Retrospective review of febrile neutropenia in the Royal Darwin Hospital, 1994–99

Healey, Tabitha; Selva-Nayagam, Sid

doi:10.1046/j.1445-5994.2001.00095.x

Cited by 11 publications

(13 citation statements)

References 15 publications

(21 reference statements)

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“…One study from Malaysia reported that 66% of FN in their cancer patients receiving chemotherapy was due to GN organisms. [1,4,5,6,7] The finding from this audit is similar to those in other developed countries including one from Darwin in Australia, [8] where most of the isolated organisms are gram positive cocci. And majority of these are coagulase negative staphylococci.…”

Section: Discussionsupporting

confidence: 71%

Bacteremia Pattern in Febrile Neutropenia among Adults Cancer Patients Receiving Chemotherapy in an Australia Regional Hospital

Ibrahim¹,

Pang²

2017

ujph

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Background: Febrile neutropenia (FN) remains one of the most concerning complications of cancer chemotherapy, and is a major cause of morbidity and mortality, consuming significant healthcare resource .This audit was carried out to determine the pattern of microbial pathogens responsible for FN in our institution as this will result in the appropriate choice of empirical antibiotic(s) for treatment of FN in the future. Methods: This is a retrospective audit of adult patients with cancer admitted with FN post chemotherapy in Goulburn valley base hospital, Shepparton, Australia between 2011-2013.Only patients who met the diagnostic criteria of FN as defined by the Infectious diseases society of America (IDSA) were included in the audit. Results: Twenty six patients presented with 31 episodes of FN between January 2013 and January 2014. 65 blood cultures (BC) were obtained with an average of 2.5 sets of BC per patients, 10.8% of these were positive. 66.7% of the BC yielded Gram Positive Cocci (GPC) (50% of which were coagulase positive staphylococci), 33.7% of the BC yielded gram negative bacilli (GNB) and 2 yielded multiple organisms. The mean neutrophil count on admission for all the 26 patients was 0.303 ± 0.25/ul. Those with positive BCs had significantly higher hs-CRP with the mean value of 223.83±94.27 mg/l, compared to those with negative BCs with 89.37±79.53 mg/l (t-test = -3.489, p=0.002).The most common malignancies were hematological and breast cancers with 8 patients each. The presumed focus of infection was mostly in the respiratory tract accounting for 42% of the cases. 30.8% of the 26 patients with FN had central venous access device(CVAD) in-situ but all had negative BCs however the odd ratio of developing FN if CVAD is present is high at 4.3(95% CI 1.01-18.0). Conclusions: the prevalence rate of bacteremia in post chemotherapy FN in our center is relatively low and GPC are the most commonly isolated organisms. Our study also support the notion that hs-CRP may be a sensitive biomaker of bacterial infection in cancer patients with post chemotherapy FN as it is significantly

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Section: Discussionsupporting

confidence: 71%

Bacteremia Pattern in Febrile Neutropenia among Adults Cancer Patients Receiving Chemotherapy in an Australia Regional Hospital

Ibrahim¹,

Pang²

2017

ujph

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“…Similar defects in neutrophil function have also been observed with other co-morbidities, such as increased alcohol consumption, renal failure and thalassemia [6], [50]–[52]. Increased incidence of melioidosis is also noted in neutropenic patients [53], [54], as well as patients with chronic granulomatous disease [55], [56]. Interestingly, the neutrophil-differentiating cytokine granulocyte colony-stimulating factor (G-CSF) has been used as a treatment for melioidosis, with mixed results; it is reported to reduce mortality of melioidosis patients in Australia [57], but is only associated with prolonged survival in Thailand patients [58].…”

Section: Introductionsupporting

confidence: 56%

Delineating the Importance of Serum Opsonins and the Bacterial Capsule in Affecting the Uptake and Killing of Burkholderia pseudomallei by Murine Neutrophils and Macrophages

et al. 2014

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Infection of susceptible hosts by the encapsulated Gram-negative bacterium Burkholderia pseudomallei (Bp) causes melioidosis, with septic patients attaining mortality rates ≥40%. Due to its high infectivity through inhalation and limited effective therapies, Bp is considered a potential bioweapon. Thus, there is great interest in identifying immune effectors that effectively kill Bp. Our goal is to compare the relative abilities of murine macrophages and neutrophils to clear Bp, as well as determine the importance of serum opsonins and bacterial capsule. Our findings indicate that murine macrophages and neutrophils are inherently unable to clear either unopsonized Bp or the relatively-avirulent acapsular bacterium B. thailandensis (Bt). Opsonization of Bp and Bt with complement or pathogen-specific antibodies increases macrophage-uptake, but does not promote clearance, although antibody-binding enhances complement deposition. In contrast, complement opsonization of Bp and Bt causes enhanced uptake and killing by neutrophils, which is linked with rapid ROS induction against bacteria exhibiting a threshold level of complement deposition. Addition of bacteria-specific antibodies enhances complement deposition, but antibody-binding alone cannot elicit neutrophil clearance. Bp capsule provides some resistance to complement deposition, but is not anti-phagocytic or protective against reactive oxygen species (ROS)-killing. Macrophages were observed to efficiently clear Bp only after pre-activation with IFNγ, which is independent of serum- and/or antibody-opsonization. These studies indicate that antibody-enhanced complement activation is sufficient for neutrophil-clearance of Bp, whereas macrophages are ineffective at clearing serum-opsonized Bp unless pre-activated with IFNγ. This suggests that effective immune therapies would need to elicit both antibodies and Th1-adaptive responses for successful prevention/eradication of melioidosis.

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“…A recent study conversely indicated that neutrophil recruitment during melioidosis may be detrimental in controlling bacterial numbers and host survival, and suggested monocytes may be important to limit B. pseudomallei infection [71]. There is indirect evidence that neutrophils may play a role in controlling melioidosis infection through correlative findings based on cellular recruitment to the infection site, predisposing conditions, and adjunctive therapies; however any protective properties have not been clearly confirmed to be attributable to neutrophils [44], [45], [46], [47], [48], [49], [50], [51], [52], [53], [54]. Notably, in vitro studies to delineate the relative abilities of neutrophils to kill B. pseudomallei have provided conflicting results [45], [55], [56], [57].…”

Section: Discussionmentioning

confidence: 99%

“…mice lacking NADPH oxidase, an important enzyme in the generation of the microbicidal respiratory burst primarily utilized by neutrophils, are more susceptible to B. pseudomallei infection [43], iv. diabetes mellitus, which is the primary predisposing condition for melioidosis, is associated with impaired neutrophil function [44], [45], [46], [47], v. neutropenic individuals are more susceptible to B. pseudomallei infection and development of fatal disease [48], [49] and, vi. granulocyte colony-stimulating factor (G-CSF), which stimulates neutrophil differentiation, prolongs the survival of melioidosis patients, though a direct link to enhanced neutrophil function has not been proven [50], [51], [52], [53], [54].…”

Section: Introductionmentioning

confidence: 99%

Capsule Influences the Deposition of Critical Complement C3 Levels Required for the Killing of Burkholderia pseudomallei via NADPH-Oxidase Induction by Human Neutrophils

2012

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Burkholderia pseudomallei is the causative agent of melioidosis and is a major mediator of sepsis in its endemic areas. Because of the low LD50 via aerosols and resistance to multiple antibiotics, it is considered a Tier 1 select agent by the CDC and APHIS. B. pseudomallei is an encapsulated bacterium that can infect, multiply, and persist within a variety of host cell types. In vivo studies suggest that macrophages and neutrophils are important for controlling B. pseudomallei infections, however few details are known regarding how neutrophils respond to these bacteria. Our goal is to describe the capacity of human neutrophils to control highly virulent B. pseudomallei compared to the relatively avirulent, acapsular B. thailandensis using in vitro analyses. B. thailandensis was more readily phagocytosed than B. pseudomallei, but both displayed similar rates of persistence within neutrophils, indicating they possess similar inherent abilities to escape neutrophil clearance. Serum opsonization studies showed that both were resistant to direct killing by complement, although B. thailandensis acquired significantly more C3 on its surface than B. pseudomallei, whose polysaccharide capsule significantly decreased the levels of complement deposition on the bacterial surface. Both Burkholderia species showed significantly enhanced uptake and killing by neutrophils after critical levels of C3 were deposited. Serum-opsonized Burkholderia induced a significant respiratory burst by neutrophils compared to unopsonized bacteria, and neutrophil killing was prevented by inhibiting NADPH-oxidase. In summary, neutrophils can efficiently kill B. pseudomallei and B. thailandensis that possess a critical threshold of complement deposition, and the relative differences in their ability to resist surface opsonization may contribute to the distinct virulence phenotypes observed in vivo.

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Retrospective review of febrile neutropenia in the Royal Darwin Hospital, 1994–99

Cited by 11 publications

References 15 publications

Bacteremia Pattern in Febrile Neutropenia among Adults Cancer Patients Receiving Chemotherapy in an Australia Regional Hospital

Bacteremia Pattern in Febrile Neutropenia among Adults Cancer Patients Receiving Chemotherapy in an Australia Regional Hospital

Delineating the Importance of Serum Opsonins and the Bacterial Capsule in Affecting the Uptake and Killing of Burkholderia pseudomallei by Murine Neutrophils and Macrophages

Capsule Influences the Deposition of Critical Complement C3 Levels Required for the Killing of Burkholderia pseudomallei via NADPH-Oxidase Induction by Human Neutrophils

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