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Frances S.P.,Australian Army Malaria Institute
Journal of the American Mosquito Control Association | Year: 2013

Field efficacy trials comparing 2 formulations of deet against mosquitoes in Redcliffe, Queensland, Australia were conducted in February 2009. A formulation containing 35% deet in a gel (Australian Defence Force deet) provided >95% protection for 3 h, while a formulation containing 40% deet in ethanol (Bushman) in a spray applicator provided >95% for 6 h. A user acceptability study showed that 82% of soldiers using the Bushman formulation during contingency operations for 14-28 days in Timor-Leste would recommend this formulation to others and believed that the formulation provided protection against mosquitoes. © 2013 by The American Mosquito Control Association, Inc. Source


Shanks G.D.,Australian Army Malaria Institute | Shanks G.D.,University of Queensland | Shanks G.D.,University of Oxford
The Lancet | Year: 2014

World War 1 was a key transition point towards scientific medicine. Medical officers incorporated Louis Pasteur's discoveries into their understanding of microorganisms as the cause of infectious diseases, which were therefore susceptible to rational control and treatment measures even in the pre-antibiotic era. Typhoid vaccination led to the successful evasion of the disastrous epidemics of previous wars. The incidence of tetanus was probably decreased by giving millions of doses of horse antitoxin to wounded soldiers. Quinine treated but could not control malaria; its use required mass compulsion. Tuberculosis was not a great military problem during World War 1, although mortality in civilian populations increased substantially. Treatment of sexually transmitted infections remained a matter of aversive conditioning, with invasive antiseptics used in the absence of antibiotics. Pandemic influenza in 1918-19 killed more people than died during the entire war, showing how much remained beyond the capability of the scientists and doctors who fought infectious diseases during World War 1. © 2014 Elsevier Ltd. Source


Russell T.L.,James Cook University | Beebe N.W.,University of Queensland | Beebe N.W.,CSIRO | Cooper R.D.,Australian Army Malaria Institute | And 2 more authors.
Malaria Journal | Year: 2013

Background: The ultimate long-term goal of malaria eradication was recently placed back onto the global health agenda. When planning for this goal, it is important to remember why the original Global Malaria Eradication Programme (GMEP), conducted with DDT-based indoor residual spraying (IRS), did not achieve its goals. One of the technical reasons for the failure to eliminate malaria was over reliance on a single intervention and subsequently the mosquito vectors developed behavioural resistance so that they did not come into physical contact with the insecticide. Hypothesis and how to test it. Currently, there remains a monolithic reliance on indoor vector control. It is hypothesized that an outcome of long-term, widespread control is that vector populations will change over time, either in the form of physiological resistance, changes in the relative species composition or behavioural resistance. The potential for, and consequences of, behavioural resistance was explored by reviewing the literature regarding vector behaviour in the southwest Pacific. Discussion. Here, two of the primary vectors that were highly endophagic, Anopheles punctulatus and Anopheles koliensis, virtually disappeared from large areas where DDT was sprayed. However, high levels of transmission have been maintained by Anopheles farauti, which altered its behaviour to blood-feed early in the evening and outdoors and, thereby, avoiding exposure to the insecticides used in IRS. This example indicates that the efficacy of programmes relying on indoor vector control (IRS and long-lasting, insecticide-treated nets [LLINs]) will be significantly reduced if the vectors change their behaviour to avoid entering houses. Conclusions: Behavioural resistance is less frequently seen compared with physiological resistance (where the mosquito contacts the insecticide but is not killed), but is potentially more challenging to control programmes because the intervention effectiveness cannot be restored by rotating the insecticide to one with a different mode of action. The scientific community needs to urgently develop systematic methods for monitoring behavioural resistance and then to work in collaboration with vector control programmes to implement monitoring in sentinel sites. In situations where behavioural resistance is detected, there will be a need to target other bionomic vulnerabilities that may exist in the larval stages, during mating, sugar feeding or another aspect of the life cycle of the vector to continue the drive towards elimination. © 2013 Russell et al.; licensee BioMed Central Ltd. Source


Shanks G.D.,Australian Army Malaria Institute | Shanks G.D.,University of Queensland | Shanks G.D.,University of Oxford | White N.J.,Mahidol University | White N.J.,Center for Tropical Medicine
The Lancet Infectious Diseases | Year: 2013

The periodicity of vivax malaria relapses may be explained by the activation of latent hypnozoites acquired from a previous malarial infection. The activation stimulus could be the febrile illness associated with acute malaria or a different febrile infection. We review historical records to examine the association between relapses of Plasmodium vivax and febrile infectious diseases. In data from British soldiers in Palestine, epidemic falciparum malaria triggered a smaller epidemic of P vivax relapses only in those who had been extensively exposed to malaria previously. Relapses did not follow pandemic influenza infection. Evidence from three simultaneous typhoid and malaria epidemics suggest that typhoid fever might activate P vivax hypnozoites. Some data lend support to the notion that vivax malaria relapse followed febrile illness caused by relapsing fever, trench fever, epidemic typhus, and Malta fever (brucellosis). These observations suggest that systemic parasitic and bacterial infections, but not viral infections, can activate P vivax hypnozoites. Specific components of the host's acute febrile inflammatory response, and not fever alone, are probably important factors in the provocation of a relapse of vivax malaria. © 2013 Elsevier Ltd. Source


Wilson N.,University of Otago | Barnard L.T.,University of Otago | Summers J.A.,University of Otago | Shanks G.D.,Australian Army Malaria Institute | Baker M.G.,University of Otago
Emerging Infectious Diseases | Year: 2012

Evidence suggests that indigenous populations have suffered disproportionately from past influenza pandemics. To examine any such patterns for Māori in New Zealand, we searched the literature and performed new analyses by using additional datasets. The Māori death rate in the 1918 pandemic (4,230/100,000 population) was 7.3× the European rate. In the 1957 pandemic, the Māori death rate (40/100,000) was 6.2× the European rate. In the 2009 pandemic, the Māori rate was higher than the European rate (rate ratio 2.6, 95% confidence interval 1.3-5.3). These findings suggest some decline in pandemic-related ethnic inequalities in death rates over the past century. Nevertheless, the persistent excess in adverse outcomes for Māori, and for Pacific persons residing in New Zealand, highlights the need for improved public health responses. Source

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