Pneumonia In Immunocompromised Hosts Research Articles

Diagnostic Approach to Pneumonia in Immunocompromised Hosts.

In immunocompromised patients, pneumonia presents a diagnostic challenge due to diverse etiologies, nonspecific symptoms, overlapping radiological presentation, frequent co-infections, and the potential for rapid progression to severe disease. Thus, timely and accurate diagnosis of all pathogens is crucial. This narrative review explores the latest advancements in microbiological diagnostic techniques for pneumonia in immunocompromised patients. It covers major available microbiological tools for diagnosing both community-acquired and hospital-acquired pneumonia, encompassing a wide spectrum of pathogens including bacterial, viral, fungal, and parasitic. While traditional culture methods remain pivotal in identifying many pneumonia-causing etiologies, their limitations in sensitivity and time to results have led to the rise of non-invasive antigen tests and molecular diagnostics. These are increasingly employed alongside cultures and microscopy for more efficient diagnosis, mainly in viral and fungal infections. Lastly, we report the future of pneumonia diagnostics, exploring the potential of metagenomics and CRISPR/Cas13a for more precise and rapid pathogen detection in immunocompromised populations.

Next-Generation Sequencing of Microbial Cell-Free DNA to Rapidly Detect Fluoribacter Bozemanae Pneumonia in an Immunocompromised Host

Background: Fluoribacter bozemanae is an uncommon pathogen that accounts for just 3-5% of cases of pneumonia caused by the different Legionella species. The mortality rate has been reported to be up to 40%. This organism is difficult to identify, making diagnosis extremely challenging with current diagnostic modalities. Case Report: We present a case of a 75-year-old female with a history of multiple myeloma undergoing active treatment with immunosuppressive agents who presented with confusion, hypoxemic respiratory failure and sepsis. Her initial presentation was consistent with Legionella infection, however, all routine testing including a Legionella urine antigen test came back negative. A CT scan of the chest was completed which showed near complete left lower lobe consolidation concerning for pneumonia. An infectious workup was initiated. Atypical and viral pneumonia polymerase chain reaction panel was negative. Microbial cell-free DNA sequencing returned positive for Fluoribacter bozemanae, a subspecies of the Legionellaceae family that is known to cause severe pneumonia in immunocompromised hosts. This information allowed a therapy adjustment resulting in rapid improvement of our patient’s symptoms. Conclusion: In cases such as this one, the diagnosis of Legionella species is often missed due to the many challenges associated with the different testing modalities. In these circumstances, next-generation genetic sequencing can be extremely useful. Now with the increasing availability of next-generation sequencing as a microbiological diagnostic tool, we can diagnose many more infections that once would have gone undiagnosed and either untreated or delayed in treatment.

Community-Acquired Pneumonia in the Immunocompromised Host: Epidemiology and Outcomes.

The epidemiology and outcomes of community-acquired pneumonia (CAP) in immunocompromised hosts (ICHs) are not well defined. The objective of this study was to define the epidemiology and outcomes of CAP in ICHs as compared with non-ICHs. This ancillary study included a prospective cohort of hospitalized adult Louisville residents with CAP from 1 June 2014 to 31 May 2016. An ICH was defined per the criteria of the Centers for Disease Control and Prevention. Geospatial epidemiology explored associations between ICHs hospitalized with CAP and income level, race, and age. Mortality for ICHs and non-ICHs was evaluated during hospitalization and 30 days, 6 months, and 1 year after hospitalization. A total of 761 (10%) ICHs were identified among 7449 patients hospitalized with CAP. The most common immunocompromising medical conditions or treatments were advanced-stage cancer (53%), cancer chemotherapy (23%), and corticosteroid use (20%). Clusters of ICHs hospitalized with CAP were found in areas associated with low-income and Black or African American populations. Mortality by time point for ICHs vs non-ICHs was as follows: hospitalization, 9% vs 5%; 30 days, 24% vs 11%; 6 months, 44% vs 21%; and 1 year, 53% vs 27%, respectively. Approximately 1 in 10 hospitalized patients with CAP is immunocompromised, with advanced-stage cancer being the most frequent immunocompromising condition, as seen in half of all patients who are immunocompromised. Risk for hospitalization may be influenced by socioeconomic disparities and/or race. ICHs have a 2-fold increase in mortality as compared with non-ICHs.

Nocardia pseudobrasiliensis Co-infection in SARS-CoV-2 Patients.

During the SARS-CoV-2 pandemic, few cases of Nocar-dia spp. co-infection have been reported during or after a COVID-19 infection. Nocardia spp. are gram-positive aerobic actinomycetes that stain partially acid-fast, can infect immunocompromised patients, and may cause dis-seminated disease. We report the case of a 52-year-old immunocompromised man who had Nocardia pseudobrasiliensis pneumonia develop after a SARS-CoV-2 in-fection. We also summarize the literature for no-cardiosis and SARS-CoV-2 co-infections. Nocardia spp. infection should remain a part of the differential diagnosis for pneumonia in immunocompromised hosts, regardless of other co-infections. Sulfonamide/carbapenem combina-tions are used as empiric therapy for nocardiosis; species identification and susceptibility testing are required to se-lect the optimal treatment for each patient.

Cell Fusion May Be Involved in the Homothallic Mating of Pneumocystis Species.

ABSTRACTPneumocystis species are obligate fungal biotrophs that colonize the lungs of mammals. They cause deadly pneumonia in immunocompromised hosts. The sexual phase seems obligate during their life cycle and essential for survival because it is believed to ensure proliferation and transmission between hosts. Here, we consider if the sexual phase is initiated by the fusion of two cells or by nucleus duplication in order to generate diploid cells that can undergo meiosis. The juxtaposition of the nucleus-associated organelles of pairs of cells with fused cytoplasmic membranes demonstrated that cell fusion can occur. Nevertheless, the frequency of cell fusion remains to be determined, and it cannot be excluded that both cell fusion and nucleus duplication are used to ensure the occurrence of the essential sexual phase. In vitro culturing of these fungi is a major milestone that could clarify the issue.

1065. Efficacy of Cefiderocol in Experimental Stenotrophomonas maltophilia Pneumonia in Persistently Neutropenic Rabbits

Background Stenotrophomonas maltophilia causes lethal pneumonia, bacteremia, and sepsis in immunocompromised patients. As a standard of care, trimethoprim-sulfamethoxazole (T/S) is considered to be the first-line therapy for Stenotrophomonas pneumonia. Cefiderocol (CFDC) is a new parenteral siderophore cephalosporin that is transported through the outer cell membrane as a siderophore mimic that then inhibits Gram-negative cell wall biosynthesis. CFDC has potent activity in vitro against S. maltophilia; however, little is known about its in vivo activity against Stenotrophomonas pneumonia in immunocompromised hosts. We therefore studied CFDC in comparison to TS in the persistently neutropenic rabbit model of Stenotrophomonas pneumonia. This rabbit model, in contrast to conventional murine models, reflects the human pattern of infection more accurately over time.MethodsWe initially studied the plasma pharmacokinetics of CFDC in non-infected and infected animals. Stenotrophomonas pneumonia was established by direct endotracheal inoculation of S. maltophilia 1×1010 CFUs for tracheobronchial colonization that evolved into bronchopneumonia. Experimental groups consisted of CFDC, T/S, and untreated controls (UC). Rabbits received CFDC at 120 mg/kg IV Q8h and T/S at 5 mg/kg IV Q12h. Profound persistent neutropenia was maintained with cytosine arabinoside. Treatment was continued for 10 days.ResultsThere were no significant differences between non-infected and infected rabbits in CFDC pharmacokinetics. Rabbits treated with CFDC and T/S demonstrated significant decreases of residual pulmonary and BAL bacterial burden vs UC (p≤0.001). CFDC achieved full clearance of S. maltophilia from lung tissue and BAL. This antibacterial activity coincided with significant reduction of lung weights (marker of organism-mediated pulmonary injury) in the CFDC group vs T/S and UC (p< 0.01). Survival was prolonged in the CFDC treatment group with 87% survival in comparison to that of T/S (25%) and UC (0%) (p< 0.01). Table 1. Efficacy of Cefiderocol in Experimental Stenotrophomonas maltophilia Pneumonia in Persistency Neutropenic Rabbits ConclusionCefiderocol is highly active in treatment of experimental S. maltophilia pneumonia in persistently neutropenic rabbits, thus laying the foundation for future clinical investigations against this lethal infection. Disclosures Naoki Ishibashi, MD, Shionogi, Inc. (Employee) Benjamin Georgiades, n/a, Shionogi, Inc. (Consultant) Roger Echols, MD, Shionogi (Consultant) Robert A. Bonomo, MD, entasis (Research Grant or Support)Merck (Grant/Research Support)NIH (Grant/Research Support)VA Merit Award (Grant/Research Support)VenatoRx (Grant/Research Support) Yoshinori Yamano, PhD, Shionogi (Employee) Thomas J. Walsh, MD, PhD (hon), Scynexis (Consultant, Grant/Research Support)Shionogi (Consultant, Grant/Research Support)

Pneumocystis jirovecii genetic diversity in a Spanish tertiary hospital.

A newly described MLST scheme aims at providing a standardized tool to study and compare Pneumocystis jirovecii epidemiology. A high diversity among P. jirovecii isolates from patients in Barcelona, Spain, and a potential association between specific STs and infection/colonization were identified.

Increased sensitivity of a new commercial reverse transcriptase-quantitative PCR for the detection of Pneumocystis jirovecii in respiratory specimens

The fungus Pneumocystis needs to be detected early in respiratory samples to prevent pneumonia in immunocompromised hosts. We evaluated a new commercial RTqPCR on 213 respiratory samples to detect Pneumocystis and found it more sensitive and faster than our routine sensitive in-house qPCR assay.

A co-infection of varicella-zoster virus and Pneumocystis jirovecii in a non-HIV immunocompromised patient: a case report

BackgroundVaricella-zoster virus (VZV) causes herpes zoster. Pneumocystis jirovecii (PJ) also causes pneumonia in immunocompromised hosts. Although both cause opportunistic infections, it is rare to have a co-infection in a non-human immunodeficiency virus carrier.Case presentationAn 84-year-old woman with hemolytic anemia referred because of acute respiratory failure. She had received prednisolone without PJ pneumonia prevention. She developed dyspnea and desaturation while eating, and thus was treated based on a presumptive diagnosis of aspiration pneumonia. Physical examination revealed a vesicular rash on the left side of her neck suggesting herpes zoster infection. Polymerase chain reaction of her sputum for PJ and VZV was positive, which confirmed a diagnosis of pneumonia due to PJ and VZV co-infection. Despite acyclovir and sulfamethoxazole and trimethoprim administration, she died on hospital day 19.ConclusionsClinicians should suspect PJP when patients on systemic corticosteroids develop pneumonia and they have not received prophylactic treatment for PJP in non-HIV carriers. When such patients have a VZV rash, clinicians should aggressively seek signs of opportunistic infections. Our case hereby highlights the importance of recognizing the possibility of a VZV and PJ co-infection.

The trophic life cycle stage of Pneumocystis species induces protective adaptive responses without inflammation-mediated progression to pneumonia.

Pneumocystis species are fungal pathogens that cause pneumonia in immunocompromised hosts. Lung damage during Pneumocystis pneumonia is predominately due to the inflammatory immune response. Pneumocystis species have a biphasic life cycle. Optimal innate immune responses to Pneumocystis species are dependent on stimulation with the cyst life cycle stage. Conversely, the trophic life cycle stage broadly suppresses proinflammatory responses to multiple pathogen-associated molecular patterns (PAMPs), including β-1,3-glucan. Little is known about the contribution of these life cycle stages to the development of protective adaptive responses to Pneumocystis infection. Here we report that CD4+ T cells primed in the presence of trophic forms are sufficient to mediate clearance of trophic forms and cysts. In addition, primary infection with trophic forms is sufficient to prime B-cell memory responses capable of clearing a secondary infection with Pneumocystis following CD4+ T cell depletion. While trophic forms are sufficient for initiation of adaptive immune responses in immunocompetent mice, infection of immunocompromised recombination-activating gene 2 knockout (RAG2-/-) mice with trophic forms in the absence of cysts does not lead to the severe weight loss and infiltration of innate immune cells associated with the development of Pneumocystis pneumonia.

Possible therapeutic effect of orally administered ribavirin for respiratory syncytial virus-induced acute respiratory distress syndrome in an immunocompetent patient: a case report

BackgroundHuman respiratory syncytial virus usually causes self-limiting upper respiratory infection and occasionally causes pneumonia in immunocompromised hosts. Respiratory syncytial virus-induced severe pneumonia or acute respiratory distress syndrome in immunocompetent adults has been rarely described. Unfortunately, optimal treatment has not been established for this potentially fatal condition. We report a case of respiratory syncytial virus-induced acute respiratory distress syndrome occurring in a previously healthy man successfully treated with orally administered ribavirin.Case presentationAn 81-year-old previously healthy Korean man presented with cough, dyspnea, and febrile sensation. He had hypoxemia with diffuse ground glass opacity evident on chest radiography, which progressed and required mechanical ventilation. All microbiological tests were negative except multiplex real-time reverse transcriptase polymerase chain reaction using respiratory specimen, which was positive for human adenovirus. Under the diagnosis of respiratory syncytial virus-induced acute respiratory distress syndrome, orally administered ribavirin was administered and he recuperated completely without complications.ConclusionThis case demonstrates the potential usefulness of orally administered ribavirin as a therapeutic option for severe respiratory syncytial virus infection, at least in an immunocompetent host.

Lung Nodules in a Patient With Recently Resected GI Stromal Tumor (GIST): Beginning of a Confusing Domino Effect

SESSION TITLE: Other Infections SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: With improved diagnostic tools, more pulmonary infections are being identified and pulmonary physicians are facing an ever expanding array of pulmonary pathology cases as a result of such infections. CASE PRESENTATION: A 50-year-old male with GIST resected 2 months ago, presented with dry cough associated with fever, night sweats, myalgias, wheezing. On exam, he had diminished bibasilar breath sounds. CT angiogram chest showed extensive pulmonary nodules with mediastinal and hilar lymphadenopathy (Fig 1-a). Urine streptococcus, legionella and histoplasma antigen, Quantiferon Gold and HIV screen were all negative. Coccidioides titer1:2. ANA and ANCA panel were negative. He underwent fluoroscopically-guided transbronchial biopsy of the lingula. Cytology of lingular wash suggested malignant cells. BAL was also positive for human metapneumovirus (HMPV). PET scan showed no uptake. Thoracoscopy and wedge resection of lingula were performed. The main histopathologic finding was non-necrotizing granulomatous inflammation with bronchiolocentric distribution (Fig 2). DISCUSSION: HMPV pneumonia may explain CT findings of ground-glass attenuation and nodular opacities. Coccidioidomycosis have been reported to manifest spiculated nodules or masses, consolidation, cavitation and lymphadenopathy on CT imaging. While histopathologic findings mimic a lymphangitic distribution, suggesting malignancy, non-necrotizing granulomatous pattern in histopathology strongly suggests pulmonary coccidioidomycosis. Focal organizing pneumonia and incidental organizing thromboembolus were simultaneously identified. This finding can be explained by HMPV pneumonia as it has been reported to cause severe pneumonia in immunocompromised hosts and develop organizing pneumonia. As of last follow up, patient is free of respiratory symptoms while steroid therapy has been tapered. Follow up CT showed near resolution of lung nodules (Fig 1-b). CONCLUSIONS: Two infectious processes, HMPV and Coccidioidomycosis led to a divergent and confusing clinical picture which includes a false alarm of malignancy, and true consequences of granulomatous disease and organizing pneumonia. While diagnosing and treating different pulmonary infections, it is getting ever more important to know and understand the possible mimics (Malignancy in our case) and consequences (Granulomatous disease and Organizing pneumonia in our case) of the infections. Reference #1: Malo J et al. Ann Am Thorac Soc 2014 Reference #2: Samuel S et al. Cancer Control 2016 Reference #3: Franquet T et al. J Comput Assist Tomogr 2005 DISCLOSURE: The following authors have nothing to disclose: Zahia Esber, Edgar Sanchez, Luis Herrera, Rumi Khan No Product/Research Disclosure Information

Pneumocystis jirovecii Pneumonia in Children

Abstract Pneumocystis jirovecii (previously known as Pneumocystis carinii), a yeast-like, atypical fungus, is an important human pathogen especially in the immunocompromised hosts. It primarily causes pneumonia (P. jirovecii pneumonia or PJP), but rarely can infect other extrapulmonary sites, such as lymph nodes, spleen, liver, and bone marrow. Though an early age of colonization/infection has been documented even in healthy children, children with human immunodeficiency virus (HIV) infection, those with immunosuppression secondary to malignancies, cancer chemotherapy, and other immunosuppressive agents, and primary immunodeficiency are the ones primarily affected with the disease. The mode of presentation is variable depending on the underlying disease, immune status, and age of the patient, but clinical features of PJP are largely nonspecific. Though diffuse, perihilar predominant, bilaterally symmetrical interstitial infiltrates with apical sparing is characteristically seen in pulmonary imaging, it is very difficult to differentiate between PJP and other causes of pneumonia in immunocompromised hosts. The growth of the organism being extremely difficult in the laboratory, direct demonstration of the organism or its DNA in pulmonary secretions (induced sputum, bronchoalveolar lavage [BAL], etc.) by either direct stains or polymerase chain reaction (PCR) is the predominant mode of diagnosis. Chemoprophylaxis is indicated for HIV-infected infants and other children with profound immunosuppression. Co-trimoxazole is the drug of choice for both prophylaxis and therapy in children with PJP; pentamidine, atovaquone, dapsone, and clindamycin/primaquine are other alternatives. Following the advent of highly active antiretroviral therapy (HAART) for the treatment of HIV disease and co-trimoxazole prophylaxis, both the incidence of PJP and associated mortality have decreased dramatically in the developing regions. Developing countries still have very high morbidity and mortality with PJP, especially in HIV-infected children.

The life cycle stages of the opportunistic fungal pathogen Pneumocystis murina provoke a differential immune response in antigen-presenting cells

Abstract Pneumocystis species are opportunistic fungal pathogens that cause severe pneumonia in immunocompromised hosts. The life cycle of Pneumocystis species consists of a trophic stage and an ascus-like cystic stage. Our lab has published data demonstrating that cysts stimulate NF-κB translocation in alveolar macrophages, but the trophic form does not. Here, we demonstrate that infection of wild-type adult mice with a normal mixture of trophic and cystic P. murina life forms elicits a more robust innate immune response in the alveolar spaces and lung parenchyma than infection with the trophic form alone. To determine the pattern recognition receptors that bind trophozoites and cysts, we examined expression of C-type lectin receptors on lung CD11c+ dendritic cells in vivo. Infection with a mixture of trophozoites and cysts resulted in the upregulation of dectin-1 and mannose receptor, while infection with trophozoites alone resulted in upregulation of dectin-2, DEC-205 and mannose receptor. In addition, we demonstrate that bone marrow-derived dendritic cells stimulated with a mixture of trophozoites and cysts produced the proinflammatory cytokines IL-1β and IL-6. In contrast, exposure to trophozoites suppressed β-glucan-induced IL-1β, IL-6, and TNFα production by bone marrow-derived dendritic cells. A targeted gene expression assay is being used to evaluate gene expression in dendritic cells following stimulation with trophozoites alone or a mixture of trophozoites and cysts. We propose that trophozoites suppress β-glucan-signaling, but are sufficient for stimulating protective responses in immunocompetent individuals.

Case of Pneumocystis jirovecii pneumonia in a non-AIDS patient

Pneumocystis jirovecii is widely known as an important cause of pneumonia in immunocompromised hosts. It remains a leading cause of opportunistic infection, morbidity and mortality in these patients. Here, a case of severe P. jirovecii pneumonia in a post-renal transplant patient is described. Giemsa and Gomor methenamine silver stain of sputum showed cysts of P. jirovecii. Despite treatment with Trimethoprim- Sulfamethoxazole, the patient developed severe respiratory failure and expired.

The trophic stage of the opportunistic fungal pathogen Pneumocystis murina suppresses β-1,3-glucan-induced cytokine production, but is sufficient for generating protective CD4+ T cell and B cell responses (MPF2P.746)

Abstract Pneumocystis species are opportunistic fungal pathogens that cause severe pneumonia in immunocompromised hosts. The life cycle of Pneumocystis species consists of a trophic stage and ascus-like cysts. Our lab has published data demonstrating that cysts stimulate NF-κB translocation in alveolar macrophages, but the trophic form does not. Here, we demonstrate that bone marrow-derived dendritic cells pulsed with mixed P. murina express more IL-1β and induce greater CD4+ T cell interferon-γ production than bone marrow-derived dendritic cells pulsed with the trophic form alone. Additionally, our data indicate that the trophic form suppresses β-1,3-glucan-induced IL-1β production by bone marrow-derived dendritic cells. β-1,3-glucan is the predominant structural component in the cyst wall, but is not produced by the trophic form. Despite evidence of immunosuppression, our data demonstrate that the trophic form stimulates protective CD4+ T cell and B cell responses. CD4+ T cells transferred from BALB/c donor mice infected with the trophic form alone mediate clearance in RAG2KO host mice infected with either the trophic form or mixed P. murina. Infection with the trophic form generates protective B cell responses that mediate clearance following reinfection with either trophozoites or mixed P. murina. We propose that the trophic stage suppresses β-1,3-glucan-induced cytokine production, but is sufficient for stimulating protective responses in immunocompetent individuals.

Susceptibility to Klebsiella pneumonaie infection in collaborative cross mice is a complex trait controlled by at least three loci acting at different time points.

BackgroundKlebsiella pneumoniae (Kp) is a bacterium causing severe pneumonia in immunocompromised hosts and is often associated with sepsis. With the rise of antibiotic resistant bacteria, there is a need for new effective and affordable control methods; understanding the genetic architecture of susceptibility to Kp will help in their development. We performed the first quantitative trait locus (QTL) mapping study of host susceptibility to Kp infection in immunocompetent Collaborative Cross mice (CC). We challenged 328 mice from 73 CC lines intraperitoneally with 104 colony forming units of Kp strain K2. Survival and body weight were monitored for 15 days post challenge. 48 of the CC lines were genotyped with 170,000 SNPs, with which we mapped QTLs.ResultsCC lines differed significantly (P < 0.05) in mean survival time, between 1 to 15 days post infection, and broad sense heritability was 0.45. Distinct QTL were mapped at specific time points during the challenge. A QTL on chromosome 4 was found only on day 2 post infection, and QTL on chromosomes 8 and 18, only on day 8. By using the sequence variations of the eight inbred strain founders of the CC to refine QTL localization we identify several candidate genes.ConclusionHost susceptibility to Kp is a complex trait, controlled by multiple genetic factors that act sequentially during the course of infection.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-865) contains supplementary material, which is available to authorized users.

Recognition of the cyst life cycle stage induces a robust immune response to the opportunistic fungal pathogen Pneumocystis murina (MPF3P.814)

Abstract Pneumocystis species are opportunistic fungal pathogens that cause severe pneumonia in immunocompromised hosts. The life cycle of Pneumocystis species consists of a vegetative trophic stage and an ascus-like cystic stage. We demonstrate that infection of wild-type adult or neonatal mice with a mixture of trophic and cystic P. murina life forms elicits a more robust CD4+ and CD8+ T cell response than infection with the trophic form alone. β-1,3-glucan is a predominant structural component in the cyst wall, but is not produced by the trophic stage. Depletion of cysts with the β-1,3-glucan synthase inhibitor anidulafungin prevents expansion of the remaining trophic organisms in immunocompromised adult mice. Depletion of cysts in immunocompetent adult mice results in fewer infiltrating CD11b+ cells in the bronchoalveolar lavage fluid. In addition, bone marrow-derived dendritic cells pulsed with mixed P. murina express more IL-1β and induce greater in vitro CD4+ T cell interferon-γ production than cells pulsed with the trophic form alone. Dendritic cells have been previously reported to activate CD4+ T cells in response to Dectin-1 stimulation by purified Pneumocystis β-1,3-glucan. We propose that dendritic cells stimulated by β-1,3-glucan on cystic Pneumocystis direct a robust pro-inflammatory response, while stimulation with the trophic form induces a less exuberant immune response that is sufficient for clearance in immunocompetent individuals.

Human rhinovirus infections of the lower respiratory tract in hematopoietic stem cell transplant recipients

BackgroundHuman rhinoviruses (HRVs) are a common cause of upper respiratory infection (URI) in hematopoietic stem cell transplant (HSCT) recipients; yet, their role in lower respiratory illness is not well understood.MethodsWe performed a retrospective chart review of HSCT recipients with HRV infection from the time molecular detection methods were implemented at our institution in 2008. Factors associated with proven or possible HRV pneumonia at the first HRV detection were evaluated by univariate and multivariate analysis. We then characterized all episodes of proven and possible HRV pneumonia from the initial HRV infection through a 1‐year follow‐up period.ResultsBetween 2008 and 2011, 63 HSCT recipients had ≥1 documented HRV infections. At first HRV detection, 36 (57%) patients had HRV URI and 27 (43%) had proven or possible HRV pneumonia; in multivariate analysis, hypoalbuminemia (odds ratio [OR] 9.5, 95% confidence interval [CI] 1.3–71.7; P = 0.03) and isolation of respiratory co‐pathogen(s) (OR 24.2, 95% CI 2.0–288.4; P = 0.01) were independently associated with pneumonia. During the study period, 22 patients had 25 episodes of proven HRV pneumonia. Fever (60%), cough (92%), sputum production (61%), and dyspnea (60%) were common symptoms. Fifteen (60%) episodes demonstrated bacterial (n = 7), fungal (n = 5), or viral (n = 3) co‐infection. Among the remaining 10 (40%) cases of HRV monoinfection, patients’ oxygen saturations ranged from 80% to 97% on ambient air, and computed tomography scans showed peribronchiolar, patchy, ground glass infiltrates.Conclusions HRV pneumonia is relatively common after HSCT and frequently accompanied by bacterial co‐infection. As use of molecular assays for respiratory viral diagnosis becomes widespread, HRV will be increasingly recognized as a significant cause of pneumonia in immunocompromised hosts.

&lt;i&gt;Bacillus cereus&lt;/i&gt; Necrotizing Pneumonia in a Patient with Nephrotic Syndrome

Bacillus cereus (B. cereus) is a Gram-positive rod that is widely distributed in the environment and can be a cause of food poisoning. We herein present a case of B. cereus necrotizing pneumonia in a patient with nephrotic syndrome under corticosteroid treatment after developing transient gastroenteritis symptoms. B. cereus was isolated from bronchial lavage fluid and transbronchial biopsy specimens. A multiplex polymerase chain reaction analysis of the toxin genes revealed a strain possessing enterotoxicity. The patient recovered after one week of intravenous meropenem followed by a combination of oral moxifloxacin and clindamycin. B. cereus is a pathogen that causes necrotizing pneumonia in immunocompromised hosts.