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Ricketssiaceae
This document summarizes various Rickettsiaceae genera including Rickettsia, Orientia, Ehrlichia, Coxiella, and Bartonella. It describes their characteristics such as being small, gram-negative, obligate intracellular parasites transmitted by arthropod vectors. Specific diseases caused by each genus are outlined, such as typhus fever caused by Rickettsia transmitted by lice and fleas, scrub typhus caused by Orientia transmitted by chiggers, and Q fever caused by Coxiella transmitted between animals and humans. Laboratory diagnosis and treatment options are also briefly discussed.
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Ricketssiaceae
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- 2. Synopsis • Genus Rickettsia •Genus Orientia • Genus Ehrlichia ---------------------------------------------------------------- • Genus Coxiella • Genus Bartonella
- 3. Introduction • Intracellular growth •Transmitted by blood sucking arthropod vectors • Howard Taylor ricketts (1906) – Discovered spotted fever rickettsia – died of typhus fever contracted during his studies
- 5. Characteristics • Small GNB •Virus like , cannot be seen under ordinary light microscope • Obligate intracellular parasite
- 7. TYPHUS FEVER GROUP •Epidemic typhus • Recrudescent typhus (Brill Zinsser disease) • Endemic typhus
- 8. Epidemic typhus • Causativeagent: R.prowazekii • Vertebrate host : Humans • Human body louse : Pediculus humanus corporis
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- 10. • Pathogenesis: Lice becomeinfected by feeding on ricketssiaemic patients multiply in the gut of lice appear in feces in 3 to 5 days infection transmitted from person to person • When the contaminated louse feces is rubbed through the minute abrasions caused by scratching • Occasionally by aersols of dried louse feces through inhalation or through the conjuctiva
- 11. • Incubation periodis 5 to 15 days • Fever with chills • Characteristic rash – 4th or 5th day • Stuporous and delirious • Case fatality – 40%
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- 13. Recrudescent typhus • Latentinfection in whom recovered from epidemic typhus • Reactivation • Hence no extrahuman reservoir
- 14. Endemic typhus • Causativeagent: R. typhi • Host: Rats, Humans • Vector: Flea – Xenopsylla cheopsis • Pathogenesis: Rickettsia multiplies in the gut of the flea shed in faeces humans
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- 16. • Humans acquirethe disease: 1. The bite of infected fleas, when their saliva or feces is rubbed in 2. Through aerosols of dried feces 3. By ingesting food recently contaminated with infected rat urine or flea feces Human infection is a dead end PERSON TO PERSON TRANSMISSION DOES NOT OCCUR
- 17. SPOTTED FEVER GROUP •Common soluble antigen • Multiply in the nucleus as well as in the cytoplasm of host cells • All transmitted by ticks except R.akari (Mite borne) • Tick typhus • Rickettsial pox
- 18. Tick typhus • Transovariantransmission – in ticks – both vector and reservoir • Larval stage or adult ticks – infective form to vertebrate hosts • Transmitted to human by tick bite
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- 20. • Rocky mountainspotted fever – most serious type • Causative agent : R.rickettsii • Indian tick typhus – R.conori • Tick: Rhipicephalus sanguineus
- 21. Rickettsial pox • Selflimited, non fatal, vesicular exanthem • Similar to chicken pox • Vesicular or varicelliform rickettsiosis • Causative agent: R.akari • Reservoir : Domestic mouse • Vector : mite (Transovarial transmission)
- 22. Pathogenesis in humans •Transmitted to humans by arthropod vectors through bite or feces • Ricketssaie multiply locally and enter the blood • Localised chiefly in the vascular endothelial cells thrombus formation occlusion of vascular lumen
- 23. • Clinical features: acute febrile illness, septicemia with maculopapular rash and fever • The long survival of rickettsiae in various organs and lymphatic tissues in infected humans and animals is a distinctive feature in its pathogenesis.
- 25. Specimen • Smears frominfected tissues • Blood
- 26. Morphology • Pleomorphic coccobacilli •Non motile , non capsulated • 0.3 – 0.6 * 0.8 – 2 um • Gram negative, but do not stain well • Under electron microscope three layered cell wall
- 27. cultivation • Unable togrow in cell free media • Growth occurs in the cytoplasm of infected cells • Optimum temperature – 32 to 35deg C • Cultivated in yolk sac of developing chick embryos, also grow on HeLa, Hep-2, Detroit 6 continuous cell lines
- 28. Resistance • Rapidly destroyedat 56degC • Destroyed at room temp also • Hence when seperated from host preserve in skimmed milk or a suspending medium containing sucrose, potassium phosphate and glutamate (SPG medium)
- 29. Antigenic structure • Spottedfever rickettsiae A, B proteins • Third surface antigen alkali stable polysaccharide found in some rickettsiae and in some strains of the Proteus bacilli
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- 31. Neil Mooser Reaction •R.typhi and R.prowazekii – similar • When male guinea pigs are inoculated intraperitoneally with blood from a case of endemic typhus or with a culture of R.typhi develop fever and characteristic scrotal inflammation. • Scrotum enlarged and testes cannot be pushed back into the abdomen because of inflammatory adhesions between the layers of the tunica vaginalis • Neil – Mooser or tunica reaction
- 33. GENUS ORIENTIA SCRUB TYPHUS(CHIGGER BORNE TYPHUS): • Causative agent: Orientia tsutsugamushi • First observed in Japan • Vector: trombiculid mites • Mite islands • Humans bitten by mite larvae (Chiggers) • Transovarian transmission in mites
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- 35. • Zoonotic tetrad O.tsutsugamushi, chiggers, rats and secondary and transitional forms of vegetation • Incubation period – 1 to 3 weeks • Characteristic Eschar, regional lymphadenopathy and maculopapular rash • Three antigenic types : Karp, Gilliam and Kato
- 37. GENUS EHRLICHIA • Small,Gram negative, obligate intracellular bacteria • Tick borne • Cytoplasm of infected phagocytic cells grow within phagosomes as mulberry like clusters Morula
- 38. • Pathogenicity: Threeinfections 1. Resembles glandular fever. Causative agent is Ehrlichia sennetsu. Endemic in Japan. Causes lymphoid hyperplasia and atypical lymphocytosis. No arthropod vector. Human infection is suspected to be caused by ingestion of fish with flukes
- 39. • 2. Humanmonocytic ehrlichiosis – caused by Ehrlichia chaffeensis. Transmitted by Amblyomma ticks. Deer and rodents are reservoir hosts. Human disease with leukopenia, thrombocytopenia and elevated liver enzymes
- 40. • 3. Humangranulocytic ehrlichiosis – either identical with or closely related to equine pathogen Ehrlichia equi. Transmitted by ticks. Deer, cattle and sheep are the suspected reservoir. Leucopenia and thrombocytopenia are seen in patients • Treatment: Doxycline for ehrlichiosis
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- 42. Specimens • Blood forculture • Tissue for culture • Serum for serological tests
- 43. Direct Microscopy • Lightmicroscope cant see individual organism, only aggregations of rickettsial particles • Giemsa stain purple coloured basophilic inclusions • Machiavello stain red coloured inclusions • Immunofluorescence microscope skin biopsies from the centre of the petechial lesions
- 45. Culture • Yolk sacof embryonated hen`s eggs • Male guinea pigs or mice • Tissue culture
- 46. Serological test Weil felixreaction: • Agglutination test in which sera are tested for agglutinins to the O antigens of certain non motile Proteus strains OX 19, OX2, OX K • Due to sharing of antigen by ricketssiae and certain strain of proteus • Tube agglutination test
- 48. Other serological tests •Complement fixation test • ELISA • RIA
- 49. Molecular methods • Polymerasechain reaction
- 50. TREATMENT • Tetracycline • Chloramphenicol •Ciprofloxacin
- 52. GENUS COXIELLA • Coxiellaburnetii • Causative agent of Q fever ( Query) • Pleomorphic bacilli • Obligate intracellular pathogen • Differs from rickettsia by being 1. More resistant to heat 2. No vector
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- 54. • Weil felixtest cannot be used to diagnose • Infection is from cattle , sheep and goats • Zoonotic disease • Bandicoot are the reservoir • Transmitted to cattle by ixodid ticks • Shed in milk of infected animals and transmitted to humans
- 55. Pathogenicity • Human diseasecharacterised by interstitial pneumonia • Coxiella may remain latent in the tissues of patients of 2 to 3 years
- 56. Laboratory diagnosis • Bloodfor microscopy • Culture and serum for serological test • PCR
- 57. Treatment • Tetracycline • Macrolideantibiotics
- 59. GENUS BARTONELLA • TinyGNB • Transmitted by arthropods • Pathogenic strains 1. B.bacilliformis 2. B.quintana 3. B.henselae
- 60. Bartonella bacilliformis • Oroyafever • High mortality • Late sequel verruga peruana • 1885 – Medical student Daniel Carrion inoculated himself with material from verruga and developed oroya fever and died • Carrion`s disease
- 61. Bartonella quintana • Firstworld war trench fever or five day fever (Million of cases) • No animal reservoir • Transmitted by body louse • Ability to grow in blood agar
- 62. Bartonella henselae • Febrileillness with lymphadenopathy following a cat scratch Cat scratch disease • Isolated from the blood of patients in blood media after prolonged incubation • Demonstrated in lymph node biospy smears and sections by Warthin-Starry staining
- 63. • Associated withHIV infected and immunodeficient personns • Bacillary angiomatosis
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