Candida Infections of The Abdomen and Thorax

Candida infections of the abdomen and thorax - UpToDate 07/04/2024 19:58
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Candida infections of the abdomen and thorax

author: Carol A Kauffman, MD
section editor: John W Baddley, MD, MSPH
deputy editor: Keri K Hall, MD, MS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2024.

This topic last updated: Aug 15, 2023.
INTRODUCTION
The clinical manifestations of infection with Candida species range from local mucous
membrane infections to widespread dissemination with multisystem organ failure.
Although Candida are considered normal microbiota in the gastrointestinal and
genitourinary tracts of humans, they have the propensity to invade and cause disease
when an imbalance is created in the ecological niche in which these organisms usually
exist.
The immune response of the host is an important determinant of the type of infection
caused by Candida. The different Candida species generally can cause all of the clinical
syndromes, although infection with Candida albicans is the most common. The major
importance of identifying the infecting organism is that some species are more resistant
to azole antifungal agents than others. (See "Management of candidemia and invasive
candidiasis in adults".)
This topic will review the manifestations of Candida infection involving the abdomen and
thorax. Candida peritonitis can complicate continuous peritoneal dialysis in patients with
end-stage kidney disease, as discussed separately (see "Fungal peritonitis in peritoneal
dialysis"). Other manifestations of Candida infections are discussed separately. (See
"Overview of Candida infections" and "Clinical manifestations and diagnosis of candidemia
and invasive candidiasis in adults" and "Chronic disseminated candidiasis (hepatosplenic
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candidiasis)" and "Candida infections in children".)
PERITONITIS AND INTRA-ABDOMINAL INFECTIONS
Risk factors — Candida species frequently contribute to polymicrobial infections that

occur following surgery on the gastrointestinal (GI) tract; upper GI tract surgery is more
likely to lead to intra-abdominal candidiasis than lower GI tract surgery [1,2]. Gut
perforation, anastomotic leaks, and acute necrotizing pancreatitis are associated with
intra-abdominal candidiasis [3-10]. A multicenter study performed from January 2015 to
December 2016 that included 26 European intensive care units (ICU) found that recurrent
gastrointestinal perforation, anastomotic leakage, presence of an abdominal drain, and
prior receipt of antifungal drugs or antibiotics were independently associated with the
development of intra-abdominal candidiasis [11].
Clinical manifestations — Intra-abdominal manifestations of Candida infection include

discrete abscesses from a GI tract, biliary, or pancreatic source, secondary peritonitis from
a GI tract, biliary, or pancreatic source, infected necrotic pancreas, gangrenous
cholecystitis, and obstruction to the common bile duct with a Candida fungus ball [7,12-
14]. Patients with intra-abdominal candidiasis may have candidemia, but the majority do
not have blood cultures yielding Candida and present a more difficult diagnostic problem
[15]. C. albicans is the predominant species isolated in intra-abdominal candidal infections,
but Candida glabrata has assumed an increasing role at some centers [16,17].
The symptoms of Candida peritonitis do not differ from those of bacterial peritonitis, and
in as many as two-thirds of patients, both bacteria and Candida are found as the cause of
peritonitis [14]. Fevers, chills, and abdominal pain are prominent symptoms. Septic shock
is commonly noted and in various studies is reported between 18 percent and 55 percent
[14,17,18].
A retrospective review of 163 patients with intra-abdominal candidiasis between 2012 and
2013 at a single center noted that 55 percent had abscesses and 33 percent had
secondary peritonitis that originated with a gastrointestinal source [14]. The remaining
patients had pancreatitis with necrosis, cholecystitis, cholangitis, and primary peritonitis.
Only 6 percent had candidemia. Source control within five days and antifungal therapy
within five days were each implemented in 72 percent of patients. Overall mortality was 28
percent, but mortality among those who had primary or secondary peritonitis was 88 and
40 percent, respectively. Abscesses, early source control, and young age were
independent predictors of decreased mortality.
A similar study retrospectively assessed outcomes for 82 patients who had intra-
abdominal candidiasis, of which 61 percent had peritonitis, 23 percent had abscesses, and
16 percent had biliary tract infections. More than half (55 percent) of the patients had
septic shock at the time intra-abdominal candidiasis was diagnosed. Appropriate source
control (HR=0.08 [0.02-0.3], p<.001), appropriate antifungal therapy (HR=0.14 [0.04-0.55],
p<.005), and a combination of both factors (HR=0.02 [0.0-0.08], p<.001]) were associated
with improved 30-day survival [18].
Diagnosis — The diagnosis is best made by aspiration of fluid under computed

tomographic (CT) or ultrasound guidance or at the time of surgery. Growth of Candida
species from an abscess or peritoneal fluid should lead to the diagnosis of invasive intra-
abdominal candidiasis and to appropriate treatment with an antifungal agent. Culture of
Candida species from an indwelling drain is not adequate for the diagnosis of infection
because it often reflects only colonization of the drain.
Blood cultures frequently show no growth in patients with intra-abdominal candidiasis

[19]. In several large studies of patients with intra-abdominal candidiasis, only 6 to 20
percent had positive blood cultures [14,17,18].
The serum beta-D-glucan (BDG) assay appears to be a useful test in patients with intra-
abdominal candidiasis [15]. BDG is present in the cell wall of many fungi, including
Candida spp and is also present in some medications and other products that are used in
the hospital setting. Because of this, a positive BDG test result cannot be used for the
diagnosis of a specific fungal infection but rather can be viewed as a marker for a possible
fungal infection that should be sought by more specific testing. In a prospective cohort
study that included 89 patients who had been in the intensive care unit for ≥72 hours and
who were considered to be at high risk for intra-abdominal candidiasis because of
recurrent gastrointestinal tract perforation or acute necrotizing pancreatitis, 29 (33
percent) developed intra-abdominal candidiasis; 27 of 29 patients (93 percent) had
negative blood cultures [20]. The sensitivity and specificity of two consecutive positive
BDG results for predicting intra-abdominal candidiasis were 65 and 78 percent,
respectively. BDG results became positive in patients with intra-abdominal candidiasis a
median of five days before the diagnosis was confirmed by culture of intra-abdominal
specimens [20].
Conversely, and more importantly, a negative BDG test in a patient at risk for intra-
abdominal candidiasis is highly predictive of the absence of invasive candidiasis and can
be used as a means by which antifungal therapy, which is often given empirically in an ICU
setting, can be safely stopped [19,21-23]. Thus, obtaining a BDG test on admission to the
intensive care unit in patients with intra-abdominal events, such as bowel perforation or
necrotizing pancreatitis, may provide a clue as to whether intra-abdominal candidiasis is a
possibility or seems unlikely. This assay does not supplant cultures, which are needed to
identify which specific fungal species might be causing infection. The BDG assay is
discussed in greater detail separately. (See "Clinical manifestations and diagnosis of
candidemia and invasive candidiasis in adults", section on 'Beta-D-glucan assay'.)
Treatment — Treatment of intra-abdominal candidiasis usually entails both surgical

intervention and antifungal therapy [23,24]. Surgical management involves drainage of
abscesses and relief of biliary tract obstruction. Adequate source control was
independently associated with improved survival in a retrospective study of intra-
abdominal candidiasis [14]. Depending on the location of the abscess, drainage can often
be performed by an interventional radiologist, obviating the need for a laparotomy. Initial
antifungal therapy is similar to that for candidemia [23].
The preferred initial treatment is an echinocandin (micafungin 100 mg intravenously [IV]

daily; anidulafungin 200 mg loading dose, then 100 mg IV daily; or caspofungin 70 mg
loading dose, then 50 mg IV daily) ( table 1). Fluconazole (800 mg [12 mg/kg] loading
dose, then 400 mg [6 mg/kg] orally daily) is an alternative that can be used in patients who
are not critically ill, who have not been treated recently with fluconazole, and who are not
considered likely to have a fluconazole-resistant isolate (eg, not colonized with a
fluconazole-resistant species, such as C. glabrata) [23]. A lipid formulation of amphotericin
B (3 to 5 mg/kg IV daily) is another alternative, but it is used infrequently because of the
greater toxicity (particularly nephrotoxicity) of this agent.
Following identification of the infecting species, treatment can be modified as follows,

provided that the patient is clinically stable:
● For fluconazole-susceptible species, such as C. albicans, Candida parapsilosis, and

Candida tropicalis, fluconazole (800 mg [12 mg/kg] loading dose, then 400 mg [6
mg/kg] orally daily) can be used. The concentrations of fluconazole achieved in bile
are as high or higher than the levels achieved in serum [13], and excellent
concentrations are achieved in peritoneal fluid. (See "Pharmacology of azoles".)
● When C. glabrata is the cause of infection, the preferred initial agent is an

echinocandin. Voriconazole has also been approved for the treatment of Candida
intra-abdominal infections and can be used for oral step-down therapy after initial
intravenous echinocandin therapy once the patient has shown improvement and the
source of the infection is adequately controlled. However, susceptibilities should be
obtained before using voriconazole for fluconazole-resistant C. glabrata isolates
because of the high probability of cross-resistance with fluconazole. (See
"Management of candidemia and invasive candidiasis in adults".)
Therapy should continue for at least two weeks and often longer, until the abscess and
signs and symptoms of peritonitis are resolved.
PNEUMONIA
Primary pneumonia due to Candida species is extremely rare. The pathogenesis of lung
involvement is that of hematogenous spread rather than aspiration of oropharyngeal
secretions. Thus, multiple microabscesses are found scattered widely throughout the lung
parenchyma, and lobar infiltrates are uncommon. Autopsy studies from cancer centers
have documented that primary Candida pneumonia, in which infection is limited to the
lungs, occurs in less than 1 percent of cases [25,26]. Much more commonly, the lungs are
one of many organs involved in the course of disseminated infection with Candida in
immunosuppressed patients [23,25]. In a review of a 20-year experience from the MD
Anderson Cancer Center, there were only 31 cases of clearly documented primary Candida
pneumonia in over 7000 autopsies in cancer patients [25].
In one study of 17 hematopoietic cell transplant recipients who had histologically proven
pulmonary candidiasis, the computed tomographic (CT) findings included multiple
nodules ranging from 3 to 30 mm in diameter in 15 patients, air-space consolidation in 11
patients, and nodules surrounded by discrete areas of ground-glass opacity (CT halo sign)
in five patients [27].
Studies in both cancer patients and nonneutropenic patients in an intensive care unit (ICU)
setting have confirmed the lack of specificity of sputum or bronchoalveolar lavage (BAL)
specimens for the diagnosis of pulmonary invasion by Candida [26,28-30]. Among 36

cancer patients with autopsy evidence of Candida pneumonia in whom sputum and/or
BAL were performed ≤4 weeks before death, the sensitivity and specificity was found to be
85 and 60 percent for sputum culture and 71 and 57 percent for BAL [26].
In a prospective study of 232 ICU patients who died with pneumonia and underwent
autopsy, none of 77 patients with Candida spp isolated from a tracheal aspirate or BAL
fluid had histopathologic evidence of Candida pneumonia [31]. Similarly, in a study of 1077
BAL specimens obtained from 555 mechanically ventilated patients in an intensive care
unit, only 8 percent yielded Candida species [30]. Of these 85 samples, 92 percent were
judged to reflect colonization only. Only two patients were treated for presumed Candida
pneumonia.
Treatment — Treatment is not recommended for Candida isolated from sputum or BAL
specimens [23]. Patients with disseminated candidiasis who develop secondary Candida
pneumonia should be treated for disseminated disease. (See "Management of candidemia
and invasive candidiasis in adults".)
EMPYEMA
In four series of patients with Candida empyema, the most common pathogen was C.
albicans, followed by either C. glabrata or C. tropicalis [32-35]. In one series including 81
patients, bacterial pathogens were isolated along with Candida in half of the patients, and
more than one bacterial species was isolated in nearly one-third of cases [32]. Most
patients were severely ill in the intensive care unit and many had antecedent surgery or an
invasive procedure on the thorax or abdomen prior to development of Candida empyema.
Spontaneous rupture of the esophagus was noted in several reports and carried a poor
prognosis [32,35].
Most patients were managed with an antifungal agent and closed drainage [32-35]; in one
study, video-assisted thorascopic surgery or open thoracotomy were also performed [32].
The overall mortality rate for the two reports that focused on Candida empyema ranged
from 27 to 62 percent [32,34]; it is uncertain whether a more aggressive drainage
approach contributed to lower mortality.
Treatment — Empiric treatment of Candida empyema consists of either an echinocandin
or an azole. Targeted treatment should be guided by microbiologic identification, species-

based risk for azole resistance, and antifungal susceptibility test results.
Data on the concentration of antifungal agents in empyema fluid are limited [36]. Most
data are from case reports that provide values for one antifungal agent in a single patient.
One series that included 81 patients noted an association between increased mortality
and use of an echinocandin rather than fluconazole (odds ratio 4.5, 95% CI 1.1-18.8),
raising questions regarding echinocandin penetration and activity in the pleural space
[32]. However, limitations of this study were the retrospective design and that only one
agent (caspofungin) was evaluated; it is possible that illness severity may have led
clinicians to select an echinocandin over fluconazole [32].
The duration of antifungal therapy should be guided by individual circumstances. A

minimum of two weeks of antifungal therapy following decortication or chest tube
removal may be sufficient; in some circumstances, a longer duration may be needed.
MEDIASTINITIS
Candida mediastinitis almost always occurs as a complication of thoracic surgical

procedures [37-40]. In a report of nine cases of Candida mediastinitis, the primary clinical
manifestations included chest wall erythema and/or drainage, fever, and sternal instability
[37]. These findings are similar to those seen with bacterial causes of postoperative
mediastinitis. (See "Postoperative mediastinitis after cardiac surgery".)
All patients had received prior antibiotic therapy, and the median time from surgery to
disease onset was 11 days (range 6 to 100 days) [37]. The course was complicated in seven
patients by contiguous or hematogenous spread. The diagnosis was delayed in three
patients because intraoperative cultures were not obtained or cultures positive for
Candida were considered contaminants.
In this study and an earlier review of 39 published cases of Candida mediastinitis, mortality
was 55 percent [37,39]. In the latter report, no patient who had not undergone a
mediastinal drainage procedure survived compared with survival in 11 of 13 patients (85
percent) who underwent mediastinal drainage [39].
Treatment — Mediastinal drainage with debridement of affected bone in combination
with antifungal therapy is essential for cure. The choice of agent should be similar to that
recommended for candidemia. Thus, an echinocandin (micafungin 100 mg intravenously
[IV] daily; anidulafungin 200 mg loading dose, then 100 mg IV daily; or caspofungin 70 mg
loading dose, then 50 mg IV daily) is recommended ( table 1). Fluconazole (800 mg [12
mg/kg] loading dose, then 400 mg [6 mg/kg] daily) can be used for susceptible species. A
lipid formulation of amphotericin B (3 to 5 mg/kg IV daily) is an alternative. Therapy is
prolonged in most cases and only stopped when all clinical and laboratory signs of
infection have resolved.
In many cases, sternal osteomyelitis accompanies mediastinal infection, which requires

prolonged therapy with oral fluconazole for susceptible species. For patients who have C.
glabrata mediastinitis and perhaps osteomyelitis, voriconazole is the most appropriate
agent for long-term oral therapy provided that the isolate is susceptible. It is important to
note that susceptibilities should be obtained before using voriconazole for fluconazole-
resistant C. glabrata isolates because of the high probability of cross-resistance with
fluconazole (see "Management of candidemia and invasive candidiasis in adults"). If
sternal involvement is present, the duration of therapy may extend to six months or
longer. Clinical response, improvement in inflammatory markers (erythrocyte
sedimentation rate, C-reactive protein), and resolution of computed tomographic scan
findings are the usual parameters that help determine length of oral therapy.
PERICARDITIS
Purulent pericarditis due to Candida species is rare but life threatening. It most often
arises as a complication of previous thoracic surgery or contiguous spread from an
adjacent focus, but hematogenous spread can occur [41-43]. C. albicans is the most
common pathogen, but infection with C. tropicalis and C. glabrata have been described
[42-44].
In a literature review of 25 cases, 21 had either undergone thoracic surgery or had

disseminated candidiasis [42]. Immunocompromise and antibiotic therapy are risk factors,
as they are for almost all Candida infections [41]. (See "Overview of Candida infections",
section on 'Risk factors for invasive infection'.)
The clinical presentation may be subtle and nonspecific in some patients [41], but other
patients will present with an enlarging cardiac shadow on chest radiography and/or signs
of cardiac tamponade. The diagnosis is confirmed by a positive culture of pericardial fluid

or finding yeast forms on pericardial biopsy.
Treatment — Untreated Candida pericarditis is almost uniformly fatal [41,42]. Tamponade

must be treated emergently with decompression and subsequently with a pericardial
window or pericardiectomy to prevent recurrent hemodynamic compromise [23,41-44].
Although not recommended, occasional patients have survived with only
pericardiocentesis and antifungal therapy [42,45]. (See "Cardiac tamponade".)
Therapy with an echinocandin (micafungin 100 mg intravenously [IV] daily; anidulafungin

200 mg loading dose, then 100 mg IV daily; or caspofungin 70 mg loading dose, then 50
mg IV daily) is recommended ( table 2) [23]. If the organism is fluconazole susceptible,
fluconazole (800 mg [12 mg/kg] loading dose, then 400 [6 mg/kg] orally daily) can be used.
A lipid formulation of amphotericin B (3 to 5 mg/kg IV daily) is an alternative. Patients
receiving an echinocandin can be switched to oral fluconazole (400 to 800 mg [6 to 12
mg/kg] daily) if the organism is susceptible when they are clinically stable.
For pericarditis due to C. glabrata, echinocandin therapy followed by oral voriconazole (400
mg orally twice daily for two doses, then 200 mg twice daily) is an option. However,
susceptibilities should be obtained before using voriconazole for fluconazole-resistant C.
glabrata isolates because of the high probability of cross-resistance with fluconazole. (See
"Management of candidemia and invasive candidiasis in adults".)
The optimal length of therapy is not known. The patient should be followed clinically and
therapy stopped only when there are no signs of ongoing pericardial inflammation and all
systemic signs of infection, such as an elevated erythrocyte sedimentation rate and
anemia, have resolved.
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and

regions around the world are provided separately. (See "Society guideline links:
Candidiasis".)
SUMMARY AND RECOMMENDATIONS
● Intra-abdominal infections
• Sources – Candida species frequently contribute to polymicrobial intra-abdominal

infections. Sources include gut perforation, anastomotic leaks after bowel
surgery, acute necrotizing pancreatitis, peritoneal dialysis infection, gangrenous
cholecystitis, and common bile duct fungus balls. Discrete abscesses with or
without peritonitis can occur. (See 'Clinical manifestations' above.)
• Microbiology – Candida albicans is the predominant species isolated in intra-

abdominal candidal infections, but Candida glabrata has assumed an increasing
role at some centers. (See 'Peritonitis and intra-abdominal infections' above.)
• Diagnosis – Growth of Candida species from an abscess or peritoneal fluid should

lead to the diagnosis of invasive intra-abdominal candidiasis and to appropriate
treatment with an antifungal agent. Culture of Candida species from an indwelling
drain is not adequate for the diagnosis of infection. The serum beta-D-glucan
(BDG) assay can be a useful adjunct to cultures of an abscess or peritoneal fluid
and may become positive before the diagnosis is established by culture. (See
'Peritonitis and intra-abdominal infections' above.)
• Treatment – Treatment usually entails both surgical intervention and antifungal

therapy. The choice of agent depends upon the Candida species. Surgical
management involves drainage of abscesses and relief of biliary tract obstruction.
An echinocandin is recommended, but fluconazole is an alternative for
fluconazole-susceptible isolates ( table 1). A lipid formulation of amphotericin B
is another alternative, but it is used infrequently because of the greater toxicity of
this agent. (See 'Treatment' above.)
● Infections of the thorax
• Pneumonia – Primary pneumonia due to Candida species is extremely rare. The

pathogenesis of lung involvement is that of hematogenous spread rather than
aspiration of oropharyngeal secretions. Thus, multiple microabscesses are found
scattered widely throughout the lung parenchyma, and lobar infiltrates are
uncommon. Treatment is not recommended for Candida isolated from sputum or
bronchoalveolar lavage specimens. Patients with disseminated candidiasis who
develop secondary Candida pneumonia should be treated for disseminated
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disease. (See 'Pneumonia' above.)
• Empyema – Empiric treatment of Candida empyema consists of either an

echinocandin or an azole. Targeted treatment should be guided by microbiologic
identification, species-based risk for azole resistance, and antifungal susceptibility
test results. (See 'Empyema' above.)
• Mediastinitis – Candida mediastinitis almost always occurs as a complication of

thoracic surgical procedures. Mediastinal drainage with debridement of affected
bone in combination with antifungal therapy is essential for cure. The choice of
agent should be similar to that recommended for candidemia. An echinocandin is
the preferred initial agent. Fluconazole is an alternative if the isolate is
susceptible. A lipid formulation of amphotericin B is a less frequently used
alternative. Therapy is prolonged in most cases and only stopped when all clinical
and laboratory signs of infection have resolved. (See 'Mediastinitis' above.)
• Pericarditis – Purulent pericarditis due to Candida species is rare but life

threatening. It most often arises as a complication of previous thoracic surgery or
contiguous spread from an adjacent focus, but hematogenous spread can occur.
An echinocandin is the preferred initial agent. Fluconazole is an alternative for
fluconazole-susceptible isolates. A lipid formulation of amphotericin B is another
alternative. (See 'Pericarditis' above.)
● Antifungal regimens
• Echinocandins – Micafungin 100 mg intravenously (IV) daily; anidulafungin 200

mg loading dose, then 100 mg IV daily; or caspofungin 70 mg loading dose, then
50 mg IV daily
• A lipid formulation of amphotericin B – 3 to 5 mg/kg IV daily
• Fluconazole – 800 mg (12 mg/kg) loading dose, then 400 mg (6 mg/kg) orally
daily\
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38. Malani PN, McNeil SA, Bradley SF, Kauffman CA. Candida albicans sternal wound
infections: a chronic and recurrent complication of median sternotomy. Clin Infect Dis
2002; 35:1316.
39. Glower DD, Douglas JM Jr, Gaynor JW, et al. Candida mediastinitis after a cardiac
operation. Ann Thorac Surg 1990; 49:157.
40. Pertowski CA, Baron RC, Lasker BA, et al. Nosocomial outbreak of Candida albicans
sternal wound infections following cardiac surgery traced to a scrub nurse. J Infect Dis
1995; 172:817.
41. Rabinovici R, Szewczyk D, Ovadia P, et al. Candida pericarditis: clinical profile and
treatment. Ann Thorac Surg 1997; 63:1200.
42. Schrank JH Jr, Dooley DP. Purulent pericarditis caused by Candida species: case report
and review. Clin Infect Dis 1995; 21:182.
43. Neughebauer B, Alvarez V, Harb T, Keefer M. Constrictive pericarditis caused by

candida glabrata in an immunocompetent patient: case report and review of
literature. Scand J Infect Dis 2002; 34:615.
44. Chaudhary K, Faidas A, Baddour LM. Candida pericarditis: unusual complication
following hiatal hernia repair. Infect Dis Clin Pract 1996; 5:339.
45. Karp R, Meldahl R, McCabe R. Candida albicans purulent pericarditis treated
successfully without surgical drainage. Chest 1992; 102:953.
Topic 2436 Version 24.0
GRAPHICS
Treatment of candidemia and invasive candidiasis in adults
Condition or Therapy
treatment
group Primary Step-down Comments
Candidemia
Nonneutropenic One of the following For patients who are When the source is
adults echinocandins clinically stable, have presumed to be the
(caspofungin 70 mg IV isolates that are CVC, remove it as early
loading dose, then 50 susceptible to as possible. For
mg IV daily; micafungin fluconazole, and have candidemia without
100 mg IV daily; negative repeat blood obvious metastatic
anidulafungin 200 mg cultures following complications, treat for
IV loading dose, then initiation of antifungal 14 days after first
100 mg IV daily) is therapy, transition from negative blood culture
recommended as initial an echinocandin or lipid result and resolution of
therapy. formulation signs and symptoms
amphotericin B to associated with
An alternative for
fluconazole is candidemia. Dilated
patients who are not
appropriate (usually funduscopic
critically ill and who are
within five to seven examination within a
considered unlikely to
days). week of diagnosis is
have fluconazole-
recommended for all
resistant Candida spp * For C. glabrata infection,
patients.
is fluconazole 800 mg transition to higher-
(12 mg/kg) oral loading dose fluconazole 800
dose, then 400 mg (6 mg (12 mg/kg) orally
mg/kg) orally ¶ daily. daily or voriconazole Δ
200 to 300 mg (3 to 4
A lipid formulation of
mg/kg) orally twice daily
amphotericin B (3 to 5
should only be
mg/kg IV daily) is an
considered for patients
alternative if there is
with fluconazole-
intolerance, limited
susceptible or
availability, or
voriconazole-
resistance to other
susceptible isolates.
antifungal agents.
For infection due to an
azole-resistant
organism, rezafungin
may be considered
because of its once-
weekly dosing.
Neutropenic One of the following Fluconazole 400 mg (6 For candidemia without

patients echinocandins mg/kg) orally ¶ daily can obvious metastatic
(caspofungin 70 mg IV be used for step-down complications,
loading dose, then 50 therapy during recommended
mg IV daily; micafungin persistent neutropenia minimum duration of
100 mg IV daily; in clinically stable therapy is 14 days after
anidulafungin 200 mg patients who have documented clearance
IV loading dose, then fluconazole-susceptible of Candida from the
100 mg IV daily) is isolates and bloodstream, provided
recommended as initial documented neutropenia and signs
therapy. bloodstream clearance. and symptoms
attributable to
A lipid formulation of Voriconazole Δ 200 to
candidemia have
amphotericin B (3 to 5 300 mg (3 to 4 mg/kg)
resolved. Dilated
mg/kg IV daily) is a less orally twice daily can be
funduscopic
attractive alternative used as step-down
examination is
because of the potential therapy during
recommended for all
for toxicity. neutropenia in clinically
patients; examination
stable patients who
For patients who are should be repeated
have voriconazole-
not critically ill and who within 7 days after
susceptible isolates and
have had no prior azole recovery from
documented
exposure, an alternative neutropenia. CVC
bloodstream clearance.
is fluconazole 800 mg removal should be
(12 mg/kg) oral loading considered on a case-
dose, then 400 mg (6 by-case basis. G-CSF-
mg/kg) orally ¶ daily. mobilized granulocyte
In situations in which transfusions can be
additional mold considered in cases of
coverage is desired, persistent candidemia
voriconazole Δ 400 mg with anticipated
orally (or 6 mg/kg IV) protracted neutropenia.
twice daily for two
doses then 200 to 300
mg orally (or 3 to 4
mg/kg IV) twice daily
can be used.
The doses above are intended for patients with normal organ function. The fluconazole dose
requires adjustment in the setting of renal insufficiency; the caspofungin and voriconazole doses
may require adjustment in hepatic insufficiency. Refer to the drug monographs included within
UpToDate for additional information including specific dose adjustment recommendations.
CVC: central venous catheter; G-CSF: granulocyte colony-stimulating factor; IV: intravenous.
* Fluconazole should be considered a first-line option only in patients who are stable, have no
previous exposure to azoles, and are not at high risk for C. glabrata infection (eg, older adults,
underlying malignancy, diabetic); refer to accompanying text.
¶ Since fluconazole is highly bioavailable, oral therapy is appropriate for most patients. IV therapy
(at the same dose) should be given to patients who are unable to take oral medications, who are
not expected to have good gastrointestinal absorption, or who are severely ill.
Δ Therapeutic drug monitoring should be considered due to widely variable pharmacokinetics;

refer to the UpToDate topic review on pharmacology of azoles for details.
Data from: Pappas PG, Kauﬀman CA, Andes DR, et al. Clinical practice guideline for the management of candidiasis: 2016
update by the Infectious Diseases Society of America. Clin Infect Dis 2016; 62:e1.
Graphic 87676 Version 9.0
Treatment of Candida endocarditis and suppurative thrombophlebitis
Condition Therapy
or
treatment
Primary Step-down Comments
group
Candida endocarditis
Native valve A lipid formulation of For patients who are Valve replacement is
endocarditis amphotericin B (3 to 5 clinically stable, have recommended;
mg/kg IV daily) with or isolates that are treatment should
without flucytosine * (25 susceptible to continue for at least 6
mg/kg orally four times fluconazole, and have weeks after surgery.
daily); negative repeat blood
For patients who cannot
cultures following
or undergo valve
initiation of a lipid
replacement, long-term
High-dose echinocandin formulation of
suppression with an oral
(caspofungin 150 mg IV amphotericin B or high-
azole (fluconazole ¶ 400
daily, micafungin 150 mg dose echinocandin
to 800 mg [6 to 12
IV daily, or anidulafungin therapy, transition to oral
mg/kg] daily if the isolate
200 mg IV daily). fluconazole ¶ 400 to 800
is susceptible ◊ ) is
mg (6 to 12 mg/kg) daily
recommended following
is appropriate.
initial antifungal therapy.
Oral voriconazole Δ 200 to
300 mg (3 to 4 mg/kg)
twice daily or delayed-
release posaconazole
tablets Δ 300 mg daily can
be used for step-down
therapy in clinically stable
patients who have
isolates susceptible to
these agents but not
susceptible to
fluconazole.
Prosthetic A lipid formulation of For patients who are Valve replacement is

valve amphotericin B (3 to 5 clinically stable, have recommended.
endocarditis mg/kg IV daily) with or isolates that are
Lifelong suppression with
without flucytosine * (25 susceptible to
an oral azole
mg/kg orally four times fluconazole, and have
(fluconazole ¶ 400 to 800
daily); negative repeat blood
or cultures following mg [6 to 12 mg/kg] daily

initiation of a lipid if the isolate is
High-dose echinocandin
formulation of susceptible ◊ ) is
(caspofungin 150 mg IV
amphotericin B or high- recommended to prevent
daily, micafungin 150 mg
dose echinocandin recurrence following
IV daily, or anidulafungin
therapy, transition to oral initial antifungal therapy
200 mg IV daily).
fluconazole ¶ 400 to 800 in all patients.
is appropriate.
Oral voriconazole Δ 200 to

300 mg (3 to 4 mg/kg)
twice daily or delayed-
release posaconazole
tablets Δ 300 mg daily can
be used for step-down
therapy in clinically stable
patients who have
isolates susceptible to
these agents but not
susceptible to
fluconazole.
Candida suppurative thrombophlebitis
A lipid formulation of For patients who are Catheter removal and

amphotericin B (3 to 5 clinically stable, have incision and drainage or
mg/kg IV daily); isolates that are resection of the vein is
susceptible to recommended if feasible.
or
fluconazole, and have
Treat with one of the
Fluconazole ¶ 400 to 800 negative repeat blood
options for primary
mg (6 to 12 mg/kg) IV or cultures following
therapy for at least two
orally daily; initiation of amphotericin
weeks after candidemia
or B or high-dose
has cleared, before
echinocandin therapy,
High-dose echinocandin transitioning to step-
transition to oral
(caspofungin 150 mg IV down therapy.
fluconazole ¶ 400 to 800
daily, micafungin 150 mg Resolution of thrombus
IV daily, or anidulafungin can be used as evidence
is appropriate.
200 mg IV daily). to discontinue antifungal
therapy if clinical and
culture data are
supportive.
The doses above are intended for patients with normal organ function. The dose of fluconazole
and flucytosine must be adjusted in the setting of renal insufficiency; the caspofungin and
voriconazole dose may require adjustment in hepatic insufficiency. Refer to the drug-specific
monographs included within UpToDate for additional information including specific dose
adjustment recommendations.
IV: intravenously.
* Toxic effects on bone marrow and liver require careful monitoring preferably with frequent
serum flucytosine levels; refer to accompanying text for discussion of benefits and risks of
combined flucytosine and amphotericin B therapy.
¶ Since fluconazole is highly bioavailable, oral therapy is appropriate for most patients. IV therapy
(at the same dose) should be given to patients who are unable to take oral medications, who are
not expected to have good gastrointestinal absorption, or who are severely ill.
Δ Therapeutic drug monitoring should be considered due to widely variable pharmacokinetics;

refer to the topic review on pharmacology of azoles for detail.
◊ In patients with endocarditis caused by a Candida species that is not susceptible to fluconazole,
oral voriconazole (200 or 300 mg [3 to 4 mg/kg] twice daily) or delayed-release posaconazole
tablets (300 mg daily) should be used for chronic suppressive therapy if the organism is
susceptible.
Data from: Pappas PG, Kauﬀman CA, Andes DR, et al. Clinical practice guideline for the management of candidiasis: 2016
update by the Infectious Diseases Society of America. Clin Infect Dis 2015; 62:e1.
Graphic 87681 Version 5.0
Contributor Disclosures
Carol A Kauffman, MD No relevant financial relationship(s) with ineligible companies to
disclose. John W Baddley, MD, MSPH Consultant/Advisory Boards: Pfizer [Rheumatology];
Pulmocide [Aspergillosis]. All of the relevant financial relationships listed have been mitigated. Keri
K Hall, MD, MS No relevant financial relationship(s) with ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,
these are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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Candida infections of the abdomen and thorax - UpToDate 07/04/2024 19:58

Official reprint from UpToDate®

Literature review current through: Mar 2024.

candidiasis)" and "Candida infections in children".)

PERITONITIS AND INTRA-ABDOMINAL INFECTIONS

Risk factors — Candida species frequently contribute to polymicrobial infections that

Clinical manifestations — Intra-abdominal manifestations of Candida infection include

Diagnosis — The diagnosis is best made by aspiration of fluid under computed

Blood cultures frequently show no growth in patients with intra-abdominal candidiasis

Treatment — Treatment of intra-abdominal candidiasis usually entails both surgical

The preferred initial treatment is an echinocandin (micafungin 100 mg intravenously [IV]

Following identification of the infecting species, treatment can be modified as follows,

● For fluconazole-susceptible species, such as C. albicans, Candida parapsilosis, and

● When C. glabrata is the cause of infection, the preferred initial agent is an

specimens for the diagnosis of pulmonary invasion by Candida [26,28-30]. Among 36

Treatment — Empiric treatment of Candida empyema consists of either an echinocandin

or an azole. Targeted treatment should be guided by microbiologic identification, species-

The duration of antifungal therapy should be guided by individual circumstances. A

Candida mediastinitis almost always occurs as a complication of thoracic surgical

Treatment — Mediastinal drainage with debridement of affected bone in combination

In many cases, sternal osteomyelitis accompanies mediastinal infection, which requires

In a literature review of 25 cases, 21 had either undergone thoracic surgery or had

of cardiac tamponade. The diagnosis is confirmed by a positive culture of pericardial fluid

Treatment — Untreated Candida pericarditis is almost uniformly fatal [41,42]. Tamponade

Therapy with an echinocandin (micafungin 100 mg intravenously [IV] daily; anidulafungin

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and

SUMMARY AND RECOMMENDATIONS

• Sources – Candida species frequently contribute to polymicrobial intra-abdominal

• Microbiology – Candida albicans is the predominant species isolated in intra-

• Diagnosis – Growth of Candida species from an abscess or peritoneal fluid should

• Treatment – Treatment usually entails both surgical intervention and antifungal

● Infections of the thorax

• Pneumonia – Primary pneumonia due to Candida species is extremely rare. The

disease. (See 'Pneumonia' above.)

• Empyema – Empiric treatment of Candida empyema consists of either an

• Mediastinitis – Candida mediastinitis almost always occurs as a complication of

• Pericarditis – Purulent pericarditis due to Candida species is rare but life

• Echinocandins – Micafungin 100 mg intravenously (IV) daily; anidulafungin 200

• A lipid formulation of amphotericin B – 3 to 5 mg/kg IV daily

Use of UpToDate is subject to the Terms of Use.

1. Carneiro HA, Mavrakis A, Mylonakis E. Candida peritonitis: an update on the latest

2. Brotfain E, Sebbag G, Friger M, et al. Invasive Candida Infection after Upper

3. Calandra T, Bille J, Schneider R, et al. Clinical significance of Candida isolated from

4. Sandven P, Qvist H, Skovlund E, et al. Significance of Candida recovered from

6. Hoerauf A, Hammer S, Müller-Myhsok B, Rupprecht H. Intra-abdominal Candida

9. de Ruiter J, Weel J, Manusama E, et al. The epidemiology of intra-abdominal flora in

10. Montravers P, Lepape A, Dubreuil L, et al. Clinical and microbiological profiles of

17. Bassetti M, Righi E, Ansaldi F, et al. A multicenter multinational study of abdominal

21. Posteraro B, De Pascale G, Tumbarello M, et al. Early diagnosis of candidemia in

24. Bassetti M, Marchetti M, Chakrabarti A, et al. A research agenda on the management

25. Haron E, Vartivarian S, Anaissie E, et al. Primary Candida pneumonia. Experience at a

cancer: an autopsy study. Clin Infect Dis 2002; 34:400.

operation. Ann Thorac Surg 1990; 49:157.

43. Neughebauer B, Alvarez V, Harb T, Keefer M. Constrictive pericarditis caused by

Treatment of candidemia and invasive candidiasis in adults

Neutropenic One of the following Fluconazole 400 mg (6 For candidemia without

UpToDate for additional information including specific dose adjustment recommendations.

Δ Therapeutic drug monitoring should be considered due to widely variable pharmacokinetics;

Graphic 87676 Version 9.0

Treatment of Candida endocarditis and suppurative thrombophlebitis

Prosthetic A lipid formulation of For patients who are Valve replacement is