Dissertation Low Temperature Effects On

Total Page:16

File Type:pdf, Size:1020Kb

Dissertation Low Temperature Effects On DISSERTATION LOW TEMPERATURE EFFECTS ON THE TRANSCRIPTOME OF YERSINIA PESTIS AND ITS TRANSMISSIBILITY BY OROPSYLLA MONTANA FLEAS Submitted by Shanna K. Williams Department of Microbiology, Immunology & Pathology In partial fulfillment of the requirements For the Degree of Doctor of Philosophy Colorado State University Fort Collins, Colorado Spring 2016 Doctoral Committee: Advisor: Brad Borlee Co-Advisor: Scott Bearden Ken Gage Mark Stenglein Shawn Archibeque Copyright by Shanna K. Williams All Rights Reserved ABSTRACT LOW TEMPERATURE EFFECTS ON THE TRANSCRIPTOME OF YERSINIA PESTIS AND ITS TRANSMISSIBILITY BY OROPSYLLA MONTANA FLEAS Yersinia pestis, the causative agent of plague, is primarily a rodent-associated, flea-borne zoonosis. Transmission to humans is mediated most commonly by the flea vector, Oropsylla montana, and occurs predominantly in the Southwestern United States. In these studies, we hypothesized that Y. pestis-infected O. montana fleas held at temperatures as low as 6ºC could serve as reservoirs of the plague bacillus during the winter months in temperate regions with endemic plague foci. With few exceptions, previous studies showed O. montana to be an inefficient vector at transmitting Y. pestis at 22-23C particularly when such fleas were fed on susceptible hosts more than a few days after ingesting an infectious blood meal. We examined whether holding fleas at sub-ambient temperatures (for purposes of these studies, ambient temperature is defined as 23C) affected the transmissibility of Y. pestis by this vector. Colony- reared O. montana fleas were given an infectious blood meal containing a virulent Y. pestis strain (CO96-3188), and potentially infected fleas were maintained at different temperatures (6ºC, 10C, 15C, or 23ºC). Transmission efficiencies were tested by allowing groups of ~15 infectious fleas to feed on each of seven naïve CD-1 mice on days 1-4, 7, 10, 14, 17, and 21, 28, 35, and 42 post infection (p.i.). Fleas held at 6ºC, 10C and 15C were able to effectively transmit at every time point p.i. The percentage of transmission to naïve mice by fleas maintained at low temperatures was higher than for fleas maintained at 23ºC and indicates that ii O. montana fleas efficiently transmit Y. pestis at low temperatures. Moreover, bacterial loads of flea cohorts maintained at temperatures of 6ºC, 10ºC and 15ºC were statistically higher than fleas maintained at 23ºC. In addition, whole transcriptomes of Y. pestis bacteria grown at 6ºC, 10C, 15C and 23ºC were analyzed to assess differential gene expression at each temperature to identify genes which may contribute to an increase in virulence or survivability of the plague pathogen at the lower temperatures when compared to ambient temperature. This is the first comprehensive study to demonstrate efficient transmission of Y. pestis by O. montana fleas maintained at temperatures as low as 6ºC. Our findings further contribute to the understanding of plague ecology in temperate climates by providing support for the hypothesis that Y. pestis is able to overwinter within the flea gut and potentially cause infection during the following transmission season. The findings also might hold implications for explaining the focality of plague in tropical regions where plague occurs in cooler environments, primarily located at higher elevations. iii ACKNOWLEDGEMENTS Foremost, I would like to express my sincere gratitude to Dr. Ken Gage and Dr. Scott Bearden for allowing me the opportunity to work in your lab while pursuing my doctorate. In addition to Dr. Gage and Dr. Bearden, I also would like to thank everyone on my committee: Dr. Brad Borlee, Dr. Mark Stenglein, and Dr. Shawn Archibeque for their encouragement, insightful comments, and guidance. My sincere thanks also goes to John Montenieri, who has been an essential part of my research studies, and always provided comic relief and constant support. I also want to thank my fellow lab mates and colleagues Sarah Maes, Tammi Johnson, Karen Boegler and Christine Graham for their assistance, discussions, and for all of the fun over the last few years. Finally, I would like to thank my family and all of my friends for the constant support and encouragement. Without each and every one of the aforementioned, it would never have been possible for me to undergo such a very difficult, but highly rewarding time in my life. I greatly appreciate everything you all have done for me. Thank you all very much. iv TABLE OF CONTENTS ABSTRACT ...................................................................................................................................ii ACKNOWLEDGEMENTS............................................................................................................iv LIST OF TABLES.........................................................................................................................vii LIST OF FIGURES .....................................................................................................................viii 1. CHAPTER 1- Literature Review-Yersinia pestis Transmission and Disease.............................................................................................................................................1 2. CHAPTER 1.1-Histoical Background and Yersinia pestis pandemics..........................…..1 3. CHAPTER 1.2-Y. pestis General Characteristics and Etiology….......................................6 4. CHAPTER 1.3- Plague as a Bioterrorism Agent.................................................................9 5. CHAPTER 1.4-Y. pestis Evolution from Y. pseudotuberculosis.......................................11 6. CHAPTER 1.5- Y. pestis Life Cycle..................................................................................14 7. CHAPTER 1.6- Y. pestis Reservoirs..................................................................................17 8. CHAPTER 1.6.1- Mammalian Hosts.................................................................................17 9. CHAPTER 1.6.2- Other Potential Reservoirs....................................................................19 10. CHAPTER 1.7- Y. pestis and fleas....................................................................................19 11. CHAPTER 1.8- Oropsylla montana..................................................................................24 12. CHAPTER 1.9- Flea (Insect) Immunity............................................................................25 13. CHAPTER 1.10- Y. pestis Transmission Mechanisms......................................................28 14. CHAPTER 1.11- Y. pestis Transmission Factors..............................................................30 15. CHAPTER 1.12- Y. pestis Virulence and Pathogenesis....................................................32 16. CHAPTER 1.13- Y. pestis Geographic Distribution and Incidence..................................37 17. CHAPTER 1.14- Y. pestis Clinical Disease Features........................................................41 18. CHAPTER 1.15- Y. pestis Diagnosis and Treatment........................................................43 19. CHAPTER 1.16- Y. pestis Surveillance and Control.........................................................49 20. CHAPTER 1.16.1- Plague Surveillance. ..........................................................................50 21. CHAPTER 1.16.2- Plague Control....................................................................................51 22. CHAPTER 1.17- Animal Models Used in Plague Research.............................................55 23. CHAPTER 1.17.1- Invertebrate Models for Studying Plague Transmission Factors…...55 24. CHAPTER 1.17.2- Mammalian Models to Study Plague Virulence and Pathogenesis....58 25. CHAPTER1.17.2A- Mouse Model....................................................................................58 26. CHAPTER 1.17.2B- Guinea Pig Model............................................................................61 27. CHAPTER 1.17.2C- Rat Model........................................................................................62 28. CHAPTER 1.17.3- Non-Human Primate (NHPs) Model..................................................64 29. CHAPTER 1.17.3A- Rhesus Macaques Model.....................…………...……….............64 30. CHAPTER 1.17.3B- African Green Monkey Model.........................................................65 31. CHAPTER 1.17.3C- Cynomolgus Macaques Model…….................................................66 32. CHAPTER 1.18- Detection Assays Used for Y. pestis Identification in Animals and Fleas………….……………………………………………………….67 33. CHAPTER 1.18.1- Rodents and Other Animal Populations.............................................67 34. CHAPTER 1.18.2- Detection of Y. pestis in Fleas............................................................68 35. CHAPTER 1.19- Next Generation Sequencing (NGS) for Transcriptomics Analysis.....69 36. CHAPTER 1 References.........................................................................................................72 v 37. CHAPTER 2- Effects of Low Temperature Flea Maintenance on the Transmissibility of Yersinia pestis by Oropsylla montana.........................................................................................121 38. CHAPTER 2.1- Introduction...........................................................................................122 39. CHAPTER 2.2- Materials and Methods..........................................................................126 40. CHAPTER 2.3- Results...................................................................................................131
Recommended publications
  • How Much Do You Know About Fleas, Ticks, Mites and Other Biters? by Vet Glen Cousquer C Norris
    Artful arthropods How much do you know about fleas, ticks, mites and other biters? By vet Glen Cousquer C Norris robably the most historically significant and well known arthropod-borne disease was the “Black Death”. This scourge of the Middle Ages, also known as the Bubonic Plague, killed Pbetween 30 and 60 per cent of Europe’s human population during the 14th Century. This bacterial disease was carried by black rats (Rattus rattus) and transmitted from the rat to humans by the Oriental rat flea (Xenopsylla cheopis). The flea was able to pick up the disease when feeding on rats and then transfer Cheyletiella mites result in the appearance the disease when feeding again on humans. At the time, the of scurf and bald patches in the fur various contributing causes of this devastating disease remained G Cousquer obscure. Our ancestors were largely ignorant of the role played transmit diseases to rabbits. Many of the most important rabbit by the rat, the flea, poor hygiene and inadequate sanitation and diseases are transmitted in this way and we need a detailed this severely hampered their attempts to deal with outbreaks. understanding of the process involved if we are to protect our Today, it is this understanding of how disease can be carried rabbits’ health and welfare. by reservoirs and then transmitted by vectors that allows us to mount more effective responses to such disease threats. So, what are the common arthropod parasites found feeding on rabbits? This feature will look at how certain arthropods play key roles in the transmission of diseases to rabbits.
    [Show full text]
  • TICKS in RELATION to HUMAN DISEASES CAUSED by <I
    University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln U.S. Navy Research U.S. Department of Defense 1967 TICKS IN RELATION TO HUMAN DISEASES CAUSED BY RICKETTSIA SPECIES Harry Hoogstraal Follow this and additional works at: https://digitalcommons.unl.edu/usnavyresearch This Article is brought to you for free and open access by the U.S. Department of Defense at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in U.S. Navy Research by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. TICKS IN RELATION TO HUMAN DISEASES CAUSED BY RICKETTSIA SPECIES1,2 By HARRY HOOGSTRAAL Department oj Medical Zoology, United States Naval Medical Research Unit Number Three, Cairo, Egypt, U.A.R. Rickettsiae (185) are obligate intracellular parasites that multiply by binary fission in the cells of both vertebrate and invertebrate hosts. They are pleomorphic coccobacillary bodies with complex cell walls containing muramic acid, and internal structures composed of ribonucleic and deoxyri­ bonucleic acids. Rickettsiae show independent metabolic activity with amino acids and intermediate carbohydrates as substrates, and are very susceptible to tetracyclines as well as to other antibiotics. They may be considered as fastidious bacteria whose major unique character is their obligate intracellu­ lar life, although there is at least one exception to this. In appearance, they range from coccoid forms 0.3 J.I. in diameter to long chains of bacillary forms. They are thus intermediate in size between most bacteria and filterable viruses, and form the family Rickettsiaceae Pinkerton. They stain poorly by Gram's method but well by the procedures of Macchiavello, Gimenez, and Giemsa.
    [Show full text]
  • WHAT IS MYXOMATOSIS? After Its Introduction to the UK in the Early 1950’S Myxomatosis Was So Virulent That an Estimated 95% of Wild and Pet Rabbits Had Died by 1955
    WHAT IS MYXOMATOSIS? After its introduction to the UK in the early 1950’s myxomatosis was so virulent that an estimated 95% of wild and pet rabbits had died by 1955. In the year 2000 we again experienced one of the worst outbreaks of Myxomatosis ever recorded, and this disease is still affecting rabbits, particularly during the late summer/ autumn season. Below: edited extracts from an article written by Dr Linda Dykes, published in Fur & Feather’s November 2000 issue. yxomatosis is a rabbit will be a pitiful sight. Severe viral disease which conjunctivitis causes blindness and decimated the wild is accompanied by swelling of the Mrabbit population when it head and genital region plus lumps arrived in Britain nearly seventy on the body. years ago. The number and The rabbit can take a fortnight to severity of outbreaks varies over die and treatment of the “classic” time as the myxomatosis virus form of myxomatosis is usually is notorious for its ability to futile. mutate from year to year, and the background immunity in There are also two atypical forms the wild rabbit population also of myxomatosis: one causes varies. pneumonia and a snuffles-like illness; the other (“nodular Be especially careful if you have a being a bit “off colour” with a few Rabbits at myxomatosis”) mainly affects skin Greatest Risk dog or cat that hunts wild rabbits, skin lesions. and carries a better prognosis. Domestic rabbits do not have as they could bring rabbit fleas Treatment is usually successful any genetically based immunity If a vaccinated rabbit does develop home or into the rabbitry on their in the vaccinated rabbit with a against myxomatosis.
    [Show full text]
  • Fleas and Flea-Borne Diseases
    International Journal of Infectious Diseases 14 (2010) e667–e676 Contents lists available at ScienceDirect International Journal of Infectious Diseases journal homepage: www.elsevier.com/locate/ijid Review Fleas and flea-borne diseases Idir Bitam a, Katharina Dittmar b, Philippe Parola a, Michael F. Whiting c, Didier Raoult a,* a Unite´ de Recherche en Maladies Infectieuses Tropicales Emergentes, CNRS-IRD UMR 6236, Faculte´ de Me´decine, Universite´ de la Me´diterrane´e, 27 Bd Jean Moulin, 13385 Marseille Cedex 5, France b Department of Biological Sciences, SUNY at Buffalo, Buffalo, NY, USA c Department of Biology, Brigham Young University, Provo, Utah, USA ARTICLE INFO SUMMARY Article history: Flea-borne infections are emerging or re-emerging throughout the world, and their incidence is on the Received 3 February 2009 rise. Furthermore, their distribution and that of their vectors is shifting and expanding. This publication Received in revised form 2 June 2009 reviews general flea biology and the distribution of the flea-borne diseases of public health importance Accepted 4 November 2009 throughout the world, their principal flea vectors, and the extent of their public health burden. Such an Corresponding Editor: William Cameron, overall review is necessary to understand the importance of this group of infections and the resources Ottawa, Canada that must be allocated to their control by public health authorities to ensure their timely diagnosis and treatment. Keywords: ß 2010 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved. Flea Siphonaptera Plague Yersinia pestis Rickettsia Bartonella Introduction to 16 families and 238 genera have been described, but only a minority is synanthropic, that is they live in close association with The past decades have seen a dramatic change in the geographic humans (Table 1).4,5 and host ranges of many vector-borne pathogens, and their diseases.
    [Show full text]
  • Wildlife Disease Monitor 2014
    WILDLIFE DISEASE MONITORING IN SWEDEN 2014 Editors: Jonas Malmsten, Erik Ågren Authors: Caroline Bröjer, Gete Hestvik, Aleksija Neimanis, Jonas Malmsten, Torsten Mörner, Henrik Uhlhorn, Erik Ågren Photo, front page: Jim Hallander Layout: Gun-Britt Rydén, Jonas Malmsten Suggested citation: Wildlife disease monitoring in Sweden 2014. National Veterinary Institute, SVA, Uppsala, Sweden. SVA´s report series 33, ISSN 1654-7098 Address: Ulls väg 2 B, 751 89 Uppsala telephone. +46 18 67 40 00 fax. +46 18 30 91 62 e-mail. [email protected] webb. www.sva.se Table of contents Foreword ....................................................... 1 Wild boar as carriers of pathogenic Wildlife disease surveillance in Sweden ......... 2 agents ..................................................... 13 Staff working with Wildlife disease Bird flu monitoring ................................... 13 investigations in 2014 ................................ 2 Investigation of moose calf mortality on Wildlife diseases and increased mortality Öland ...................................................... 14 events of interest 2014 .................................. 3 Pasteurellosis in fallow deer .................... 14 Bird flu virus in harbour seals .................... 3 PCR diagnosis of trichomonas infection in Fox tapeworm – EchinococcosIS .............. 3 wild birds ................................................. 14 Mortality event in fallow deer ..................... 3 Salmonella in hedgehogs ........................ 15 Trichomoniasis in Greenfinches ...............
    [Show full text]
  • DOMESTIC RATS, FLEAS and NATIVE RODENTS
    DOMESTIC RATS, FLEAS and NATIVE RODENTS In Relation To Plague In The United States By Entomologist Carl 0. Mohr INTRODUCTION and finally to the lungs causing pneumonic plague. ubonic plague is a rodent and rodent - Pneumonic plague is extremely fatal and flea disease caused by the plague bacil­ highly infectious when sputum droplets pass Blus Pasturella pest is which is transmitted direct from person to person. The death from animal to animal and thence to man by rate due to it is practically 100 percent. fleas. It is highly fatal. At least half Plague is dreaded particularly where of the human cases result in death without living conditions are such as to bring modern medication. (Table I — last two human beings into close contact with large columns). Because of their close associa* oriental-rat-flea populations, and where tion with man, domestic rats* and their crowded conditions permit rapid pneumonic fleas, especially the oriental rat flea transmission from man to man. Xenopsylla cheopis, are responsible for most human epidemics. Only occasional cases ANCIENT AMERICAN DISEASE OR RECENT are caused by bites of other fleas or by INTRODUCTION direct infection from handling rodents. Infection due to bites of fleas or due to Two widely different views exist con­ direct contact commonly results in swollen cerning the arrival of plague in North lymph glands, called buboes, hence the name America. The prevalent view is that it was bubonic plague. Infection may progress to introduced from the Orient into North the blood stream causing septicemic plague, America at San Francisco through ship- * Rattus rattus and Rattus norvegicus.
    [Show full text]
  • CDFA List of Reportable Conditions for Animals and Animal Products
    January 2021 ANIMAL HEALTH BRANCH LIST OF REPORTABLE CONDITIONS FOR ANIMALS AND ANIMAL PRODUCTS* *Pursuant to Section 9101 of the California Food and Agricultural Code, Title 3 California Code of Regulations § 797 and Title 9 Code of Federal Regulations Section 161.4(f) WHO MUST REPORT: Any licensed veterinarian, any person operating a diagnostic laboratory, or any person who has been informed, recognizes or should recognize by virtue of education, experience, or occupation, that any animal or animal product is or may be affected by, or has been exposed to, or may be transmitting or carrying any of the following conditions, must report that information. WHAT TO REPORT: Immediately report any animal disease not known to exist in the United States, any event with increased mortality and/or morbidity of unknown cause or source and any toxicology condition likely to contaminate animals or animal products (meat, milk or eggs). CALL IF YOU SEE: high morbidity or mortality, vesicles, CNS signs, uncommon ticks, hemorrhagic septicemias, unusual larvae in wounds, unusual or unexplained illness. Report any emergency, regulatory, or monitored condition within the provided time frame. Some diseases are listed under the major species of concern; if you see compatible signs for such conditions in another species, please report! EMERGENCY CONDITIONS REGULATORY CONDITIONS MONITORED CONDITIONS Report within 24 Hours of Discovery Report within Two Days of Discovery Report within 30 Days of Discovery MULTIPLE SPECIES MULTIPLE SPECIES MULTIPLE SPECIES • Brucellosis (B. melitensis, B. abortus, B. suis)1 • Bluetongue General, non-specific conditions: Unexplained high • Pseudorabies (Aujeszky’s disease) • Echinococcosis/hydatidosis (Echinococcus species) mortality or diseased animals; livestock exposed to toxic • Tuberculosis (Mycobacterium bovis)1 • Epizootic hemorrhagic disease substances.
    [Show full text]
  • Gr up Industrial Microbiology & Biotechnology
    SMGr up Industrial Microbiology & Biotechnology Sandeep Tiwari1, Syed Babar Jamal1, Paulo Vinícius Sanches Daltro de Carvalho1, Syed Shah Hassan1, Artur Silva2 and Vasco Azevedo1 1Universidade Federal de Minas Gerais, UFMG, Brazil 2Universidade Federal do Pará, Belém, PA, Brazil. *Corresponding author: Vasco Azevedo, Universidade Federal de Minas Gerais/Instituto de CiênciasBiológicas, Minas Gerais, Brazil, Email: [email protected] Published Date: February 15, 2015 ABSTRACT Microbes are small living organisms, quite diverse and adapt to various environments. They live on our planet long before that markedly effects the human, animals and plants life. Biotechnologically, molecular genetics of microbes is systematically manipulated, enable them possible through transfer of human insulin gene to a bacterium to treat diabetes, a milestone in for the production of beneficial products. The large-scale production of insulin was made the history of biotechnology. The microbial cultures are managed, monitored and maintained for their genotype/phenotype stability. Bacteria are one of the biotechnologically important microbes for example Escherichia coli, some species of lactic acid bacteria, and some viruses Using such as bacteriophages etc. recognized as anti-cancer oncolytic viruses. Moreover, yeast has also been used with broad-spectrum applications, such as Saccharomyces cerevisiae. biologically active primary and secondary metabolites like ethanol and antibiotics have been diverse genetic technologies, a number of beneficial products like microbial polymers, produced so far and used. Here, it would be injustice not to comment on the importance of vaccines for several infectious diseases through their ability to trigger the host immune system. Furthermore, roles of microorganisms in the production of pharmaceutical proteins A Text Book of Biotechnology | www.smgebooks.com 1 Copyright Azevedo V.
    [Show full text]
  • Improved Taxonomy of the Genus Streptomyces
    UNIVERSITEIT GENT Faculteit Wetenschappen Vakgroep Biochemie, Fysiologie & Microbiologie Laboratorium voor Microbiologie Improved taxonomy of the genus Streptomyces Benjamin LANOOT Scriptie voorgelegd tot het behalen van de graad van Doctor in de Wetenschappen (Biochemie) Promotor: Prof. Dr. ir. J. Swings Co-promotor: Dr. M. Vancanneyt Academiejaar 2004-2005 FACULTY OF SCIENCES ____________________________________________________________ DEPARTMENT OF BIOCHEMISTRY, PHYSIOLOGY AND MICROBIOLOGY UNIVERSITEIT LABORATORY OF MICROBIOLOGY GENT IMPROVED TAXONOMY OF THE GENUS STREPTOMYCES DISSERTATION Submitted in fulfilment of the requirements for the degree of Doctor (Ph D) in Sciences, Biochemistry December 2004 Benjamin LANOOT Promotor: Prof. Dr. ir. J. SWINGS Co-promotor: Dr. M. VANCANNEYT 1: Aerial mycelium of a Streptomyces sp. © Michel Cavatta, Academy de Lyon, France 1 2 2: Streptomyces coelicolor colonies © John Innes Centre 3: Blue haloes surrounding Streptomyces coelicolor colonies are secreted 3 4 actinorhodin (an antibiotic) © John Innes Centre 4: Antibiotic droplet secreted by Streptomyces coelicolor © John Innes Centre PhD thesis, Faculty of Sciences, Ghent University, Ghent, Belgium. Publicly defended in Ghent, December 9th, 2004. Examination Commission PROF. DR. J. VAN BEEUMEN (ACTING CHAIRMAN) Faculty of Sciences, University of Ghent PROF. DR. IR. J. SWINGS (PROMOTOR) Faculty of Sciences, University of Ghent DR. M. VANCANNEYT (CO-PROMOTOR) Faculty of Sciences, University of Ghent PROF. DR. M. GOODFELLOW Department of Agricultural & Environmental Science University of Newcastle, UK PROF. Z. LIU Institute of Microbiology Chinese Academy of Sciences, Beijing, P.R. China DR. D. LABEDA United States Department of Agriculture National Center for Agricultural Utilization Research Peoria, IL, USA PROF. DR. R.M. KROPPENSTEDT Deutsche Sammlung von Mikroorganismen & Zellkulturen (DSMZ) Braunschweig, Germany DR.
    [Show full text]
  • The Evolution of Flea-Borne Transmission in Yersinia Pestis
    Curr. Issues Mol. Biol. 7: 197–212. Online journal at www.cimb.org The Evolution of Flea-borne Transmission in Yersinia pestis B. Joseph Hinnebusch al., 1999; Hinchcliffe et al., 2003; Chain et al., 2004). Presumably, the change from the food- and water-borne Laboratory of Human Bacterial Pathogenesis, Rocky transmission of the Y. pseudotuberculosis ancestor to Mountain Laboratories, National Institute of Allergy the flea-borne transmission of Y. pestis occurred during and Infectious Diseases, National Institutes of Health, this evolutionarily short period of time. The monophyletic Hamilton, MT 59840 USA relationship of these two sister-species implies that the genetic changes that underlie the ability of Y. pestis to use Abstract the flea for its transmission vector are relatively few and Transmission by fleabite is a recent evolutionary adaptation discrete. Therefore, the Y. pseudotuberculosis –Y. pestis that distinguishes Yersinia pestis, the agent of plague, species complex provides an interesting case study in from Yersinia pseudotuberculosis and all other enteric the evolution of arthropod-borne transmission. Some of bacteria. The very close genetic relationship between Y. the genetic changes that led to flea-borne transmission pestis and Y. pseudotuberculosis indicates that just a few have been identified using the rat flea Xenopsylla cheopis discrete genetic changes were sufficient to give rise to flea- as model organism, and an evolutionary pathway can borne transmission. Y. pestis exhibits a distinct infection now be surmised. Reliance on the flea for transmission phenotype in its flea vector, and a transmissible infection also imposed new selective pressures on Y. pestis that depends on genes that are specifically required in the help explain the evolution of increased virulence in this flea, but not the mammal.
    [Show full text]
  • Common Rabbit Pathogens
    Common Rabbit Pathogens Encephalitozoon Cuniculi Encephalitozoonosis is caused by Encephalitozoon cuniculi. About 80% of healthy rabbits carry the pathogen, without any clinical signs developing. Clinical disease can present with the following clinical signs: torticollis, ataxia, uveitis, posterior paresis and urinary incontinence. Other clinical signs can occur depending on the particular organs involved (such as hepatic and renal disease). Transmission is by infectious spores excreted primarily in the urine but also in the faeces and transmission can occur both orally and nasally. A pregnant doe can pass the pathogen on to her offspring in utero. The disease is a zoonosis and is an emerging human pathogen. Detection is now available by two methods both the traditional serology, giving antibody titres, to enable monitoring of clinical cases or detection of active shedding by PCR. The options available to help diagnose E. cuniculi are: Serology An IgG titre is the most commonly used test, this indicates long term exposure. Levels continue to rise steadily from 30 days post primary infection until they peak at 70 days. An IgM titre is now also available and can be used in conjunction with the IgG. IgM indicates early exposure and new infection in the initial 35 days prior to IgG detection. The sample required is serum (not from a gel tube). PCR No special medium is required for this test, a sample of urine, CSF or faeces simply needs to be placed in to a sterile universal tube. The sensitivity of this test is 96%, the specificity has yet to be measured. E. cuniculi can be intermittently shed, so a 3 day pooled sample should be taken.
    [Show full text]
  • Biological Observations on the Oriental Rat Flea, Xenopsylla Cheopsis
    BIOLOGICAL OBSERVATIONS ON THE ORIENTAL RAT FLEA, Xenopsylla cheopis (ROTHSCHILD), WITH SPECIAL STUDIES ON THE EFFECTS OF THE CHEMOSTERILANT TRIS (1-AZIRIDINYL) PHOSPHINE OXIDE By ROBERT LOOMIS LINKFIELD A DISSERTATION PRESENTED TO THE GRADUATE COUNCIL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA December, 1966 ACKNOWLEDGEMENTS The author wishes to express his sincere gratitude to the Chairman of his Supervisory Committee, Dr. J. T. Creighton, Department of Entomology, University of Florida, and the Co-Chairman, Dr. P. B. Morgan, United States Department of Agriculture, for their advice and assistance. For their criticism of the manuscript, appreciation is also expressed to committee members Dr. F. S. Blanton and Mr. W. T. Calaway, and to Dr. A. M. Laessle who read for Dr. Archie Carr. Special thanks are due to Dr. C. N. Smith for the use of facilities at the U.S.D.A. Entomology Research Division Laboratory; to Dr. G. C. LaBrecque for his suggestions and encouragement; and to all the U.S.D.A. staff who assisted. Dr. William Mendenhall, Chairman of the Department of Statistics, assigned Mr. Marcello Pagano to aid in.certain statistical analyses; the Computer Center allotted 15 minutes of computer time. Their cooperation is gratefully acknowledged. Last, but not least, appreciation goes to my wife, Ethel, who typed the preliminary copies of this manuscript and who gave affectionate encouragement throughout the course of this study. ii . TABLE OF CONTENTS . Page ACKNOWLEDGEMENTS. ii LIST OF TABLES V "' LIST OF FIGURES . vii INTRODUCTION . 1 REVIEW OF LITERATURE 5 Chemosterilants 1 .
    [Show full text]