therapy.
CJ
Aseptic meningitis syndrome is defined as the presence of clinical and laboratory findings consistent
with meningitis in a patient who has normal cerebrospinal fluid stains and culture on initial evaluation.
Polymerase chain reaction is both sensitive and specific for diagnosing enteroviral meningitis and is also
useful for diagnosing aseptic meningitis due to herpes
simplex virus.
Treatment of enteroviral meningitis is supportive.
Bacteria! Meningitis
Cause
Streptococcus pneumoniae is the most common cause ofbacterial meningitis in the United States. Approximately 70% of
patients with S. pneumoniae meningitis have otitis media,
sinusitis, pneumonia, basilar skull fracture with CSF leak, or
are immunocompromised (splenectomy or asplenia,
hypogammaglobulinernia, multiple myeloma, alcoholism,
chronic liver or kidney disease, malignancy, or HIV infection).
Neisseria meningitidis meningitis most often occurs in
children and young adults and in patients with properdin
and terminal complement (CS, C6, C7, C8, and perhaps
C9) deficiencies. Listeria monocytogenes meningitis develops
most frequently in neonates, older adults (>50 years of age ),
and in those who are immunocomprornised (diabetes mellitus, liver or kidney disease, collagen vascular disorders, disorders ofiron overload, HIV infection, transplant recipients,
and patients taking anti-tumor necrosis factor a agents such
as infliximab and etanercept), although cases have been
reported in patients with no underlying disorders.
Outbreaks have been associated with ingestion of contarninated coleslaw, soft cheeses, raw vegetables, alfalfa tablets,
cantaloupes, and frankfurters and other processed meats.
The incidence of invasive listeriosis has been decreasing,
most likely as a result of decreased contamination by
L. monocytogenes in ready-to-eat foods .
Meningitis due to group B streptococci ( Streptococcus
agalactiae) most commonly occurs in neonates. Because of
this risk, the Centers for Disease Control and Prevention
( CDC) and the American College of Obstetricians and
2
TABLE 2.
States
Percentage of Total Cases
1986"
1995b
2003-2007
Haemophilus influenzae
45
Neisseria meningitidis
14
25
14
Streptococcus pneumoniae
18
47
58
Streptococcus agalactiae
12
18
Listeria monocytogenes
Pathogen
Hospitai-Acquired lnfections
TABLE 44.
Period
Risk Factors
Preoperative
CONT.
KEY POINTS
Diagnosis
SSI typically manfests during the second or third posroperative week, although it can occur much la ter if an in1plant was
placed during surgery. Diagnosis of superficial incisional SSI
is typically based on signs and symptoms, including purulent
drainage, pain, tenderness, redness, or heat. Patients with
r <top'"';"
Treatment
Surgical opening of the incision with debridement and
removal of necrotic tissue is the most important aspect of
treatment of deep incisional and organ/ space SSis.
Antimicrobial therapy is an important adjunct. The type of
debridement and duration of postoperative antimicrobial
therapy depend on tl1e anatomic site of infection, the invasiveness of tl1e SSI, and whetl1er foreign material was
implanted or fillly removed.
Prevention
The major measures to prevent SSis are listed in Table 45 .
Checklists have played an important role in decreasing SSI
rates, because they help to ensure compliance with multiple
infection controlmeasures. The impact of preoperative nasal
79
Hospitai-Acquired lnfections
TABLE 45.
Comments
Comments
Avoid shaving of ha ir
Non e
Non e
Comments
Maintaining plasma glucose levels below 200 mg/dl (11.1 mmoi/L) for
48 h postoperatively is recommended
Non e
SSI
I:J decolonization of
CONT.
Diagnosis
CLABSI should be h.ighly suspected in patients who do not
!uve an obvious source ofinfection from a si te other than tl1e
centralline and in whom tl1e same pathogen is isolated from
a peripheral blood culture specimen and from either a blood
culture specimen obtained by aspirating blood tlrrough tl1e
centralline or a culture of the catheter ti p. lt is important to
recognize that central venous catl1eter tips are often colonized
with bacteria in the absence of clinical infection. Thus, a positive culture of a central venous catheter performed as part of
a routine screening protocol in the absence of positive blood
cultures or signs of infection does not require treatment.
Blood cultures (at least t:wo sets) should be obta.ined from different anatomic si tes (at least one peripheral si te). A threefold
greater colony count from the culture drawn through a
catheter compared with a peripheral blood culture is a strong
predictor for CLABSI. "Time to positivity" is the time
between blood culture incubation and growth detection .
When blood cultures are drawn from a centralline and from
--~~----
Hospitai-Acquired lnfections
TABLE 46.
Period
Risk Factors
Premature birth
Neutropenia
Prolonged hospitalization
Prolonged duration of
catheterization
Total parenteral nutrition
delivered through the
catheter
Heavy microbial colonization
of the catheter hub
aFemoral vein placement is associated with greatest infection risk, and interna! jugular
vein placement with the second greatest infection risk.
Note: Female sex and subclavian vein insertion site were independently associated with
decreased risk for infection.
L __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _
CJ
CONT.
a peripheral si te \Vithin 30 minutes of one another, if the centralline culture turns positive at least 2 hours before growth
is reponed on the peripheral culture, a central line infection
is strongly supported. The semiquantitative roll-plate method
for culturing the distal tip of a central venous catheter is a validated method for detecting catheter colonization and contributes diagnostic information when the same pathogen is
recovered rrom both the catheter tip and the blood culture
specimen. Typically, blood cultures should become negative
once an infected central !ine is removed and appropriate therapy is administered. If bacteremia persists, a diagnostic
workup for a deeper source of infection is appropriate.
Treatment
Removal of the centralline is the most important intervention
in treating CLABSI and is especially important when the
pathogen is S. aureus, Pseudomonas aeruginosa, or Candida
species. If salvage of a central line is attempted, use of an
antibiotic lock is an opcional adjunct to administration of systemic antibiotics.
Prevention
Early CLABSI occurs in the first 5 to 7 days following central
line insertion and is typically caused by pathogens introduced
during insertion. Late ' CLABSI occurs 5 to 7 days or more
after insertion and is generally caused by pathogens introduced during catheter use or care. Methods to prevent early
CLABSI mostly relate to improving catheter insertion techniques. Hand hygiene, basic aseptic techniques, and fui!
----
--
---
----- -
Hospitai-Acquired lnfections
stabilized ( typically on hospital da y 3 or 4 ), is another important component of treating HAP. Treatrnent for 8 days is sufficient for patients with VAP, as long as empiric therapy was
effective and patients do not have pneumonia due to
Pseudomonasspecies or Acinetobacterspecies. The four important components of treating HAP and VAP are to ( l) treat
early, (2) administer empiric broad-spectrum antimicrobial
agents, ( 3) de-escalare antimicrobial coverage when appropriate, and (4) consider short-duration therapy (8 days)
whenever feasible.
Prevention
The most effective way to prevent VAP is to avoid wmecessary mechanical ventilation. Use of noninvasive ventilation
techniques whenever possible and aggressive weaning efforts
for patients who do require mechanical ventilation are advocated. Adherence to an evidence-based VAP-prevention
"bundle" of interventions is recommended, which includes
( l) keeping the head of the bed elevated at greater than 30
degrees, (2) daily assessments of readiness to wean, and ( 3)
use of chlorhexidine mouth care. Respiratory equipment has
been associated with outbreaks of VAP, and equipment
should be disinfected or sterilized according to published
guidelines. Continuous intermittent subglottic suctioning
has been demonstrated to reduce the risk for VAP. The data
regarding use of endotracheal tu bes coated with antiseptics
in preventing VAP are promising, but coated tubes are not
currently recommended by guidelines. Selective use of oral
and digestive decontamination has been demonstrated to be
an effective preventive intervention in Europe but not in the
United States, where the prevalence of antibiotic-resistant
pathogens is higher. Cl
KEY POINTS
Hospital-acquired pneumonia is defined as a pneumonia that occurs 48 hours or more after hospital
admission that was not incubating at the time of
admission.
Ventilator-associated pneumonia is defined as pneu monia that develops more than 48 to 72 hours after
beginning mechanical ventilation.
Mechanical ventilation is the single strongest independent risk factor for development of hospital-acqtred
pneumonia and ventilator-associated pneumonia.
The four important components for treating hospitalacquired pneumopia and ventilator-associated pneumonia are to (l ) treat early, (2) administer empiric broadspectrum antimicrobial agents, (3) de-escalare
antimicrobial coverage when appropriate, and (4) consider short-duration therapy (8 days) whenever feasible.
CJ
Hospitai-Acquired lnfections
Caused by Multidrug-Resistant
Organisms
Hospital-acquired infections (HAis) are commonly caused by
multidrug-resistant organisms. Examples of gram-positive
multidrug-resistant organisms include MRSA and vancomycin-resistant enterococci. The vast majority of HAis
caused by MRSA are due to hospital-acquired MRSA,
although community-associated MRSA has also been implicated. Frequently encmmtered gram-negative multidrugresistant organisms include extended-spectrum ~-lactamase
(ESBL)-producing Enterobacteriaceae, carbapenem-resistant Enterobacteriaceae, Acinetobacter baumannii, and multidrug-resistant strains of P. aeruginosa.
The prevalence of multidrug-resistant organisms as
causative pathogens for HAis is continually increasing.
lnfections caused by multidrug-resistant organisms are associated with worse outcomes compared with infections caused by
drug-susceptible strains of tl1e same species. Multidrug-resistant infections were historically acquired only in nosocomial settings but are now being encountered in long-term care facilities (for example, nursing homes) and in patients without any
contact with health care environments. Although the development of multidrug resistance is complex, its rapid expansion
and increasing clinical significance highlight the need for diligent stewardship in using antibiotics in all settings.
Treatment of HAls caused by multidrug-resistant
organisms is frequently complicated by delays in beginning
effective antimicrobial therapy. Treatrnent principies include
the foUowing:
l. MRSA infection is often treated with vancomycin.
However, ifthe minimal inhibitory concentration to vancomycin is elevated (;:::2, micrograms/mL) and the patient
is not clinically responding to therapy, other agents may be
considered, such as linezolid or clindan1ycin for pneumonia and daptomycin for bloodstream infections.
2. Linezolid and daptomycin are generally used to treat invasive infections due to vancomycin-resistant enterococci.
However, if an1picillin is active against the causative organism, it should be used as the preferred therapeutic agent.
3. Carbapenems are the antibiotics of choice for invasive
infections such as bacteremia caused by ESBL-producing
pathogens. Group l carbapenems (for example,
ertapenem) can be used to treat these infections as long
as they are not caused by Pseudomonas or Acinetobacter
species. Fluoroquinolones are also a therapeutic option if
tl1e pathogen is susceptible. Cephalosporins and penicillins, including cefepime and ~-lactam/~-lactanlase
combinations, should not be used.
4. Therapeutic options for infections caused by carbapenemresistant Enterobacteriaceae are limited. Polymyxins, tigecycline, and sometimes, anlinoglycosides are often the only
83
KEY POINTS
Recommended Prophyladic
Regimens
In patients who meet current AHA infective endocarditis cri teria, a single dose of a prophylactic antimicrobial agent
should be given 30 to 60 minutes before all dental procedures
involving manipulation of gingival tissue, tl1e periapical region
of teeth, or perforation of the oral mucosa in those patients
with cardiac conditions discussed previously. If the antimi crobial agent is inadvertently not administered before the
procedure, the medication may be given up to 2 hours after
the procedure. Table 48 lists the preferred antimicrobial regimens for use before a dental procedure.
TABLE 48.
Although a link between invasive respiratory tract procedures and infective endocarditis has never been demonstrated,
antimicrobial prophylaxis (see Table 48) may be considered for
patients with the cardiac conditions discussed previously who
undergo an invasive respiratory tract proccdure. Infective
endocarditis prophylaxis is not recommcnded for paticnts who
undergo gen.itourinary or gastrointestinal procedures, including upper endoscopy or colonoscopy with or without biopsy.
Appropriate treatment for patients with bacteriuria is recommended to prevent wound infection or infcction from
gen.itourinary tract proccdures. In patients at risk for infective
endocarditis who are about to undergo a surgical procedure
that involves infected skin and/or related tissues, it is recommended that the treatment regimen for the infection have
adequate activity against staphylococci and ~-hemolytic streptococci, because these organ.isms have a greater propensity to
cause infective endocarditis. Cl
KEY POINTS
Situation
Agent"
Adults
Children
Oral
Amoxicillin
2g
50 mglkg
Ampicillin
2 g IM or IV
50 mg/kg IM or IV
Cefazolin or ceftriaxone
1 g IM or IV
50 mg/kg IM or IV
Cephalexin
2g
50 mglkg
600mg
20 mg/kg
or
or
Clindamycin
or
Azithromycin or clarithromycin
Allergic to penicillin or ampicillin and
unable to take oral medication
Cefazolin or ceftriaxone
500 mg
15 mglkg
1 g IM or IV
50 mg/kg IM or IV
600 mg IM or IV
20 mg/kg IM or IV
or
Clindamycin
ot a single dose 30 to 60 minutes before the dental procedure. or, if inadvertently not administered, drug may be given up to 2 hours alter the procedure.
Adapted from Wi lson W, Taubert KA, Gewitz M, et al; American Heart Association. Prevention of infective endocarditis: guidelines from the American Heart Association : a guideline from the
American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council
on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research lnterdisciplinary Working Group. J Am Dent Assoc. 2008; 139 Suppi:3524S. [PMID: 18167394].
Copyright 2008 American Dental Association.
85
C]
HIV/AIDS
TABLE 50 .
Lymphadenopathy
Fevers, night sweats
Fatigue
Weight loss
Chronic diarrhea
Seborrheic dermatitis, psoriasis, t inea, onychomycosis
Oral aphthous ulcers, oral hairy leukoplakia,
gingivit is/periodontit is
Peripheral neuropathy
Leukopenia, anemia, thrombocytopenia
Nephropathy
KEY POINTS
pregnancy to implement measures to minimize perinatal transmission. In addition, in 2012, the FDA approved an at-home,
rapid HIV screening test. The self-administered test uses swabs
of oral fluids from the upper and lower gums to identif)r HIV
antibodies, and results are available within 20 to 40 minutes.
Physicians should advise patients that a positive test result
requires confirmatory testing in the office. Moreover, because
HIV antibodies may not appear during the window period (see
Acute Retroviral System, discussed previously) patients with negative home test results should undergo repeat testing within
3 months.
The diagnosis of HIV infection is established by a twostage serologic testing process. The initial test is an enzyme
inummoassay (EIA). A negative EIA is generally considered
adeq uate to exclude infection except during the acute phase fol lowing primary infection (the window period) before seroconversion occurs and when serologic testing, including Western
blot assay, may be falsely negative. In these patients, EIA testing should be repeated 6 to 12 weeks later when seroconversion
is established. If an acute diagnosis is necessary during the window period, a specific viral test such as the quantitative RNA
polymerase chain reaction assay may be useful; in acute infection, the viral load is usually very high (ofi:en > 100,000
copies/ mL). However, use of a viral load study for routine diagnosis or in sinations other than during the acute phase ofinfection is discouraged because of decreased sensitivity and specificity of the test at lower viral loads and the significant cost
relative to EIA. In a patient with a positive EIA, the test should
be repeated. Repeatedly positive EIA results are confirmed by
Western blot assay. Combination testing with EIA followed by
Western blot assay has a sensitivity of 99.5% and specificity of
99.99%. Rapid HIV tests are now available in k.its that can be
used in the clinical setting. These are EIA tests, and positive
results reqtre standard follow-up confirmatory testing. Because
the EIA requires confirmatory testing, it is never appropriate to
tell patients they have HIV infection based on results of any EIA
alone before the Western blot results are known.
A negative Western blot assay indicares a false-positive
EIA result. An indeterminate Western blot assay indica tes the
presence of antibody bands to certain viral antigens, but
results are insufficient to establish the diagnosis ofHIV infection. This may occur during the "window period" of acute
infection when patients are just beginning to develop antibodies to HIV. Repeatedly indeterminate Western blot results
usually indicare a cross-reacting antibody caused by infections
or imm unologic diseases other than HIV infection.
Indications for HIV testing are shown in Table 51.
KEY POINTS
HIV/AIDS
lipoatrophy may be reduced with avoidance of the thymidine analogue reverse transcrip ase inhibitors (RTis)
(stavudine and zidovudine) .
Mitochondrial toxicity leading to lactic acidosis, which
can be fatal if not recognized early, has decreased with
replacement of stavudine, didanosine, and zidovudine with
larnivudine or emtricitabine and tenofovir in most regimens.
Osteopenia and osteoporosis may also be increased in
patients with HIV infection; bone densitometry screening is
not recommended for all patients but should be considered
for those older than 50 years or with other risk factors.
HIV can also lead to chronic kidney disease through
development ofHIV-associated nephropathy. HIV-associated
nephropathy, when diagnosed early, can be reversed with treatment ofHIV. Patients in whom HIV-associated nephropathy
progresses may require kidney dialysis or transplantation.
Liver disease is also increasing in patients with HIV infection, partly beca use of tl1e high prevalence of coinfection with
HBV or hepatitis C virus (HCV). Patients with HIV infection
with chronic HBV infection requiring treatment should be
given a multidrug regimen with agents active against both
HBV and HIV infection. Patients co-infected with HIV and
HCV have an increased risk for progression to chronic liver
disease and cirrhosis.
KEY POINT
Cardiovascular Disease
An increased risk for cardiovascular disease is associated not
only with the use of sorne antiretroviral agents but also with
HIV infection itself. The SMART study, which randomized
subjects with CD4 cell counts greater than 350/microliter
to continuous ART versus CD4 cell count- guided treatment interruptions, found that patients in the treatmentinterruptions arm not only had more infectious complications (as expected), but they also experienced more
cardiovascular disease end points and deatl1, which led to
early termination of the study. These results suggest that
any increased cardiovascular risk caused by the metabolic
side effects of treatment is more than offset by the risk from
uncontrolled HIV infection, at least in those patients with
CD4 cell counts less than 350/microliter. This increased
risk is thought to be related to ongoing chronic inflammation, contributing to increased atherosclerosis. Chronic care
of patients with HIV infection requires attention to madifiable cardiovascular risk factors, such as smoking, hyperlipidemia, hypertension, and diabetes.
90
KEY POINTS
Any increased cardiovascular risk caused by the metabolic side effects ofHIV treatment is more than offset by the risk from uncontrolled HIV infection.
Chronic care of patients with HIV infection requires
attention to modifiable cardiovascular risk factors,
such as smoking, hyperlipidemia, hypertension, and
diabetes mellitus.
CJ
With the initiation of ART, viral load levels fall sharply, CD4
cell cow1ts increase, and immune responses in1prove. In the
presence of an opporumistic infection, which may not have
been clinically recognized previously, this reconstiUJtion of the
inlmune response can lead to drarnatic inflailiDlatory responses
as the newly revived immune system reacts to high burdens of
antigens. This inflanmutory presentation ofinfections is called
inlmune reconstirution inflaiTimatory syndrome (IRIS) a11d
usually occurs a few weeks to a few months after initiation of
ART. IRIS occurs witl1 various opportunistic infections but
most commonly in patients with mycobacterial infections, such
as tuberculosis or M. avium complex, or disseminated fungal
infections. Continuation of treatment is appropriate in patients
with IRIS, but concomitant corticosteroids may be required to
moderare excessive inflanmution. CJ
KEY POINTS
Opportunistic lnfections
Most opportunistic infections are unlikely to occur in patients
with a CD4 cell cow1t higher than 200/nlicroliter, which is
why tllis is the threshold value used to define AIDS.
Oral candidiasis ( thrush) may occur in patients with CD4
cell counts greater than 200/microliter, especially in those
with other risk factors, such as history of use ofinhaled corticosteroids or broad-spectrum antibiotics, but extension to
esophageal candidiasis occurs more often in patients with
AIDS. Diagnosis is usually based on findings ofvisual inspection shmving characteristic whitish plaques on tl1e oral
mucosa. Treatment of oral candidiasis includes topical agents
such as clotrimazole troches. Dysphagia or other swallowing
symptoms in patients with visible thrush suggest esophageal
[:J
HIV/AIDS
luscum contagiosum.
91
HIV/AIDS
Cl
CONT.
92
HIV/AIDS
Antiretroviral Regimens
The objective of HIV treatment..is to fully suppress viral replication to prevent the development of viral drug resistance,
resu.lting in a rapid and progressive decrease of viral load levels
within the first few weeks of treatment, and, within a few
months of treatment, undetectable viral load levels that remain
undetectable during therapy. Adhering to such a regimen
requires a level of conunitment often clifficult for patients to
maintain. Consequently, clinicians must discuss adherence with
patients befare initiation of therapy and at every follow-up visit.
Maximal suppression ofthe virus generally requires the use of at
least three drugs from at least two different classes. See Table 55
for a list of agents currently in use in the United States.
The current preferred initial regimen in patients without
viral drug resistance combines two nucleoside analogue RTis
(tenofovir and emtricitabine ) with a nonnucleoside RTI
(efavirenz ), available as a once-daily, combination single pill.
The use of a combination pill improves adherence and effectiveness. However, efavirenz shou.ld not be used in women
TABLE 55.
Class
Agentsa
Abacavir
Didanosine
Emtricitabine
Lamivud ine
St avudine
Tenof ovir
Zidovudine
Nonnudeoside RTis
Efavirenz
Etravirine
Nevirapine
Rilpivirine
Atazanavir
Darunavi r
Fosamprenavir
lnd inavir
Lopinavir
Nelfinavir
Ritonavir
Saquinavir
Tipranavir
Entry in hibitors
Enfuvirtide
M araviroc
Integrase inhibitor
Ra lteg ravir
Resistance Testing
Baseline testing of a patient's HIV isolate for antiretroviral
resistan ce should be performed to guide the choice of agents,
because previous infection with a resistant virus may have
occurred. Resistance testing is also appropriate in the setting
of treatment failure as evidenced by suboptimally controlled
viral loads (lack of decreased or suppressed viral load, or previously undetectable viralloads that have become detectable
on repeated testing). Generally, about 500 copies of
virus/ mL of blood are required for resistance testing to be
adequately performed. Testing for treatment failure should be
done while the patient is still receiving therapy, because false negative results may occur with removal ofthe selective pressure provided by the drugs.
93
Directions
Ea eh of the numbered items is fo/lowed by lettered answers. Select the ONE lettered answer that is BEST in each case.
ltem 1
An 18-year-old womaJ) is evaluated 4 weeks following hospitalization for her second episode of pneumococcal pneumonia in 18 months. She received the pneumococcal vaccine 20 months ago. The patient was also diagnosed with
giardiasis 2 years ago. She also has a history of asthma. Her
mother has selective IgA deficiency, and her brother has
lymphoma . Her review of systems is negative for findings
associated with autoimmLme disorders, including systemic
lupus erythematosus.
On physical examination, vital signs are normal . Faint
crackles are heard at the posterior left lung base.
Laboratory studies show a hemoglobin level of 8.6
g/ dL (86 g/ L), a mean corpuscular volume ofl20 fL, and
a leukocyte count of 6800/pL (6.8 x 109/L) with a normal differential . HIV serology results are negative .
(A) Caspofungin
(B) Convencional an1photericin B
(C) Fluconazole
(D ) Liposomal amphotericin B
(E ) Voriccmazole
ltem 2
ltem 4
A 42-year-old manis evaluated for recurrent diarrhea . Four
weeks ago, the patient was diagnosed with a mild Clostridium difficile infection and treated with a 14-day COLirSe of
metronidazole, 500 mg orally every 8 hours, with resolu tion ofhis symptoms. He currently takes no medications.
One week after his last dose of metronidazole, he again
develops recurrent watery stools without fever or otl1er
symptoms. There is no visible blood or mucus in tl1e stools.
Physical examination findings are noncontributory.
Results oflaboratory studies show a leukocyte count of
10,400/ pL (10.4 x 109 / L) anda normal serum creatinine
leve!. A stool sample tests positive for occult blood, and
results of a repeat stool assay are again positive for C. difficile toxin.
CJ ltem 3
ltem S
A 28-year-old woman is evaluated for a 2-day history of
painful genitallesions accompanied by dysuria, generalized
myalgia, malaise, and fever. She is sexually active.
111