ORIGINAL ARTICLE
Necrotizing Pneumonia in Cancer Patients
A Retrospective Observational Study, 1987–2011
Abraham Tareq Yacoub, MD,* Joseph Halliday, DO,† Mitusya Katayama, MD,† Yanina Pasikhova, PharmD,‡
Adam Katzman, BS,§ Alexander Ralys, MS,║ Ramon L. Sandin, MD, MS, FCAP,¶#
and John Greene, MD, FACP‡#
Background: Necrotizing pneumonia (NP) is a rare, pathologic process
similar to lung abscess defined by multiple, small (<2 cm) cavitary lesions that
has a variety of causes. Risk factors include potential for aspiration, frequent or
prolonged hospitalization, and immunosuppression. Common pathogens in-
clude staphylococcus, streptococcus, anaerobes, aerobic gram-negative bacilli,
mycobacteria, Nocardia, and fungi. The purpose of our study was to character-
ize the causes of NP in cancer patients and to appreciate the different etiologies
when hematologic malignancy (HM) patients are compared with solid tumor
patients because of differences in immunosuppression.
Methods: Our study entailed a retrospective chart review conducted at the
Moffitt Cancer Center in Tampa, Fla, within the past 24 years (January 1, 1987,
to June 1, 2011) between the ages of 18 and 85 years diagnosed with NP. The
patients were identified through review of our institutional databases. Patients
were initially screened through visual review of computed tomography scans
for cavitary lesions and then confirmed via radiology reports demonstrating
an NP or lung abscess and by clinical notes. Patients without a primary lung
infectious microorganism confirmed by reliable culture were placed into
2 groups based on presentation and speed of cavitation from the onset of symp-
toms, with 7 days being the cutoff. Neutropenia was defined as an absolute
neutrophil count of less than 500/μL. Small versus large cavitary lesions were
distinguished by a cutoff of 2 cm. For demographic, descriptive and clinical
data, standard descriptive statistics were used. For comparisons between groups
involving nominal data, χ2 tests were used. One-way analysis of variance tests
were performed for comparisons between multiple groups with numerical data.
P < 0.05 was considered statistically significant where appropriate.
Results: We identified 65 cases of NP, with 44 (68%) having positive
cultures for 1 or more organisms. Methicillin-resistant Staphylococcus
aureus, Pseudomonas aeruginosa, Klebsiella species, mycobacteria,
streptococci, and other unidentified fast-growing organisms were more
common in lung cancer and obstructive lung disease compared with HM
(9.1% vs 3.0%, 18.2% vs 6.1%, 4.5% vs 3.0%, 13.6% vs 0%, 9.1% vs
0%, and 13.6% vs 12.1%, respectively). Conversely, Aspergillus,
Nocardia, unidentified slow-growing organisms, and other rare organisms
were more common in HM (15.2% vs 13.6%, 6.1% vs 4.5%, 24.2% vs
4.5%, and 21.2% vs 13.6%, respectively). Neutropenia at the time of diag-
nosis was observed in 15 patients with HM (45%), 1 patient with nonlung
solid organ cancer (9%), and none of the patients with lung cancer. Hema-
tologic malignancy had significantly more deaths due to respiratory failure
and other causes (18% and 12%, respectively) compared with lung disease
(5% and 0%, respectively). The association between infecting organism
and speed of progression to NP was not significant (P = 0.11).
From the *H. Lee Moffitt Cancer Center and Research Institute; †Division of
Infectious Diseases and International Medicine, University of South Florida;
‡Infectious Diseases, H. Lee Moffitt Cancer Center and Research Institute;
and §University of South Florida Morsani College of Medicine, Tampa; ║Lake
Erie College of Osteopathic Medicine, Bradenton; and ¶Clinical Microbiology
and Virology Laboratories, Moffitt Cancer Center, and #University of South
Florida College of Medicine, Tampa, FL.
Correspondence to: John Greene, MD, FACP, University of South Florida
College of Medicine, 12902 Magnolia Drive, Tampa, FL 33612.
E-mail: john.greene@moffitt.org.
The authors have no funding or conflicts of interest to disclose.
Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
ISSN: 1056-9103
Infectious Diseases in Clinical Practice • Volume 23, Number 2, March 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Conclusions: We found that HM patients with NP had a higher mortality
and more opportunistic and slow-growing organisms when compared with
cancer patients with lung disease or other solid tumors. Further study is
needed to determine the role that neutropenia, duration of illness, and
isolated pathogen play in the treatment of cancer patients with NP.
Key Words: necrotizing pneumonia, cancer, neutropenia
(Infect Dis Clin Pract 2015;23: 85–88)
N ecrotizing pneumonia (NP), a rare complication of community-
acquired pneumonia (CAP), is the destruction of pulmo-
nary parenchymal tissue and can result from infection by a
variety of organisms.1 It encompasses a spectrum of lung
parenchymal necrosis, including lung abscess, which is de-
fined as the formation of a cavity with an air-fluid level due
to infection that is greater than 2 cm.2,3 Patients with malignant
neoplasms were considered at an increased risk for infection
due to intensive chemotherapy, but the risk can extend even
into complete remission.4,5 Therefore, although NP is attrib-
uted to infection mainly by aerobic and anaerobic bacteria, in-
vasive mold and some other bacteria have also been reported as
causative agents in immunocompromised patients.1,4–6 The in-
citing microorganism is important in the progression of the dis-
ease and subsequent morbidity and mortality.1
Previous studies have demonstrated NP is most commonly
caused by anaerobic bacteria such as Prevotella, Peptostreptococcus,
and some Bacteroides species.1 Aerobic bacteria associated with NP
include Staphylococcus aureus, Klebsiella pneumoniae, Pseudo-
monas aeruginosa, and Nocardia.1,4,6 Because of the immune-
compromised state of cancer patients, fungi such as Aspergillosis
and Mucor species are commonly found.2 Symptoms can be present
from weeks to months and include fever, chills, cough productive
of sputum, weight loss, night sweat, pleurisy, and hemoptysis.4
There are 2 main pathological mechanisms for developing
NP and lung abscess in immunocompromised patients, each in-
volving different microorganisms and needing different clinical
considerations when considering cancer patients. The first is an
obstructive lung disease such as lung adenocarcinoma, bronchiec-
tasis, and so on, which can lead to inadequate drainage or aspira-
tion and infection via bacteria from the oropharynx.3,7,8 The other
group is hematologic malignancy (HM) who may have neutrope-
nia and T-cell immunodeficiency, especially following bone
marrow transplantation (BMT), and predispose patients to lung
colonization by a wide variety of microorganisms, including
molds and Nocardia, which can be slower growing.1,2,8 Also,
immunocompromised individuals are predisposed to bacteremia
and can develop septic emboli to the lungs.3,8
MATERIALS AND METHODS
The inclusion criteria for this study was all neoplastic malig-
nancy patients at Moffitt Cancer Center in Tampa, Fla, within the
past 24 years (January 1, 1987, to June 1, 2011) between the ages
of 18 and 85 years who have been diagnosed with NP infection by
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Yacoub et al Infectious Diseases in Clinical Practice • Volume 23, Number 2, March 2015

a wide range of microorganisms. Patients were initially screened (63%) alive as of their last follow-up, 10 (15%) discharged to a
for by looking through computed tomography (CT) scans for cav- hospice center, 7 (11%) died of respiratory failure, and 4 (6%) died
itary lesions and then confirmed via radiological reports and clin- of another cause, most commonly related to their cancer.
ical notes demonstrating an NP or lung abscess.
Patients were identified through review of Moffitt’s institu- Analysis by Preexisting Cancer Condition
tional databases: Cerner/PowerChart and Emageon at Moffitt
Comparison of aforementioned data was made between
Cancer Center. Through these databases, access to pathology re-
groups with lung cancer/obstructive lung disease (n = 22), HM
ports, operative reports, laboratory values, clinical notes, radiologic
(n = 33), and other solid organ cancers (n = 9). There was no sig-
reports, and radiology images was given. For patients treated be-
nificant difference between the ages of the patients between
fore the creation of PowerChart and Emageon, archived paper
groups. There was a significant difference between the microor-
charts were reviewed.
ganisms found in each group; MRSA, P. aeruginosa, Klebsiella,
Data were collected via a retrospective hospital chart review
Mycobacterium, Streptococcus, and unknown fast-growing infec-
using the above databases. Patients without a primary lung infec-
tions were more common in lung cancer and obstructive disease
tious microorganism confirmed by reliable culture were placed
than in hematologic malignancies (9.1% to 3.0%, 18.2% to
into 2 groups based on presentation and speed of cavitation from
6.1%, 4.5% to 3.0%, 13.6% to 0, 9.1% to 0, and 13.6% to
the onset of symptoms, with 7 days being the cutoff. For this
12.1%, respectively). Conversely, Aspergillus, Nocardia, slow-
study, neutropenia was defined as an absolute neutrophil count
growing unknown infections, and other rare infections were more
(ANC) of less than 500/μL. Also, lesion size was distinguished
common in hematologic malignancies than in lung disease
between small and large with the cutoff as 2 cm, the size deter-
(15.2% to 13.6%, 6.1% to 4.5%, 24.2% to 4.5%, and 21.2% to
mined to qualify as an abscess.
13.6%, respectively). The most common infections in the other
For demographic, descriptive, and clinical data, standard de-
malignancies group were unknown fast-growing (44.4%), Myco-
scriptive statistics were used. For comparisons between groups
bacterium (22.2%), and P. aeruginosa, Klebsiella, and rare infec-
involving nominal data, χ2 tests were used. One-way analysis of
tion (all 11.1%).
variance tests were performed for comparisons between multiple
Neutropenia at the time of NP was observed in 15 (45%) of
groups with numerical data. P < 0.05 was considered statistically
the HM patients, and 1 (9%) of the other solid organ cancer pa-
significant where appropriate.
tients, which was statistically significant. Because almost all the
neutropenic patients were in the HM group, the summary statistics
RESULTS were very similar to the overall population described earlier. The
difference between the groups in speed of progression to NP from
Population Description onset was not statistically significant; however, other malignancy
had the most rapidly growing infections (5.3 ± 6.7 days), followed
A total of 65 cases of NP in cancer patients were found dur-
by lung cancer (14.2 ± 14.3 days), then HM infections (19.0 ±
ing the retrospective chart review. The average age at NP diagno-
32.4 days) were the slowest. There was a significant difference
sis was 54 ± 15 years (range, 22–81 years), and the population was
in hospitalization length, with HM patients hospitalized the lon-
predominantly white with slightly more males than females. Of
gest (21.7 ± 15.6 days), followed by lung (13.7 ± 10.7 days) and
the 65 cases, 44 (68%) had positive cultures for 1 or more organ-
then closely by other (10.9 ± 7.2 days).
isms. The most common were Aspergillus (n = 7), S. aureus and
Regarding CT lesions, there was a significant difference in
MRSA (methicillin-resistant S. aureus) (n = 5), P. aeruginosa
size and placement between the groups with HM and lung groups
(n = 7), Klebsiella (n = 3), various types of mycobacteria
having more lesions greater than 2 cm and other relatively equal,
(n = 7), Nocardia (n = 3), and Streptococcus (n = 3).
and with HM lesions predominantly bilateral where lung and other
The most common preexisting conditions prior to NP diag-
cancer lesions were predominantly in the upper right lobe.
nosis were leukemia (26%; primarily acute myeloid leukemia
Presenting symptoms differed significantly between the
[AML], 21%), cancer of lung origin (18%), other obstructive lung
groups, with HM cases more likely to present with fever and then
disease: chronic obstructive pulmonary disease/emphysema/
cough and weight loss versus lung cases where cough and fever
bronchiectasis) (22%), lymphoma (16%), and metastatic cancers
were equally likely and more hemoptysis was observed. Prophy-
of nonlung, nonhematologic origin (15%).
lactic coverage differed greatly between the groups. Cases of
Neutropenia at the time of NP was found in 16 cases (25%),
HM were significantly more likely to have coverage over the cul-
with an average length of neutropenia of 47.2 (±99.3) days
tured microorganism (39%), compared with lung cases (10%) and
and an average time between onset of neutropenia and NP diagno-
other malignancy (0%).
sis of 15.0 (±20.6) days. The average white blood cell count
Lastly, there was also a significant difference between the
and ANC for those patients were 0.20 cells/uL (±0.14) and
clinical outcomes between the groups. Cases of HM had signifi-
0.82 cells/uL (±0.62), respectively. Computed tomography lesions
cantly more deaths due to both respiratory failure and other causes
were predominantly greater than 2 cm (57%) and located in the
(18% and 12%, respectively) compared with lung cases (5% and
upper right lobe (32%) or bilaterally (23%).
0%, respectively), and other malignancy had no deaths as of last
The most prevalent presenting symptoms on either hospital
follow-up. Hospice discharge, however, was more common in
admission or infectious disease consultation were fever (60%) and
lung cases (27%) than HM (12%) and other (0).
cough (40%); however, other constitutional symptoms were re-
ported. The average time between onset of symptoms or admission
to NP diagnosis was 15.4 (±25.1) days, and the average longest hos- Analysis by Microorganism
pitalization for NP was 17.6 (±13.6) days. A total of 15 patients The same data were broken down according to the microor-
(23%) were on prophylactic antibiotic treatment prior to their NP, ganism causing the primary lung infection leading to the NP.
which had coverage for the microorganisms that were ultimately There was no significant difference between the ages of all the
found on culture. All patients were treated with antibiotics and/or groups. Different organisms were found in neutropenic versus
antifungals for their cultured or assumed microorganism subse- nonneutropenic patients. A significantly greater proportion of
quent to their diagnosis. The overall outcomes were 41 patients neutropenics were found to be infected by Klebsiella (1, 100%),

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Infectious Diseases in Clinical Practice • Volume 23, Number 2, March 2015
unknown slow-growing bacteria (7, 62%), mycobacteria (1, 50%),
and Aspergillus (3, 43%) than in MRSA (1, 33%), unknown fast-
growing infections (2, 20%), P. aeruginosa, and Nocardia (all
0 cases). Of the groups that contained more than 1 patient, there
was a significant difference between the average length of neutro-
penia between the groups: Aspergillus (32.3 ± 2.1 days) and un-
known slow infections (24.9 ± 24.9 days) were significantly
greater than unknown fast infections (15.0 ± 1.4 days). There
was no significant difference between the groups regarding the
amount of time between the start of neutropenia and the NP diag-
nosis. The white blood cell count was significantly lower for
Aspergillus, both unknown groups and rare infections, Klebsiella,
MRSA, and Mycobacterium; however, there was no difference be-
tween groups in ANC.
The association between infecting microorganism and speed of
progression to NP was not significant (P = 0.11); however Klebsiella,
MRSA, P. aeruginosa, unknown fast infections, and other rare infec-
tions were faster to necrotize than Aspergillus, Mycobacterium avium
complex (MAC), Nocardia, Mycobacterium, multiorganism, and un-
known slow infections. Also, there was no significant difference in
hospitalization time between the groups.
Lesion size was significantly different between the groups
with Nocardia and unknown slow infections more likely to be
greater than 2 cm, Aspergillus, MRSA, mycobacteria, P. aeruginosa,
rare infections, unknown fast and multiorganism infections about
equal proportion large and small, and Klebsiella and MAC having
predominantly less-than-2-cm lesions. However, there was no signif-
icant difference between groups in the location of the lesions.
There was a significant association between type of microor-
ganism and whether prophylactic antibiotics given covered it with
Klebsiella, MRSA, and Nocardia more likely to be covered than
Aspergillus, MAC, Mycobacterium, P. aeruginosa, rare infections,
and multiorganism infections. Finally, there was a significant dif-
ference in clinical outcomes between the groups with Nocardia,
MRSA, and the unknown microorganism infections more likely
to have death or hospice discharge.
DISCUSSION
NP in Lung Cancer and Obstructive Lung Disease
Patients with lung cancer are at a greater risk for developing
pneumonia because of the tumor obstructing the airway along
with comorbidity with other obstructive lung diseases such as
chronic obstructive pulmonary disease.8 Postobstructive pneumo-
nia after time, especially in the immune-compromised patient
such as a cancer patient on chemotherapy, can become necrotiz-
ing; previous studies demonstrated the most common initial path-
ogens in this scenario to be P. aeruginosa, S. aureus and MRSA,
upper respiratory anaerobes, and other gram-negative bacilli.1,4,6,8
This study found similar results with the exception of a few Myco-
bacterium cases seen in lung cancer patients. One study had found
MAC in lung cancer patients seen affecting primarily distal airways.9
The nonsignificance in progression to a necrotizing lesion
between the lung cancer group and others can be attributed to
the small sample size and large scatter within groups, although
the means did appear as expected, with the lung cancer patients
progressing more rapidly than do patients with hematologic ma-
lignancies. The differences observed in survival between NP in
lung cancer versus HM, with HM being significantly greater,
can most likely be attributed to the cancer condition itself and as-
sociated confounding variables rather than just the inciting micro-
organisms being more virulent.
Approximately 3 times as many MRSA and P. aeruginosa
cases were seen in lung cancer than HM groups with these
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Necrotizing Pneumonia in Cancer Patients
microorganisms necrotizing the lung tissue faster than others
and having worse outcomes. Necrotizing pneumonia due to
MRSA is often severe and can be fatal.6 The data demonstrated
that MRSA, along with Nocardia and unknown infections, were
more likely to result in either death or hospice discharge.
Community-acquired MRSA has the capacity to produce a wide
variety of virulence factors, notably Panton-Valentine leukocidin,
which has a mortality rate up to 75% despite treatment.6 However,
the scope of this study did not encompass examining effects of viru-
lence factors or cytotoxins produced by the different microorganisms.
Likewise, P. aeruginosa is also common for an early, virulent
NP infection.8,10 Although most of the P. aeruginosa cases were
seen in the lung cancer group, 2 cases in this study resulted in
P. aeruginosa infection via septic emboli from P. aeruginosa bac-
teremia. One proposed mechanism of NP by P. aeruginosa is the
production of exoenzyme A, which was shown to damage bron-
chial endothelium, type 1 pneumocytes, and capillary endothelial
cells.10 Treatment for these aforementioned initial pathogens seen
commonly in obstructive lung cancer is antimicrobials covering
the intended pathogen over a course of 6 weeks to 3 months, de-
pending on progression and mitigation of the obstruction via che-
motherapy, radiation, or resection.8
NP in Hematologic Malignancy
Dysregulation of immune system function predisposed HM
patients to lung infections.7,8 Almost all cases of neutropenia asso-
ciated with NP were in the HM group; depending on the stage of
neutropenia, different pathogens must be considered. Short-term
neutropenia (less than a week) presents with similar etiology that
was discussed with the fast-acting virulent pathogens common
in lung cancer.8 However, prolonged neutropenia increases the
probability of molds causing the NP.
The HM patients were the slowest to show a necrotizing le-
sion and had significantly more Aspergillus, Nocardia, and other
rare infections, which capitalized on weakened immunity. In this
study, the HM cases also tended to present with larger necrotizing
lesions on CT, because of the relatively large amount of Aspergil-
lus cases with central necrosis. Because of the fact that many were
seen for BMT consultation, these patients were much more likely
than lung cancer and other cancer to receive prophylactic coverage
of antibiotics, which ended up covering their ultimately diagnosed
pathogen. However, as mentioned earlier, outcomes were still sig-
nificantly worse because of higher levels of immune dysfunction.
Prolonged neutropenia increases the risk for the most common
NP-inducing Aspergillus species, Aspergillus fumigatus. These in-
fections were seen to take a significantly longer time to necrose
from the initial onset of pneumonia symptoms. Again, these
showed on CT as larger lesions.
These cavitary infiltrates can also be caused, albeit less com-
monly, by Nocardia and Mycobacterium species.7,8 Nocardia and
mycobacteria were likewise demonstrated to be slow growing as
Aspergillus. Nocardia did have worse outcomes than Aspergillus
or Mycobacterium; however, when the groups were split by micro-
organisms, there were very few in each group.
NP by Other Rare Infections and in Nonlung Solid
Organ Cancers
The other rare infectious agents were those in the study, which
had only 1 patient and included Rhodococcus, Acinetobacter,
Prevotella, Scedosporium, Paelomyces, Strenotrophomonas, Cryp-
tococcus, Mycobacterium tuberculosis, Bacteroides, Fusobacterium,
Morganella, Cupriavidus, and viral (parainfluenza 3 and Haemophilus
influenzae). They were predominantly seen in HM. Opportunistic
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Yacoub et al Infectious Diseases in Clinical Practice • Volume 23, Number 2, March 2015
infections that would not normally cause NP can be seen in immune-
compromised patients such as HM, especially with BMT.4,8
The group of patients with nonlung solid organ cancers in
this study was likewise a disjointed group without many signifi-
cant deviations, falling between lung cancer and HM in many pa-
rameters. The most common pathogens seen in these cancers were
either unidentified or Mycobacterium.
NP in Cancer Patients With Undetermined Etiology
A total of 21 of the 65 patients in this study had no positive
cultures but were included in order to increase the sample size
and to examine their characteristics in light of all the other pa-
tients. The 2 groups were separated into slow and fast growing
based on the time between the onset of symptoms and the first
NP lesion on CT. The fast-growing NP group was similar to the
other virulent and fast-progressing pathogens such as MRSA, P.
aeruginosa, and Klebsiella. There were significantly fewer neu-
tropenic patients than in those in the slow growing. Contrarily,
the group with slow-growing organisms shared similarities with
HM pathogens such as Aspergillus. However, there was no signif-
icant difference between the 2 groups in clinic outcomes, probably
because of the limited number of patients in each group.
The first, and perhaps the most important, aspect of treat-
ment is the need for rapid institution of appropriate antibiotic ther-
apy.11 For health care–associated MRSA or community-acquired
MRSA pneumonia, intravenous vancomycin or linezolid 600 mg
orally/intravenously twice daily or clindamycin 600 mg orally/
intravenously 3 times daily, if the strain is susceptible, is recom-
mended for 7 to 21 days, depending on the extent of infection.12
In hospital-acquired pneumonia caused by gram-negative
rods with no risk factors for multidrug resistance, antibiotics such
as levofloxacin, moxifloxacin or ceftriaxone, or ampicillin/
sulbactam or ertapenem should be instituted.13 In patients with
risk factors for multidrug resistance, broad-spectrum antibiotics
such as cefepime, ceftazidime or imipenem, meropenem or
piperacillin-tazobactam + or ciprofloxacin, levofloxacin or genta-
micin, tobramycin, or amikacin +/− vancomycin or linezolid.13
In K. pneumonia, carbapenemase tigecycline and colistin can
be instituted14,15
With aspergillosis, the most compelling data come from
large, randomized trials showing superiority of posaconazole
compared with fluconazole or itraconazole in preventing invasive
aspergillosis in neutropenic patients.16 Voriconazole showed a
survival advantage over amphotericin B in patients with HM with
prolonged neutropenia.16 Clinicians can also institute lipid formu-
lation amphotericin and combination therapy.
CONCLUSIONS
We found that HM patients with NP had a higher mortality
and more opportunistic and slow-growing organisms when com-
pared with cancer patients with lung disease or other solid tumors.
Further study is needed to determine the role that neutropenia, du-
ration of illness, and isolated pathogen play in the treatment of
cancer patients with NP.
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REFERENCES
1. Tzeng DZ, Markman M, Hardin K. Necrotizing pneumonia and
pulmonary gangrene: difficulty in diagnosis, evaluation, and treatment.
Clin Pulm Med. 2007;14(3):166–170.
2. Gadkowski LB, Stout JE. Cavitary pulmonary disease. Clin Microbiol
Rev. 2008;21(2):305–333.
3. Long S. Necrotizing pneumonia and lung abscess. In: Principles and
Practice of Pediatric Disease. 3rd ed. Churchill Livingstone; 2009.
4. Poole PS, Stark HE, Stark P. Necrotizing pneumonia, pulmonary abscess,
and lung gangrene: multiple pathways to lung parenchymal destruction.
Contemp Diagn Radiol. 2011;34(13):1–6.
5. Muto H, Kaneko S, Machino T, et al. Quinupristin/dalfopristin and
voriconazole controlled Staphylococcus epidermidis pneumonia and
chronic necrotizing aspergillosis in a patient with severe lung degradation
consequent to multiple treatments for Hodgkin’s lymphoma. J Infect
Chemother. 2006;12(6):391–395,
6. Jung N, Lehmann C, Hellmann M, et al. Necrotizing pneumonia caused
by Panton-Valentine leucocidin-producing Staphylococcus aureus
originating from a Bartholin’s abscess. Infect Dis Obstet Gynecol. 2008;
2008:491401.
7. Sawicki GS, Lu FL, Valim C, et al. Necrotising pneumonia is an
increasingly detected complication of pneumonia in children. Eur Respir J.
2008;31(6):1285–1291.
8. Akinosoglou KS, Karkoulias K, Marangos M. Infectious complications in
patients with lung cancer. Eur Rev Med Pharmacol Sci. 2013;17(1):8–18.
9. Lande L, Peterson DD, Gogoi R, et al. Association between pulmonary
Mycobacterium avium cellulare infection and lung cancer. J Thorac Oncol.
2012;7(9):1345–1351.
10. Woods DE, Hwang WS, Sharhabadi MS, et al. Alteration of pulmonary
structure by Pseudomonas aeruginosa exoenzyme S. J Med Microbiol.
1988;26(2):133–141.
11. Rubinstein E, Kollef MH, Nathwani D. Pneumonia caused by
methicillin-resistant Staphylococcus aureus. Clin Infect Dis. 2008;46(5):
S378–S385.
12. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the
Infectious Diseases Society of America for the treatment of
methicillin-resistant Staphylococcus aureus infections in adults and
children. Clin Infect Dis. 2011;52(3):e18–e55.
13. Kollef MH, Morrow LE, Baughman RP, et al. Health care–associated
pneumonia (HCAP): a critical appraisal to improve identification,
management, and outcomes—proceedings of the HCAP Summit. Clin
Infect Dis. 2008;46(suppl 4):S296–S334; quiz 335–338.
14. Deresinski SC, Schirmer P. Management of infections due to
KPC-producing Klebsiella pneumoniae. F1000 Med Rep. 2009;1.pii:79.
15. Daly MW, Riddle DJ, Ledeboer NA, et al. Tigecycline for treatment of
pneumonia and empyema caused by carbapenemase-producing Klebsiella
pneumoniae. Pharmacotherapy. 2007;27(7):1052–1057.
16. Limper AH, Knox KS, Sarosi GA, et al. An official American
Thoracic Society statement: treatment of fungal infections in adult
pulmonary and critical care patients. Am J Respir Crit Care Med.
2011;183(1):96–128.
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