Treponema Pallidum Ssp

Total Page:16

File Type:pdf, Size:1020Kb

Treponema Pallidum Ssp SPIROCHAETALES Katalin Kristóf 2014 Spirochaetales • 2 Familiae • Spirochetaceae • Treponema • Borrelia • Leptospiraceae • Leptospira Common feature: ••• thin, coiled, spiral shaped bacteria Length: 10-30 µm ••• Too thin (0,1-0,2 µµµm) to be seen with light microscopy stained with Gram => Darkfield illumination; IF; silver-impregnation • periplasmic flagellae (endoflagellae) Spirochaetales Associated Human Diseases Genus Species Disease Treponema pallidum ssp. pallidum Syphilis pallidum ssp. endemicum Bejel pallidum ssp. pertenue Yaws carateum Pinta Borrelia burgdorferi Lyme disease (borreliosis) recurrentis Epidemic relapsing fever Many species Endemic relapsing fever Leptospira interrogans Leptospirosis (Weil’s Disease) Treponemal infections Apathogen: T. minutum, T. reiteri, T. denticola, T. phagedenis Plaut-Vincent angina Nonvenereal Treponemal diseases (treponematosis): • Treponema pallidum ssp. endemicum ⇒ bejel (endemic syphilis) - spread person to person by contaminated eating utensils - initial oral lesions, secondary skin lesions - Africa, Asia, Australia (endemic) • Treponema pallidum ssp. pertenue ⇒ yaws - granulomatosous disease, skin lesion - South America, Central Africa, Southeast Asia • Treponema carateum ⇒pinta - skin lesions – spread by direct contact with infected lesions - South America Lues tests – positive! Vincent’s angina Ulcerative tonsillitis causing tissue necrosis often due to extension of acute ulcerative gingivitis Fusobacterium nucleatum in combination with oral spirochates (Treponema vincentii and others) causes the fusospirochaetal infections Treponema pallidum Morphology: - thin, coiled spirochetes (0,1 to 0,2 X 6-20 µm) - Three periplasmic flagellae are inserted at each ends (endoflagellae) - Outer membrane proteins: - TrompI, TrompII, TrompIII - Inner proteins:15kDa, 17kDa, 45.5kDa, 47kDa (endoflagellum, cytoplasma membrane, cytoplasma) Multiplication : by binary transverse fission Cultivation: can not be cultivated on cell-free artificial culture media - Kept alive in rabbit testis ! - rabbit epithelial cells (GT 30h, only a few generations) Treponema pallidum – virulance factors, pathogenesis • Outer membrane proteins promote adherence to host cells • Hyaluronidase may facilitate perivascular infiltration • Coating of fibronectin protects against phagocytosis • Tissue destruction primarily results from host’s immune response to infection • Destroy cytoplasma membrane, mitochondrial membrane => Cholesterol, Lecithine, Kardiolipin Ag free ( RPR, VDRL) • Endarteriitis, Periarteriitis» inflammation, necrosis • T-cell dependent late hypersensitivity »Granuloma • Gumma I. Acquired syphilis (venereal disease) Spread: sexually (STD) The “great imitator”! 3 phases: 1) primary phase – 1-2 weeks incubaton period - The initial syphylitic chancre develops at the site where the spirochete is inoculated - Generally on the genitalia, rare: oral cavity, perianal region - localised replication of bacteria =>Papule, macule =>erodes => chancre – ulcus durum: hard, painless ulceration - Painless lymphotic nodes „bubo indolens” - mucocutan lesion is very infectious! - spontaneous remission may occur after 2-6 weeks (50%) 2. Stage develops after 4 to 8 weeks from the primer infection (haematogen spreading) disseminated disease - with generalised mucocutaneous rash , - superficial sores (mucous patches) may occur on mucous membranes of the mouth, vagina, or anus, - while wart-like lesions called condylomata lata may form in moist intertriginous areas. - Hepatitis - Neurological signs - High fever Highly - micropolyadenopathy contagious! - spontaneous remission may occur; after 1-2 years these symptoms can reoccur latent persistence 3. Stage (late phase) after 3-30 years from the primer infection - all tissues are involved - gumma (granulomatous lesions) in bone, vessels, skin - neurosyphilis: tabes dorsalis, paralysis progressiva (encephalopathy), ataxia, dementia, N. opticus degeneration - cardiovascular syphilis: aortitis, aorta aneurysm (rupture) Progression of Untreated Syphilis Late benign Gummas in skin and soft tissues Tertiary Stage II. Congenital (connatal) syphilis • T pallidum subsp pallidum also damages foetuses (from 4 gw) • Approximately 50 percent of foetuses are aborted or stillborn ; • In early congenital syphilis (before the age of two years ~ II): mucocutaneous lesions, osteochondritis, anaemia, and hepatosplenomegaly. • In late congenital syphilis (> 4 years, ~III) : interstitial keratitis and blindness, tooth deformation (notched incisors and moon molars), eighth-nerve deafness, neurosyphilis, rhagades (fissures at mucocutaneous junctions), cardiovascular lesions, Clutton's joints (fluid accumulation on knee), and bone deformation of the legs, nasal septum, and hard palate. • Can be preventing with penicillin treatment of the Treponema infected pregnant woman! early congenital syphilis late congenital syphilis • Plexus brachialis • Hutchinson's triad: paralysis • interstitial keratitis, • notched incisors • and eighth-nerve deafness • Tibia deformation Hutchinson’s teeth – the incisors are smaller than normal, with sloping sides and central semilunar notches. Diagnosis • Sample: exudates, punctuates from the mucocutan lesion, (1-2 phase) • Microscopy: • Too slender (0,1-0,2 µm) to be seen with light microscopy stained with Gram • Live treponemes can be visualized by using dark-field microscopy • (rapid rotation about its longitudinal axis and bending, flexing, and snapping about its full length) • Fluorescent labelled antitreponemal antibodies • Silver-impregnation • PCR • Serology Serology I. Non specific treponemal II. Specific treponemal tests tests reaginic antibodies detection of specific - developed against lipids released from Immobilizin Ab ( treponemal) damaged cells during the early stage of disease and present on the cell surface of the treponema • TPIT • KKR • FTA-Abs • VDRL • TPHA, TPPA • RPR • TP-ELISA • Western Blot, Immunoblot Ag: Cardiolipin (from extraction of Treponemal Ag: TP proteins, beef heart), lecitin, cholesterol lipoproteins I. Non –treponemal tests • VDRL-test (Venereal Disease Research Laboratory) - Ag = freshly prepared cardiolipin suspension - patient's serum is inactivated at 56 oC, for 30 min - a drop of the cardiolipin suspension is placed on a glass slide - mixed with a drop of the inactivated serum Negative: Cardiolipin suspension remain dispersed. Positive: Cardiolipin forms visible clumps when combining with reagin. • RPR –test (Rapid Plasma Reagin) Ag = cardiolipin suspension attached to latex particles patient's serum should not be inactivated Negative: Cardiolipin-latex suspension remains intact. Positive: Cardiolipin-latex is agglutinated and sediments as rough granula - Flocculation Flocculation: granules => Ab equally Ag Dilution of patient serum! II. (Specific) treponemal tests 1. FTA-ABS = F luorescent Treponemal Antibody-absorption • Ag = killed, fixed T.pallidum on glass slide • Overlayed with the patient’s serum, which has been mixed with an extract of nonpathogenic treponemes (T. reiteri ) • fluorescein labelled antihuman immunglobulin (IgG, IgM) • fluorescein microscopy • The most sensitive and specific /2.TPI = Treponema pallidum immobilisation test living T.pallidum = Antigen inactivated patient’s serum, complement of guinea pigs The reaction is based on that T. pallidum cells are inhibited in their movement if they are exposed to specific IgG antibodies in the presence of complement. Negative: T. pallidum cells exhibit locomotion. Positive: T. pallidum cells do not show movement. / II. Treponemal tests 3.TPHA, TPPA T. pallidum ha emagglutination test • T. pallidum particle agglutination • Bird red blood cells sensitized • Gelatin particles sensitized with T. with T. pallidum antigens pallidum antigens (E.coli Tp15, Tp17, Tp 47 - (Bacillus subtilis Tp15, Tp17,Tp47 - recombinant) recombinant) • Neg/Pos (1:80) • Neg/Pos (1:80) • Titer • Titer • IgG, IgM and IgA • IgG, IgM and IgA II. Treponemal tests: 4. TP-ELISA • Rekombinant Ag-s Tp15, Tp17, Tp47 II. Treponemal tests: 5. Western blot • Immunoblot strip • 15, 17, 45.5 and 47 kDa recombinant proteins • IgG, IgM BAP (biologically aspecific positivity) : Sensitivity of serological tests in untreated syphilis Test Primary Secondary Latent Tertiary VDRL 78 (74-87) 100 95 (88-100) 71 (37-94) RPR 86 (77-99) 100 98 (95-100) 73 FTA-ABS 84 (70-100) 100 100 96 Treponemal 76 (69-90) 100 97 (97-100) 94 Agglutination EIA 93 100 100 The use of only one type of serologic test is insufficient for diagnosis. Summary of serological tests: For screening • TPPA/TPHA • FTA-Abs • Tp-ELISA For verification • Western blot RPR/ VDRL • Determination of the stage • To monitor the effectiveness of therapy • To detect reinfection Treatment, control • penicillin treatment eradicates all stages, including congenital infection in pregnancy • /Doxycyclin, Azithromycin/ • Jarisch-Herxheimer • lysis of the treponemes causes the release of huge amount antigenes => high fever, anaphylaxia, abortion • (steroid) Prevention: safe sex • For sex partners of patients with syphilis in any stage: • Draw syphilis serology • Perform physical exam • Congenital - Can be preventing with penicillin treatment of the Treponema infected pregnant woman – screening! Epidemiology of Borrelia Infections Borrelia Pediculus humanus recurrentis Ornithodoros spp. Borrelia spp. Ixodes spp. Borrelia burgdorferi Borrelia genus • Morphology: 4- 18 µm, spirochete, have fewer coils. Seven to twenty periplasmic flagella originate at each end and overlap
Recommended publications
  • LYME DISEASE Other Names: Borrelia Burgdorferi
    LYME DISEASE Other names: Borrelia burgdorferi CAUSE Lyme disease is caused by a spirochete bacteria (Borrelia burgdorferi) that is transmitted through the bite from an infected arthropod vector, the black-legged or deer tick Ixodes( scapularis). SIGNIFICANCE Lyme disease can infect people and some species of domestic animals (cats, dogs, horses, and cattle) causing mild to severe illness. Although wildlife can be infected by the bacteria, it typically does not cause illness in them. TRANSMISSION The bacteria has been observed in the blood of a number of wildlife species including several bird species but rarely appears to cause illness in these species. White-footed mice, eastern chipmunks, and shrews serve as the primary natural reservoirs for Lyme disease in eastern and central parts of North America. Other species appear to have low competencies as reservoirs for the bacteria. The transmission of Lyme disease is relatively convoluted due to the complex life cycle of the black-legged tick. This tick has multiple developmental stages and requires three hosts during its life cycle. The life cycle begins with the eggs of the ticks that are laid in the spring and from which larval ticks emerge. Larval ticks do not initially carryBorrelia burgdorferi, the bacteria must be acquired from their hosts they feed upon that are carriers of the bacteria. Through the summer the larval ticks feed on the blood of their first host, typically small mammals and birds. It is at this point where ticks may first acquireBorrelia burgdorferi. In the fall the larval ticks develop into nymphs and hibernate through the winter.
    [Show full text]
  • Are You Suprised ?
    B DAMB 721 Microbiology Final Exam B 100 points December 11, 2006 Your name (Print Clearly): _____________________________________________ I. Matching: The questions below consist of headings followed by a list of phrases. For each phrase select the heading that best describes that phrase. The headings may be used once, more than once or not at all. Mark the answer in Part 2 of your answer sheet. 1. capsid 7. CD4 2. Chlamydia pneumoniae 8. Enterococcus faecalis 3. oncogenic 9. hyaluronidase 4. pyruvate 10. interferon 5. Koplik’s spot 11. hydrophilic viruses 6. congenital Treponema pallidum 12. Streptococcus pyogenes 1. “spreading factor” produced by members of the staphylococci, streptococci and clostridia 2. viral protein coat 3. central intermediate in bacterial fermentation 4. persistant endodontic infections 5. a cause of atypical pneumonia 6. nonspecific defense against viral infection 7. has a rudimentary life cycle 8. HIV receptor 9. Hutchinson’s Triad 10. measles 11. resistant to disinfection 12. β-hemolytic, bacitracin sensitive, cause of suppurative pharyngitis 2 Matching (Continued): The questions below consist of diseases followed by a list of etiologic agents. Match each disease with the etiologic agent. Continue using Part 2 of your answer sheet. 1. dysentery 6. Legionnaire’s 2. botulism 7. gas gangrene 3. cholera 8. tuberculosis 4. diphtheria 9. necrotizing fascitis 5. enteric fever 10. pneumoniae/meningitis 13. Clostridium botulinum 14. Vibrio cholera 15. Mycobacterium bovis 16. Shigella species 17. Streptococcus pneumoniae 18. Clostridium perfringens 19. Salmonella typhi 20. Streptococcus pyogenes 3 II. Multiple Choice: Choose the ONE BEST answer. Mark the correct answer on Part 1 of the answer sheet.
    [Show full text]
  • Pronunciation Guide to Microorganisms
    Pronunciation Guide to Microorganisms This pronunciation guide is provided to aid each student in acquiring a greater ease in discussing, describing, and using specific microorganisms. Please note that genus and species names are italicized. If they cannot be italicized, then they should be underlined (example: a lab notebook). Prokaryotic Species Correct Pronunciation Acetobacter aceti a-se-toh-BAK-ter a-SET-i Acetobacter pasteurianus a-se-toh-BAK-ter PAS-ter-iann-us Acintobacter calcoacetius a-sin-ee-toe-BAK-ter kal-koh-a-SEE-tee-kus Aerococcus viridans (air-o)-KOK-kus vi-ree-DANS Agrobacterium tumefaciens ag-roh-bak-TEAR-ium too-me-FAY-she-ens Alcaligenes denitrificans al-KAHL-li-jen-eez dee-ni-TREE-fee-cans Alcaligenes faecalis al-KAHL-li-jen-eez fee-KAL-is Anabaena an-na-BEE-na Azotobacter vinelandii a-zoe-toe-BAK-ter vin-lan-DEE-i Bacillus anthracis bah-SIL-lus AN-thray-sis Bacillus lactosporus bah-SIL-lus LAK-toe-spore-us Bacillus megaterium bah-SIL-lus Meg-a-TEER-ee-um Bacillus subtilis bah-SIL-lus SA-til-us Borrelia recurrentis bore-RELL-ee-a re-kur-EN-tis Branhamella catarrhalis bran-hem-EL-ah cat-arr-RAH-lis Citrobacter freundii sit-roe-BACK-ter FROND-ee-i Clostridium perfringens klos-TREH-dee-um per-FRINGE-enz Clostridium sporogenes klos-TREH-dee-um spore-AH-gen-ease Clostridium tetani klos-TREH-dee-um TET-ann-ee Corynebacterium diphtheriae koh-RYNE-nee-back-teer-ee-um dif-THEE-ry-ee Corynebacterium hofmanni koh-RYNE-nee-back-teer-ee-um hoff-MAN-eye Corynebacterium xerosis koh-RYNE-nee-back-teer-ee-um zer-OH-sis Enterobacter
    [Show full text]
  • Canine Lyme Borrelia
    Canine Lyme Borrelia Borrelia burgdorferi bacteria are the cause of Lyme disease in humans and animals. They can be visualized by darkfild microscopy as "corkscrew-shaped" motile spirochetes (400 x). Inset: The black-legged tick, lxodes scapularis (deer tick), may carry and transmit Borrelia burgdorferi to humans and animals during feeding, and thus transmit Lyme disease. Samples: Blood EDTA-blood as is, purple-top tubes or EDTA-blood preserved in sample buffer (preferred) Body fluids Preserved in sample buffer Notes: Send all samples at room temperature, preferably preserved in sample buffer MD Submission Form Interpretation of PCR Results: High Positive Borrelia spp. infection (interpretation must be correlated to (> 500 copies/ml swab) clinical symptoms) Low Positive (<500 copies/ml swab) Negative Borrelia spp. not detected Lyme Borreliosis Lyme disease is caused by spirochete bacteria of a subgroup of Borrelia species, called Borrelia burgdorferi sensu lato. Only one species, B. burgdorferi sensu stricto, is known to be present in the USA, while at least four pathogenic species, B. burgdorferi sensu stricto, B. afzelii, B. garinii, B. japonica have been isolated in Europe and Asia (Aguero- Rosenfeld et al., 2005). B. burgdorferi sensu lato organisms are corkscrew-shaped, motile, microaerophilic bacteria of the order Spirochaetales. Hard-shelled ticks of the genus Ixodes transmit B. burgdorferi by attaching and feeding on various mammalian, avian, and reptilian hosts. In the northeastern states of the US Ixodes scapularis, the black-legged deer tick, is the predominant vector, while at the west coast Lyme borreliosis is maintained by a transmission cycle which involves two tick species, I.
    [Show full text]
  • Borrelia Burgdorferi and Treponema Pallidum: a Comparison of Functional Genomics, Environmental Adaptations, and Pathogenic Mechanisms
    PERSPECTIVE SERIES Bacterial polymorphisms Martin J. Blaser and James M. Musser, Series Editors Borrelia burgdorferi and Treponema pallidum: a comparison of functional genomics, environmental adaptations, and pathogenic mechanisms Stephen F. Porcella and Tom G. Schwan Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, NIH, Hamilton, Montana, USA Address correspondence to: Tom G. Schwan, Rocky Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840, USA. Phone: (406) 363-9250; Fax: (406) 363-9445; E-mail: [email protected]. Spirochetes are a diverse group of bacteria found in (6–8). Here, we compare the biology and genomes of soil, deep in marine sediments, commensal in the gut these two spirochetal pathogens with reference to their of termites and other arthropods, or obligate parasites different host associations and modes of transmission. of vertebrates. Two pathogenic spirochetes that are the focus of this perspective are Borrelia burgdorferi sensu Genomic structure lato, a causative agent of Lyme disease, and Treponema A striking difference between B. burgdorferi and T. pal- pallidum subspecies pallidum, the agent of venereal lidum is their total genomic structure. Although both syphilis. Although these organisms are bound togeth- pathogens have small genomes, compared with many er by ancient ancestry and similar morphology (Figure well known bacteria such as Escherichia coli and Mycobac- 1), as well as by the protean nature of the infections terium tuberculosis, the genomic structure of B. burgdorferi they cause, many differences exist in their life cycles, environmental adaptations, and impact on human health and behavior. The specific mechanisms con- tributing to multisystem disease and persistent, long- term infections caused by both organisms in spite of significant immune responses are not yet understood.
    [Show full text]
  • Investigation of the Lipoproteome of the Lyme Disease Bacterium
    INVESTIGATION OF THE LIPOPROTEOME OF THE LYME DISEASE BACTERIUM BORRELIA BURGDORFERI BY Alexander S. Dowdell Submitted to the graduate degree program in Microbiology, Molecular Genetics & Immunology and the Graduate Faculty of the University of Kansas in partial fulfillment of the requirements for the degree of Doctor of Philosophy. _____________________________ Wolfram R. Zückert, Ph.D., Chairperson _____________________________ Indranil Biswas, Ph.D. _____________________________ Mark Fisher, Ph.D. _____________________________ Joe Lutkenhaus, Ph.D. _____________________________ Michael Parmely, Ph.D. Date Defended: April 27th, 2017 The dissertation committee for Alexander S. Dowdell certifies that this is the approved version of the following dissertation: INVESTIGATION OF THE LIPOPROTEOME OF THE LYME DISEASE BACTERIUM BORRELIA BURGDORFERI _____________________________ Wolfram R. Zückert, Ph.D., Chairperson Date Approved: May 4th, 2017 ii Abstract The spirochete bacterium Borrelia burgdorferi is the causative agent of Lyme borreliosis, the top vector-borne disease in the United States. B. burgdorferi is transmitted by hard- bodied Ixodes ticks in an enzootic tick/vertebrate cycle, with human infection occurring in an accidental, “dead-end” fashion. Despite the estimated 300,000 cases that occur each year, no FDA-approved vaccine is available for the prevention of Lyme borreliosis in humans. Development of new prophylaxes is constrained by the limited understanding of the pathobiology of B. burgdorferi, as past investigations have focused intensely on just a handful of identified proteins that play key roles in the tick/vertebrate infection cycle. As such, identification of novel B. burgdorferi virulence factors is needed in order to expedite the discovery of new anti-Lyme therapeutics. The multitude of lipoproteins expressed by the spirochete fall into one such category of virulence factor that merits further study.
    [Show full text]
  • Information to Users
    INFORMATION TO USERS This manuscript bas been reproJuced from the microfilm master. UMI films the text directly ftom the original or copy submitted. Thus, sorne thesis and dissertation copies are in typewriter face, while others may be itom any type ofcomputer printer. The quality oftbis reproduction is depeDdeDt apoD the quality of the copy sablDitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthlough, substandard margins, and improper alignment can adversely affect reproduction. In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will he noted. Also, if unauthorized copyright material had to be removed, a note will indicate the deletion. Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, beginning at the upper left-hand corner and continuing trom left to right in equal sections with sma1l overlaps. Each original is a1so photographed in one exposure and is included in reduced fonn at the back orthe book. Photographs ineluded in the original manuscript have been reproduced xerographically in this copy. Higher quality 6" x 9" black and white photographie prints are available for any photographs or illustrations appearing in this copy for an additional charge. Contact UMI directly to order. UMI A Bell & Howell Information Company 300 North Zeeb Raad, ADn AJbor MI 48106-1346 USA 313n61-4700 8OO1S21~ NOTE TO USERS The original manuscript received by UMI contains pages with slanted print. Pages were microfilmed as received. This reproduction is the best copy available UMI Oral spirochetes: contribution to oral malodor and formation ofspherical bodies by Angela De Ciccio A thesis submitted to the Faculty ofGraduate Studies and Research, McGill University, in partial fulfillment ofthe requirements for the degree ofMaster ofScience.
    [Show full text]
  • Relapsing Fever in Young Refugees from East Africa Spinello Antinori1,2* , Valeria Colombo1 and Mario Corbellino1,2
    Antinori et al. Critical Care (2017) 21:205 DOI 10.1186/s13054-017-1777-z LETTER Open Access Relapsing fever in young refugees from East Africa Spinello Antinori1,2* , Valeria Colombo1 and Mario Corbellino1,2 See related letter by Cutuli et al. https://ccforum.biomedcentral.com/articles/10.1186/s13054-017-1666-5 We read with interest the letter by Cutuli et al. [1] leptospirosis, all other findings can be observed in describing a case of severe co-infection by Leptospira patients with severe clinical presentation of both dis- spp. and Borrelia recurrentis in a young female refugee eases. However, in the recent wave of LBRF observed in from East Africa. We would like to comment on several Europe, intensivists were faced with severe cases of issues raised by their paper. LBRF presenting with shock solely as a consequence of First, the authors state “nits were present on her the Jarisch-Herxheimer reaction precipitated by adminis- scalp…”. In our opinion, this sentence may mislead tration of antibiotics [4]. readers as meaning that “head lice” (Pediculus humanus A final point that deserves comment concerns the capitis) are the vectors of louse-borne relapsing fever microbiology diagnosis. Molecular biology by means of (LBRF). Indeed, body lice (Pediculus humanus humanus) real-time polymerase chain reaction in this case pro- are to date the only demonstrated vectors of the disease. vided the correct diagnosis of both infections. Although We are aware of only two reports providing proof that not clearly stated, the authors report that malaria was head lice can harbor B. recurrentis and consequently excluded among other possible differential diagnoses.
    [Show full text]
  • The Relapsing Fever Agent Borrelia Hermsii Has Multiple
    Copyright Q 1992 by the Genetics Societyof America The Relapsing Fever AgentBorrelia hermsii Has Multiple Copiesof Its Chromosome and Linear Plasmids Todd Kitten and Alan G. Barbour Departments of Microbiology and Medicine, The Universityof Texas Health Science Center, Sun Antonio, Texas 78284 Manuscript received March 17, 1992 Accepted for publicationJune 25, 1992 ABSTRACT Borrelia hermsii, a spirochete which causes relapsing fever in humans and other mammals, eludes the immune responseby antigenic variationof the “Vmp” proteins.This occurs by replacement of an expressed vrnp gene with a copy of a silent vrnp gene. Silent and expressedvrnp genes are located on separate linearplasmids. To further characterize vrnp recombination, copy numbers were determined for two linear plasmids and for the l-megabase chromosome by comparing hybridization of probes to native DNA with hybridization to recombinant plasmids containing borrelial DNA. Plasmid copy numbers were also estimated by ethidium bromide fluorescence. Total cellular DNA content was determined by spectrophotometry. For borreliasgrown in mice, copy numbers and 95% confidence intervals were 14 (12-17)for an expression plasmid,8 (7-9) for a silent plasmid, and 16 (13-18) for the chromosome. Borrelias grown in broth mediumhad one-fourth to one-half this number of plasmids and chromosomes. Staining of cells with4’,6-diamidino-2-phenylindole revealed DNA to be distributed throughout most of the spirochete’s length. These findings indicate that borrelias organize their total cellular DNA into several complete genomes and thatcells undergoing serotype switches do one or more of the following: (1) coexpress Vmps from switched and unswitched expression plasmids for at least three to five generations, (2)suppress transcription from some expressionplasmid copies, or (3) partition expression plasmids nonrandomly.The lower copy number ofthe silentplasmid indicates that nonreciprocal Vmp gene recombination may result from loss of recombinant silent ” plasmids by segregation.
    [Show full text]
  • Product Description EN Bactoreal® Kit Chlamydiaceae
    Product Description BactoReal® Kit Chlamydiaceae For research only, not for diagnostic use BactoReal® Kit Chlamydiaceae Order no. Reactions Pathogen Internal positive control DVEB03113 100 FAM channel Cy5 channel DVEB03153 50 FAM channel Cy5 channel DVEB03111 100 FAM channel VIC/HEX channel DVEB03151 50 FAM channel VIC/HEX channel Kit contents: Detection assay for Chlamydia and Chlamydophila species Detection assay for internal positive control (control of amplification) DNA reaction mix (contains uracil-N glycosylase, UNG) Positive control for Chlamydiaceae Water Background: The Chlamydiaceae family currently includes two genera and one candidate genus: genus Chlamydia (including the species Chlamydia muridarum, Chlamydia suis, Chlamydia trachomatis), genus Chlamydophila (including the species Chlamydophila abortus, Chlamydophila caviae Chlamydophila felis, Chlamydia pecorum, Chlamydophila pneumoniae, Chlamydophila psittaci), and candidatus Clavochlamydia. All Chlamydiaceae are obligate intracellular Gram-negative bacteria that cause diseases in humans and animals worldwide. Description: BactoReal® Kit Chlamydiaceae is based on the amplification and detection of the 23S rRNA gene of C. muridarum, C. suis, C. trachomatis, C. abortus, C. caviae, C. felis, C. pecorum, C. pneumoniae and C. psittaci using real-time PCR. It allows the rapid and sensitive detection of the 23S rRNA gene of Chlamydiaceae from DNA samples purified from different sample material (e.g. with the QIAamp DNA Mini Kit). For subtyping please contact ingenetix. PCR-platforms: BactoReal® Kit Chlamydiaceae is developed and validated for the ABI PRISM® 7500 instrument (Life Technologies), LightCycler® 480 (Roche) and Mx3005P® QPCR System (Agilent), but is also suitable for other real-time PCR instruments. Sensitivity and specificity: BactoReal® Kit Chlamydiaceae detects at least 10 copies/reaction.
    [Show full text]
  • Import of an Extinct Disease?
    OBSERVATION Pinta in Austria (or Cuba?) Import of an Extinct Disease? Ingrid Woltsche-Kahr, MD; Bruno Schmidt, PhD; Werner Aberer, MD; Elisabeth Aberer, MD Background: Pinta, 1 of the 3 nonvenereal treponema- detection of spirochetes in the trunk lesion indicated early toses, is supposed to be extinct in most areas in South and secondary syphilis, but an extensive case history and the Central America, where it was once endemic. Only scat- clinical appearance fulfilled all criteria for pinta. tered foci may still remain in remote areas in the Brazilian rain forest, and the last case from Cuba was reported in 1975. Conclusion: The acquisition of a distinct clinical en- tity, pinta, in a country where it was formerly endemic Observation: A native Austrian woman, who had lived but now is believed to be extinct raises the question of for 7 years in Cuba and was married to a Cuban native, whether the disease is in fact extinct or whether syphilis developed a singular psoriasiform plaque on her trunk and pinta are so similar that no definite distinction is pos- and several brownish papulosquamous lesions on her sible in certain cases. palms and soles during a visit to her home in Austria. Positive serological findings for active syphilis and the Arch Dermatol. 1999;135:685-688 HE NONVENEREAL trepone- after the appearance of pintids), lesions matoses yaws, endemic marked by vitiligolike depigmentation are syphilis (bejel), and pinta the leading feature. These lesions are not are caused by an organism believed to be infectious. Histopathologi- that is morphologically and cal investigations show moderate acan- Tantigenically identical to the causative agent thosis, spongiosis, sometimes hyperkera- of venereal syphilis, Treponema pallidum.
    [Show full text]
  • Taxonomy JN869023
    Species that differentiate periods of high vs. low species richness in unattached communities Species Taxonomy JN869023 Bacteria; Actinobacteria; Actinobacteria; Actinomycetales; ACK-M1 JN674641 Bacteria; Bacteroidetes; [Saprospirae]; [Saprospirales]; Chitinophagaceae; Sediminibacterium JN869030 Bacteria; Actinobacteria; Actinobacteria; Actinomycetales; ACK-M1 U51104 Bacteria; Proteobacteria; Betaproteobacteria; Burkholderiales; Comamonadaceae; Limnohabitans JN868812 Bacteria; Proteobacteria; Betaproteobacteria; Burkholderiales; Comamonadaceae JN391888 Bacteria; Planctomycetes; Planctomycetia; Planctomycetales; Planctomycetaceae; Planctomyces HM856408 Bacteria; Planctomycetes; Phycisphaerae; Phycisphaerales GQ347385 Bacteria; Verrucomicrobia; [Methylacidiphilae]; Methylacidiphilales; LD19 GU305856 Bacteria; Proteobacteria; Alphaproteobacteria; Rickettsiales; Pelagibacteraceae GQ340302 Bacteria; Actinobacteria; Actinobacteria; Actinomycetales JN869125 Bacteria; Proteobacteria; Betaproteobacteria; Burkholderiales; Comamonadaceae New.ReferenceOTU470 Bacteria; Cyanobacteria; ML635J-21 JN679119 Bacteria; Proteobacteria; Betaproteobacteria; Burkholderiales; Comamonadaceae HM141858 Bacteria; Acidobacteria; Holophagae; Holophagales; Holophagaceae; Geothrix FQ659340 Bacteria; Verrucomicrobia; [Pedosphaerae]; [Pedosphaerales]; auto67_4W AY133074 Bacteria; Elusimicrobia; Elusimicrobia; Elusimicrobiales FJ800541 Bacteria; Verrucomicrobia; [Pedosphaerae]; [Pedosphaerales]; R4-41B JQ346769 Bacteria; Acidobacteria; [Chloracidobacteria]; RB41; Ellin6075
    [Show full text]