Behavioral Effects of Tularemia and Sandfly Fever in Man

Alluisi, Earl A.; Beisel, William R.; Bartelloni, Peter J.; Coates, Glynn D.

doi:10.1093/infdis/128.6.710

Cited by 28 publications

(16 citation statements)

References 18 publications

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“…[15][16][17][18][19] Jones et al 7 recently combined a number of these data-sets and fitted Weibull and log-normal cumulative distribution functions to model the probability of infection given dose. These authors also considered the Saslaw et al 16 results alone due to complications arising from pooling multiple data-sets.…”

Section: Infectious Dosementioning

confidence: 99%

“…The dotted box in Figure 2A corresponds to the results of McCrumb, where, among the control subjects, clinically overt disease appeared within 3 to 5 days following exposure to a challenge varying from 200 to 20,000 organisms. 15 In addition, Alluisi et al 19 exposed 16 men to an aerosol containing 20,000 to 30,000 organisms and found that clinical illness began after incubation periods of 2 to 4 days. Similarly, Hornick and Eigelsbach found a mean incubation period of 3 days with volunteers exposed to 25,000 organisms.…”

Section: Infectious Dosementioning

confidence: 99%

See 1 more Smart Citation

Modeling Inhalational Tularemia: Deliberate Release and Public Health Response

Egan¹,

Hall²

2011

Biosecurity and Bioterrorism: Biodefense Strategy, Practice, an

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Two epidemic modeling studies of inhalational tularemia were identified in the published literature, both demonstrating the high number of potential casualties that could result from a deliberate aerosolized release of the causative agent in an urban setting. However, neither study analyzed the natural history of inhalational tularemia nor modeled the relative merits of different mitigation strategies. We first analyzed publicly available human/primate experimental data and reports of naturally acquired inhalational tularemia cases to better understand the epidemiology of the disease. We then simulated an aerosolized release of the causative agent, using airborne dispersion modeling to demonstrate the potential number of casualties and the extent of their spatial distribution. Finally, we developed a public health intervention model that compares 2 mitigation strategies: targeting antibiotics at symptomatic individuals with or without mass distribution of antibiotics to potentially infected individuals. An antibiotic stockpile that is sufficient to capture all areas where symptomatic individuals were infected is likely to save more lives than treating symptomatic individuals alone, providing antibiotics can be distributed rapidly and their uptake is high. However, with smaller stockpiles, a strategy of treating symptomatic individuals alone is likely to save many more lives than additional mass distribution of antibiotics to potentially infected individuals. The spatial distribution of symptomatic individuals is unlikely to coincide exactly with the path of the dispersion cloud if such individuals are infected near their work locations but then seek treatment close to their homes. The optimal mitigation strategy will depend critically on the size of the release relative to the stockpile level and the effectiveness of treatment relative to the speed at which antibiotics can be distributed.

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Section: Infectious Dosementioning

confidence: 99%

Section: Infectious Dosementioning

confidence: 99%

Modeling Inhalational Tularemia: Deliberate Release and Public Health Response

Egan¹,

Hall²

2011

Biosecurity and Bioterrorism: Biodefense Strategy, Practice, an

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show abstract

“…The severity and rapidity of the disease caused by Francisella, especially in the lungs, are likely the result of an exploitation and/or failure of one or more components of innate immunity, leading ultimately to the inability of macrophages to control infection. Failure of the innate immune response to control F. tularensis infection of human macrophages is corroborated by the short incubation time of 1 to 2 days in human volunteers for developing symptomatic disease following aerosol challenge of F. tularensis (3,41) and in nonhuman primates challenged with the virulent Schu 4 strain (54).…”

mentioning

confidence: 99%

Characterization of the Receptor-Ligand Pathways Important for Entry and Survival ofFrancisella tularensisin Human Macrophages

et al. 2006

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Inhalational pneumonic tularemia, caused by Francisella tularensis, is lethal in humans. F. tularensis is phagocytosed by macrophages followed by escape from phagosomes into the cytoplasm. Little is known of the phagocytic mechanisms for Francisella, particularly as they relate to the lung and alveolar macrophages. Here we examined receptors on primary human monocytes and macrophages which mediate the phagocytosis and intracellular survival of F. novicida. F. novicida association with monocyte-derived macrophages (MDM) was greater than with monocytes. Bacteria were readily ingested, as shown by electron microscopy. Bacterial association was significantly increased in fresh serum and only partially decreased in heat-inactivated serum. A role for both complement receptor 3 (CR3) and Fc␥ receptors in uptake was supported by studies using a CR3-expressing cell line and by down-modulation of Fc␥ receptors on MDM, respectively. Consistent with Fc␥ receptor involvement, antibody in nonimmune human serum was detected on the surface of Francisella. In the absence of serum opsonins, competitive inhibition of mannose receptor (MR) activity on MDM with mannan decreased the association of F. novicida and opsonization of F. novicida with lung collectin surfactant protein A (SP-A) increased bacterial association and intracellular survival. This study demonstrates that human macrophages phagocytose more Francisella than monocytes with contributions from CR3, Fc␥ receptors, the MR, and SP-A present in lung alveoli.

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“…Average effi ciency in overall performance on a battery of tasks, as a percentage of baseline (pre-infection) measurements, fell during symptoms by 33% in the former and 25% in the latter study. Alluisi et al [4] found similar drops in overall performance of 31 % and 20% during infection with Francisella tularensis, another bacterial infection, and sandfly fever virus, respectively. These studies provided the origi nal evidence for performance impairment associated with illness.…”

mentioning

confidence: 86%

“…4 The first 3 days of a trial were considered a quarantine prior to virus challenge and volunteers developing colds in this period were excluded. Performance measures were taken during this period to ascertain baseline levels.…”

Section: Introductionmentioning

confidence: 99%

Selective Effects of Colds and Influenza on Human Performance Efficiency: A Critical Appraisal

Savory¹

1992

Neuropsychobiology

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This paper provides an appraisal of the results published from the MRC Common Cold Unit on human performance efficiency during minor upper respiratory tract infection, i.e. colds and influenza. Despite strict controls employed in the methods of data collection, the robustness of the results and some of the conclusions drawn are questioned. In particular, the claim that colds and influenza lead to selective (and different) effects is criticised as being based on incomplete data. The lack of replication, the small sample sizes, possible response biases and use of controls are considered. Overall, it is argued that there are insufficient data to provide conclusive evidence for selective effects and that over-generalisation from such studies can be misleading.

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Behavioral Effects of Tularemia and Sandfly Fever in Man

Cited by 28 publications

References 18 publications

Modeling Inhalational Tularemia: Deliberate Release and Public Health Response

Modeling Inhalational Tularemia: Deliberate Release and Public Health Response

Characterization of the Receptor-Ligand Pathways Important for Entry and Survival ofFrancisella tularensisin Human Macrophages

Selective Effects of Colds and Influenza on Human Performance Efficiency: A Critical Appraisal

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