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Uva-DARE (Digital Academic Repository) UvA-DARE (Digital Academic Repository) Psittacosis : molecular tools for detection and typing of Chlamydophila psittaci Heddema, E.R. Publication date 2007 Document Version Final published version Link to publication Citation for published version (APA): Heddema, E. R. (2007). Psittacosis : molecular tools for detection and typing of Chlamydophila psittaci. Mercis. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. 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UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl) Download date:26 Sep 2021 Psittacosis Molecular tools for detection and typing of Chlamydophila psittaci Edou Redbad Heddema Cover design © Mercis publishing, used with permission ISBN 10: 9073838970 ISBN 13: 97873838970 Printed by F&N Eigen Beheer, Amsterdam This thesis was financially supported by Bayer Healthcare, Oxoid, Pfizer, Roche Diagnostics, and the University of Amsterdam Psittacosis Molecular tools for detection and typing of Chlamydophila psittaci Academisch Proefschrift ter verkrijging van de graad van doctor aan de Universiteit van Amsterdam op gezag van de Rector Magnificus prof. dr. J. W. Zwemmer ten overstaan van een door het college voor promoties ingestelde commissie, in het openbaar te verdedigen in de Aula der Universiteit op donderdag 22 maart 2007, te 14.00 uur door Edou Redbad Heddema geboren te Weststellingwerf Promotiecommissie Promotor: Prof. dr. C. M. J. E. Vandenbroucke-Grauls Co-promotores: Dr. Y. Pannekoek Dr. C. E. Visser Overige leden: Dr. R. E. Jonkers Prof. dr. P. A. Kager Dr. J. T. Lumeij Prof. dr. P. Speelman Dr. J. van Steenbergen Prof. dr. D. Vanrompay Faculteit der Geneeskunde Table of contents Contents Chapter 1. Introduction: Chlamydophila psittaci infections with the emphasis on zoonotic infections 7 Chapter 2. A woman with a lobar infiltrate due to psittacosis detected by polymerase chain reaction 31 Chapter 3. Development of an internally controlled real-time PCR assay for detection of Chlamydophila psittaci in the LightCycler 2.0 system 39 Chapter 4. An outbreak of psittacosis due to Chlamydophila psittaci genotype A in a veterinary teaching hospital 55 Chapter 5. Prevalence of Chlamydophila psittaci in fecal droppings from feral pigeons in Amsterdam, The Netherlands 69 Chapter 6. Genotyping of Chlamydophila psittaci strains in human clinical samples by ompA sequence analysis 79 Chapter 7. Summarizing discussion: molecular tools for the detection and typing of Chlamydophila psittaci strains causing human and avian infections 85 Chapter 8. Nederlandse samenvatting, Dankwoord, Curriculum vitae, Publicaties 95 Chapter 1 Introduction: Chlamydophila psittaci infections with the emphasis on zoonotic infections Edou R. Heddema 1, Yvonne Pannekoek 1, Caroline E. Visser 1, Christina M.J.E. Vandenbroucke-Grauls 1,2 1) Department of Medical Microbiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. 2) Department of Medical Microbiology & Infection Control, VU University Medical Center, Amsterdam, the Netherlands. 7 Chapter 1 History In 1881, Jacob Ritter wrote an article in which he described seven cases of psittacosis in one family related to parrots and finches caged in the study of his brother's house in Uster, Switzerland. Three people died, including one of his brothers (29,54). Ritter accurately identified the study as the site of the source of infection, considered the birds as vectors, and determined both the incubation period and the nontransmissibility of the disease from human to human. The main pathologic finding was pneumonia. Besides the respiratory symptoms, the disease presented with headache and a slow pulse rate compared with the body temperature (relative bradycardia), that was often seen in “typhus” (typhoid fever), an endemic disease in Europe at that time. Therefore, he named the disease “pneumothyphus”. Ritter's article is a precise description of the clinical presentation, epidemiology, pathologic findings, and natural history of psittacosis. Several outbreaks were reported since Ritter’s description. One of the largest outbreaks in the 19 th century was in Paris in 1896 which involved more than 70 people. In 1893 a Frenchman, named Nocard, isolated a Gram-negative bacterium belonging to the Salmonella group from an ill bird. The bacterium was named Nocard’s bacillus and seen as the causative agent of psittacosis. Only seldom this easy to culture bacterium could be isolated from birds involved in outbreaks of psittacosis. In 1929 and 1930 a sharp increase in psittacosis cases was observed worldwide. This is the so-called psittacosis pandemic. Two reasons for this increase were established. Firstly, an outbreak of psittacosis occurred among bird flocks in Argentina that were meant for international bird trade. Thus, worldwide distribution of infected birds occurred. Secondly, keeping birds for hobby flourished in the late 1920’s because of good economic times (63). It took until 1930 before the true psittacosis agent was identified and cultured (3,4). At first, the psittacosis agent could only be propagated in birds, but later peritoneal inoculation in mice became the preferred culture technique (26). The agent was classified as a virus belonging to the psittacosis-lymphogranuloma venereum group. The “virus” was stained with Giemsa, Macchiavello or Castaneda technique. Some properties of the agent revealed a size of 0.22-0.33 µm, a unique developmental-cycle and it was considered a large virus with bacterial affinities (38). 8 Chapter 1 For diagnostic purposes, culture was a quite cumbersome procedure. Laboratory associated infections occurred and the poor growth in culture of some strains were major problems. Therefore serologic tests were developed quite soon after the discovery of the causative agent. In 1935 Bedson and co-workers described the complement fixation reaction (CF) (2). With this test it was possible to diagnose psittacosis when the “virus” could not be grown. But for many years this method was not very standardized concerning the antigen used and the amount of complement added (16). Despite these shortcomings , it became the preferred method for detection of psittacosis cases. In the 1950’s it became clear that psittacosis could be effectively treated with tetracycline. In 1966 all “viruses” in the psittacosis-lymphogranuloma venereum group were finally assigned to the bacterial genus Chlamydia. (48). Already in 1928 psittacosis became a notifiable disease in the Netherlands. The disease was included in the “wet op de besmettelijke ziekten” (law for the prevention of infectious diseases). In the Netherlands, one of the first reports on psittacosis was by Herderschêe in 1930 (31). Six people were described who had close contact with recently acquired parrots. Two of them died and again the main pathologic finding was pneumonia. In 1937, laboratories in Amsterdam succeeded in isolating the “psittacosis virus” from a patient with “atypical pneumonia” by use of mouse inoculation. They stained the “virus” with the modified Castaneda technique according to Bedson. By use of the CF test they were able to find serologic evidence for presumed psittacosis patients in the Netherlands, but they were unable to isolate the “virus” (72). In 1949 Dekking pointed at racing pigeons as a potential source for infection (17). Quite soon thereafter, several authors described cases of psittacosis related to parakeets and pigeons (5,7,34). Most of these cases were diagnosed by serological tests (CF). 9 Chapter 1 Microbiology The bacterium The causative agent of psittacosis is Chlamydophila psittaci . This pathogen is an obligate intracellular Gram-negative bacterium. Chlamydophila psittaci (formerly Chlamydia psittaci ) has, like all other members of the order Chlamydiales , a unique developmental-cycle which was already recognized by Bland and Canti in 1935. Two distinct forms of this pathogen are recognized: the extracellular infectious, spore-like elementary bodies (EB) and the intracellular non-infectious fragile, metabolically active reticulate bodies (RB). The EB is approximately 0.3 µm in size and derives its rigidity from intensive disulfide bridges between the cysteine rich residues in the so-called cysteine rich outer membrane envelope proteins ( envA and envB ). The RB is about 1 µm in size and is the replicative form. The developmental cycle starts with attachment and entry of the EB. Invasion is probably by receptor mediated endocytosis. To date the precise structure of the receptor is still unknown. Once inside the cell the EB’s are surrounded by a membrane bound vacuole termed an inclusion that avoids fusion with lysosomes. In the case of C. trachomatis infection, after entry, EB inclusions start to fuse into larger vacuoles. This fusion is not observed in C. caviae
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