The author(s) hereby affirms that the manuscript entitled: ....................................................................................... ............................................. to be published in Journal of Microbiology and InfectiousDiseases is original, that all statements as facts are based on author(s) investigation and research, that the manuscript does not, in whole or in part, violate any copyright or any
The author(s) hereby affirms that the manuscript entitled: ...... ............................................................................................................................ .. to be published in Journal of Microbiology and InfectiousDiseases is original, that all statements as facts are based on author(s) investigation and research, that the manuscript does not, in whole or in part, violate any copyright or any law of pri- vacy or other personal or property right. The manuscript has not been published elsewhere in total or in part; is not being submitted and/or considered for publication in total or in part elsewhere; and that the author(s) has full authority to enter into this copyright agreement and to make the grants con- tained herein. In signing this form, each author acknowledges that he/she participated in the work in a substantive way and is prepared to take public responsibility for the work. Please sign in the same order in which the authors’ names appear on the title page of manuscript.
Psychiatric symptoms can be associated with several systemic and central nervous system infec- tions and they can be the initial presenting symptoms, occurring in the absence of neurological symptoms in some disorders as in some cases of viral encephalitis. They could also be part of the clinical picture in other cases such as psychosis or mood symptoms secondary to brucellosis or toxoplasmosis. Late-onset neuropsychiatric complications may also occur several years following the infection such as in the case of subacute sclerosing panencephalitis due to measles. Some In- fectious diseases may have possible etiological role for major psychiatric disorders, based on yet unconfirmed reports for viral infectiousdiseases (e.g. Influenza virus and HSV-1) which are thought to have risk for developing schizophrenia and psychosis. Neuropsychiatric adverse effects can occur due to drugs (e.g. mefloquine, interferon-alpha) that are used for treatment of infectiousdiseases. Psychiatric symptoms can also be reactivated resulting from chronic, complicated and serious infections such as HIV that can lead to depression, anxiety or adjustment disorders, al- though CNS involvement can also be a possible etiological factor. Patients suffering from primary and severe psychiatric disorders are at increased risk of contracting infection; that is mainly re- lated to high risk behaviors in patients with mania or schizophrenia. It is also important to con- sider that the co-occurrence of psychiatric symptoms and infection can be incidental (i.e. infec- tious diseases can occur in psychiatric patients regardless of the above mentioned factors). Early identification of the underlying etiology for organic/secondary psychiatric symptoms is essential for appropriate intervention and early treatment of the primary condition that could be the etiol- ogy of psychiatric symptoms so as to avoid unnecessary long-term psychiatric treatment and to avoid complications of possible misdiagnosis or delayed diagnosis of the primary condition.
In this time of unprecedented global change, infectiousdiseases will impact humans and wildlife in novel and unknown ways. Climate change, the introduction of invasive species, urbanization, agricultural practices and the loss of biodiversity have all been implicated in increasing the spread of infectious pathogens. In many regards, deforestation supersedes these other global events in terms of its immediate potential global effects in both tropical and temperate regions. The effects of deforestation on the spread of pathogens in birds are largely unknown. Birds harbor many of the same types of pathogens as humans and in addition can spread infectious agents to humans and other wildlife. It is thought that avifauna have gone extinct due to infectiousdiseases and many are presently threatened, especially endemic island birds. It is clear that habitat degradation can pose a direct threat to many bird species but it is uncertain how these alterations will affect disease transmission and susceptibility to disease. The migration and dispersal of birds can also change with habitat degradation, and thus expose populations to novel pathogens. Some recent work has shown that the results of landscape transformation can have confounding effects on avian malaria, other haemosporidian parasites and viruses. Now with advances in many technologies, including mathematical and computer modeling, genomics and satellite tracking, scientists have tools to further research the disease ecology of deforestation. This research will be imperative to help predict and prevent outbreaks that could affect avifauna, humans and other wildlife worldwide.
The epidemiology of infectiousdiseases is a complex and multi-factoral subject [16, 151, 74]. As such, no single review can hope to cover all aspects. Here we fo- cus largely on the population dynamics of infectiousdiseases – how the number of individuals infected changes dynamically over time. This article therefore relies heavily on tools from mathematics and theoretical physics (the theory of differential equations and dynamical systems, statistical mechanics, and stochastic processes). However, there are multiple disciplines that feed into epidemiology that we do not cover. Statistics is one with which many readers will be familiar; statistics plays a vital role in both inter- preting the observed infection data (accounting for the many biases in reporting) and in parameter inference when we attempt to fit models to data. Obviously, a range of biological sciences from microbiology to immunology to ecology are needed to inform our understanding of the pathogen, the host and their interaction; while we do not attempt a comprehensive review of such knowledge, the next section does provide suf- ficient biological background to motivate and justify the choice of model formulation. Finally, in recent years it has become apparent that other disciplines have a role to play: economics is vital to underpin cost-effectiveness studies that are key to assessing control programmes; sociology and psychology help to explain and predict human response to outbreaks or new treatments; while medical insights are needed to understand the link between the individual as a host for the pathogen and the individual as a patient that requires treatment. Therefore, when developing models for the spread of an infectious disease we not only need a range of mathematical skills but must account for the in- sights provided by many other disciplines. Throughout, we had attempted to draw on citations from the mathematical and biological literature whenever possible, so as to introduce the reader to this (possible novel) fields of scientific publication.
My field placement for the Master of Applied Epidemiology (MAE) commenced on 25 February 2013, in the Vaccine Preventable Diseases Surveillance section (VPDS), Health Emergency and Management Branch (HEMB), Office of Health Protection (OHP), Australian Department of Health (the Department of Health). My field supervisor was the director of VPDS, Ms Rhonda Owen. During this time I worked on diseases managed by this section including influenza, Human Pappillomavirus (HPV) and legionellosis. Collaboration and supervision was provided for each project by specialists in their fields including Dr. Julia Brotherton from the Victorian Cytology Service (VCS), Christina Bareja (VPDS), Kate Pennington (VPDS) and Amy Bright (VPDS). As part of my placement I also worked with the Australian Capital Territory Health Protection Service (HPS) to investigate an outbreak of gastroenteritis. I was seconded to HPS for 2 weeks to assist with the investigation.